COLLAGEN DISEASES characterized by brittle, osteoporotic, and easily fractured bones. It may also present with blue sclerae, loose joints, and imperfect dentin formation. Most types are autosomal dominant and are associated with mutations in COLLAGEN TYPE I.
The process of bone formation. Histogenesis of bone including ossification.
Bone lengthening by gradual mechanical distraction. An external fixation device produces the distraction across the bone plate. The technique was originally applied to long bones but in recent years the method has been adapted for use with mandibular implants in maxillofacial surgery.
Bone-forming cells which secrete an EXTRACELLULAR MATRIX. HYDROXYAPATITE crystals are then deposited into the matrix to form bone.
Renewal or repair of lost bone tissue. It excludes BONY CALLUS formed after BONE FRACTURES but not yet replaced by hard bone.
A biosynthetic precursor of collagen containing additional amino acid sequences at the amino-terminal and carboxyl-terminal ends of the polypeptide chains.
Process by which organic tissue becomes hardened by the physiologic deposit of calcium salts.
A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.
The largest and strongest bone of the FACE constituting the lower jaw. It supports the lower teeth.
A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly conserved DNA-binding domain known as the runt domain and is involved in genetic regulation of skeletal development and CELL DIFFERENTIATION.
The SKELETON of the HEAD including the FACIAL BONES and the bones enclosing the BRAIN.
External devices which hold wires or pins that are placed through one or both cortices of bone in order to hold the position of a fracture in proper alignment. These devices allow easy access to wounds, adjustment during the course of healing, and more functional use of the limbs involved.
Bone-marrow-derived, non-hematopoietic cells that support HEMATOPOETIC STEM CELLS. They have also been isolated from other organs and tissues such as UMBILICAL CORD BLOOD, umbilical vein subendothelium, and WHARTON JELLY. These cells are considered to be a source of multipotent stem cells because they include subpopulations of mesenchymal stem cells.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC
Extracellular substance of bone tissue consisting of COLLAGEN fibers, ground substance, and inorganic crystalline minerals and salts.
A potent osteoinductive protein that plays a critical role in the differentiation of osteoprogenitor cells into OSTEOBLASTS.
The bony deposit formed between and around the broken ends of BONE FRACTURES during normal healing.
The second longest bone of the skeleton. It is located on the medial side of the lower leg, articulating with the FIBULA laterally, the TALUS distally, and the FEMUR proximally.
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
The most common form of fibrillar collagen. It is a major constituent of bone (BONE AND BONES) and SKIN and consists of a heterotrimer of two alpha1(I) and one alpha2(I) chains.
X-RAY COMPUTERIZED TOMOGRAPHY with resolution in the micrometer range.
A bone fixation technique using an external fixator (FIXATORS, EXTERNAL) for lengthening limbs, correcting pseudarthroses and other deformities, and assisting the healing of otherwise hopeless traumatic or pathological fractures and infections, such as chronic osteomyelitis. The method was devised by the Russian orthopedic surgeon Gavriil Abramovich Ilizarov (1921-1992). (From Bull Hosp Jt Dis 1992 Summer;52(1):1)
Thin outer membrane that surrounds a bone. It contains CONNECTIVE TISSUE, CAPILLARIES, nerves, and a number of cell types.
An autosomal dominant disorder of tooth development characterized by opalescent dentin resulting in discoloration of the teeth. The dentin develops poorly with low mineral content while the pulp canal is obliterated.
Intraoral OSTEOTOMY of the lower jaw usually performed in order to correct MALOCCLUSION.
The growth and development of bones from fetus to adult. It includes two principal mechanisms of bone growth: growth in length of long bones at the epiphyseal cartilages and growth in thickness by depositing new bone (OSTEOGENESIS) with the actions of OSTEOBLASTS and OSTEOCLASTS.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The physiological restoration of bone tissue and function after a fracture. It includes BONY CALLUS formation and normal replacement of bone tissue.
Vitamin K-dependent calcium-binding protein synthesized by OSTEOBLASTS and found primarily in BONES. Serum osteocalcin measurements provide a noninvasive specific marker of bone metabolism. The protein contains three residues of the amino acid gamma-carboxyglutamic acid (Gla), which, in the presence of CALCIUM, promotes binding to HYDROXYAPATITE and subsequent accumulation in BONE MATRIX.
The differentiation of pre-adipocytes into mature ADIPOCYTES.
The development of bony substance in normally soft structures.
A highly glycosylated and sulfated phosphoprotein that is found almost exclusively in mineralized connective tissues. It is an extracellular matrix protein that binds to hydroxyapatite through polyglutamic acid sequences and mediates cell attachment through an RGD sequence.
The growth action of bone tissue as it assimilates surgically implanted devices or prostheses to be used as either replacement parts (e.g., hip) or as anchors (e.g., endosseous dental implants).
Mature osteoblasts that have become embedded in the BONE MATRIX. They occupy a small cavity, called lacuna, in the matrix and are connected to adjacent osteocytes via protoplasmic projections called canaliculi.
The longest and largest bone of the skeleton, it is situated between the hip and the knee.
The formation of cartilage. This process is directed by CHONDROCYTES which continually divide and lay down matrix during development. It is sometimes a precursor to OSTEOGENESIS.
Abnormally small jaw.
A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter.
Fractures of the lower jaw.
Bone-growth regulatory factors that are members of the transforming growth factor-beta superfamily of proteins. They are synthesized as large precursor molecules which are cleaved by proteolytic enzymes. The active form can consist of a dimer of two identical proteins or a heterodimer of two related bone morphogenetic proteins.
The surgical cutting of a bone. (Dorland, 28th ed)
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The stable placement of surgically induced fractures of the mandible or maxilla through the use of elastics, wire ligatures, arch bars, or other splints. It is used often in the cosmetic surgery of retrognathism and prognathism. (From Dorland, 28th ed, p636)
Diseases of BONES.
A type of fibrous joint between bones of the head.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Synthetic or natural materials for the replacement of bones or bone tissue. They include hard tissue replacement polymers, natural coral, hydroxyapatite, beta-tricalcium phosphate, and various other biomaterials. The bone substitutes as inert materials can be incorporated into surrounding tissue or gradually replaced by original tissue.
Increase in the longest dimension of a bone to correct anatomical deficiencies, congenital, traumatic, or as a result of disease. The lengthening is not restricted to long bones. The usual surgical methods are internal fixation and distraction.
The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth.
A non-vascular form of connective tissue composed of CHONDROCYTES embedded in a matrix that includes CHONDROITIN SULFATE and various types of FIBRILLAR COLLAGEN. There are three major types: HYALINE CARTILAGE; FIBROCARTILAGE; and ELASTIC CARTILAGE.
Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.
Breaks in bones.
Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere.
Genes whose loss of function or gain of function MUTATION leads to the death of the carrier prior to maturity. They may be essential genes (GENES, ESSENTIAL) required for viability, or genes which cause a block of function of an essential gene at a time when the essential gene function is required for viability.
Cell growth support structures composed of BIOCOMPATIBLE MATERIALS. They are specially designed solid support matrices for cell attachment in TISSUE ENGINEERING and GUIDED TISSUE REGENERATION uses.
The continuous turnover of BONE MATRIX and mineral that involves first an increase in BONE RESORPTION (osteoclastic activity) and later, reactive BONE FORMATION (osteoblastic activity). The process of bone remodeling takes place in the adult skeleton at discrete foci. The process ensures the mechanical integrity of the skeleton throughout life and plays an important role in calcium HOMEOSTASIS. An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as OSTEOPOROSIS.
The amount of mineral per square centimeter of BONE. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by X-RAY ABSORPTIOMETRY or TOMOGRAPHY, X RAY COMPUTED. Bone density is an important predictor for OSTEOPOROSIS.
The grafting of bone from a donor site to a recipient site.
The mineral component of bones and teeth; it has been used therapeutically as a prosthetic aid and in the prevention and treatment of osteoporosis.
Organic compounds which contain P-C-P bonds, where P stands for phosphonates or phosphonic acids. These compounds affect calcium metabolism. They inhibit ectopic calcification and slow down bone resorption and bone turnover. Technetium complexes of diphosphonates have been used successfully as bone scanning agents.
Fractures occurring as a result of disease of a bone or from some undiscoverable cause, and not due to trauma. (Dorland, 27th ed)
Generating tissue in vitro for clinical applications, such as replacing wounded tissues or impaired organs. The use of TISSUE SCAFFOLDING enables the generation of complex multi-layered tissues and tissue structures.
Artificial substitutes for body parts and materials inserted into organisms during experimental studies.
General disorders of the sclera or white of the eye. They may include anatomic, embryologic, degenerative, or pigmentation defects.
A plant family of the order Rhamnales, subclass Rosidae class Magnoliopsida. The plants have a characteristic silvery or rusty-colored sheen, caused by tiny distinctive scales. Flowers have a tubular structure of four sepals. Root nodules host the Frankia (ACTINOMYCETES) nitrogen-fixing symbionts.
Removal of mineral constituents or salts from bone or bone tissue. Demineralization is used as a method of studying bone strength and bone chemistry.
The inner and longer bone of the FOREARM.
Persistent flexure or contracture of a joint.
A condition in which one of a pair of legs fails to grow as long as the other, which could result from injury or surgery.
Preprosthetic surgery involving rib, cartilage, or iliac crest bone grafts, usually autologous, or synthetic implants for rebuilding the alveolar ridge.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A family of peptidyl-prolyl cis-trans isomerases that bind to CYCLOSPORINS and regulate the IMMUNE SYSTEM. EC 5.2.1.-
The molecular unit of collagen fibrils that consist of repeating three-stranded polypeptide units arranged head to tail in parallel bundles. It is a right-handed triple helix composed of 2 polypeptide chains. It is rich in glycine, proline, hydroxyproline, and hydroxylysine.
A negatively-charged extracellular matrix protein that plays a role in the regulation of BONE metabolism and a variety of other biological functions. Cell signaling by osteopontin may occur through a cell adhesion sequence that recognizes INTEGRIN ALPHA-V BETA-3.
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
A heterogeneous group of bone dysplasias, the common character of which is stippling of the epiphyses in infancy. The group includes a severe autosomal recessive form (CHONDRODYSPLASIA PUNCTATA, RHIZOMELIC), an autosomal dominant form (Conradi-Hunermann syndrome), and a milder X-linked form. Metabolic defects associated with impaired peroxisomes are present only in the rhizomelic form.
A heterogeneous group of autosomally inherited COLLAGEN DISEASES caused by defects in the synthesis or structure of FIBRILLAR COLLAGEN. There are numerous subtypes: classical, hypermobility, vascular, and others. Common clinical features include hyperextensible skin and joints, skin fragility and reduced wound healing capability.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
An extracellular endopeptidase which excises a block of peptides at the amino terminal, nonhelical region of the procollagen molecule with the formation of collagen. Absence or deficiency of the enzyme causes accumulation of procollagen which results in the inherited connective tissue disorder--dermatosparaxis. EC
Surgical procedures used to treat disease, injuries, and defects of the oral and maxillofacial region.
Calcium salts of phosphoric acid. These compounds are frequently used as calcium supplements.
Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., COLLAGEN; ELASTIN; FIBRONECTINS; and LAMININ).
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
The area between the EPIPHYSIS and the DIAPHYSIS within which bone growth occurs.
Biocompatible materials placed into (endosseous) or onto (subperiosteal) the jawbone to support a crown, bridge, or artificial tooth, or to stabilize a diseased tooth.
A nonhormonal medication for the treatment of postmenopausal osteoporosis in women. This drug builds healthy bone, restoring some of the bone loss as a result of osteoporosis.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The properties, processes, and behavior of biological systems under the action of mechanical forces.
Congenital structural abnormalities and deformities of the musculoskeletal system.
A set of twelve curved bones which connect to the vertebral column posteriorly, and terminate anteriorly as costal cartilage. Together, they form a protective cage around the internal thoracic organs.
Premature closure of one or more CRANIAL SUTURES. It often results in plagiocephaly. Craniosynostoses that involve multiple sutures are sometimes associated with congenital syndromes such as ACROCEPHALOSYNDACTYLIA; and CRANIOFACIAL DYSOSTOSIS.
A mobile chain of three small bones (INCUS; MALLEUS; STAPES) in the TYMPANIC CAVITY between the TYMPANIC MEMBRANE and the oval window on the wall of INNER EAR. Sound waves are converted to vibration by the tympanic membrane then transmitted via these ear ossicles to the inner ear.
Genes that influence the PHENOTYPE both in the homozygous and the heterozygous state.
A bone morphogenetic protein that is widely expressed during EMBRYONIC DEVELOPMENT. It is both a potent osteogenic factor and a specific regulator of nephrogenesis.
A dark-gray, metallic element of widespread distribution but occurring in small amounts; atomic number, 22; atomic weight, 47.90; symbol, Ti; specific gravity, 4.5; used for fixation of fractures. (Dorland, 28th ed)
A bone morphogenetic protein that is a potent inducer of bone formation. It also functions as a regulator of MESODERM formation during EMBRYONIC DEVELOPMENT.
A biocompatible polymer used as a surgical suture material.
Genes that influence the PHENOTYPE only in the homozygous state.
Fractures of the femur.
A purely physical condition which exists within any material because of strain or deformation by external forces or by non-uniform thermal expansion; expressed quantitatively in units of force per unit area.
Cyanogen bromide (CNBr). A compound used in molecular biology to digest some proteins and as a coupling reagent for phosphoroamidate or pyrophosphate internucleotide bonds in DNA duplexes.
Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis (OSTEOPOROSIS, POSTMENOPAUSAL) and age-related or senile osteoporosis.
Congenital absence of or defects in structures of the jaw.
The quality of surface form or outline of CELLS.
Rods of bone, metal, or other material used for fixation of the fragments or ends of fractured bones.
Glycoproteins which contain sialic acid as one of their carbohydrates. They are often found on or in the cell or tissue membranes and participate in a variety of biological activities.
Numerical expression indicating the measure of stiffness in a material. It is defined by the ratio of stress in a unit area of substance to the resulting deformation (strain). This allows the behavior of a material under load (such as bone) to be calculated.
A fracture in which union fails to occur, the ends of the bone becoming rounded and eburnated, and a false joint occurs. (Stedman, 25th ed)
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The spinal or vertebral column.
Mandibulofacial dysostosis with congenital eyelid dermoids.
A large multinuclear cell associated with the BONE RESORPTION. An odontoclast, also called cementoclast, is cytomorphologically the same as an osteoclast and is involved in CEMENTUM resorption.
A severe form of neonatal dwarfism with very short limbs. All cases have died at birth or later in the neonatal period.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Surgical insertion of an appliance for the replacement of areas of the mandible.
An infant during the first month after birth.
A prosthetic appliance for the replacement of areas of the mandible missing or defective as a result of deformity, disease, injury, or surgery.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
The fibrous CONNECTIVE TISSUE surrounding the TOOTH ROOT, separating it from and attaching it to the alveolar bone (ALVEOLAR PROCESS).
Injuries of tissue other than bone. The concept is usually general and does not customarily refer to internal organs or viscera. It is meaningful with reference to regions or organs where soft tissue (muscle, fat, skin) should be differentiated from bones or bone tissue, as "soft tissue injuries of the hand".
A family of structurally related collagens that form the characteristic collagen fibril bundles seen in CONNECTIVE TISSUE.
Fixation and immobility of a joint.
Synthetic or natural materials, other than DRUGS, that are used to replace or repair any body TISSUES or bodily function.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Bone loss due to osteoclastic activity.
The white, opaque, fibrous, outer tunic of the eyeball, covering it entirely excepting the segment covered anteriorly by the cornea. It is essentially avascular but contains apertures for vessels, lymphatics, and nerves. It receives the tendons of insertion of the extraocular muscles and at the corneoscleral junction contains the canal of Schlemm. (From Cline et al., Dictionary of Visual Science, 4th ed)
The susceptibility of CAPILLARIES, under conditions of increased stress, to leakage.
Elements of limited time intervals, contributing to particular results or situations.
Congenital or acquired asymmetry of the face.
Polymorphic cells that form cartilage.
A bone morphogenetic protein family member that includes an active tolloid-like metalloproteinase domain. The metalloproteinase activity of bone morphogenetic protein 1 is specific for the removal of the C-propeptide of PROCOLLAGEN and may act as a regulator of EXTRACELLULAR MATRIX deposition. Alternative splicing of MRNA for bone morphogenetic protein 1 results in the production of several PROTEIN ISOFORMS.
An individual in which both alleles at a given locus are identical.
A prosthesis that gains its support, stability, and retention from a substructure that is implanted under the soft tissues of the basal seat of the device and is in contact with bone. (From Boucher's Clinical Dental Terminology, 4th ed)
The region of the HAND between the WRIST and the FINGERS.
An individual having different alleles at one or more loci regarding a specific character.
Fenestra or oval opening on the lateral wall of the vestibular labyrinth adjacent to the MIDDLE EAR. It is located above the cochlear round window and normally covered by the base of the STAPES.
Dense fibrous layer formed from mesodermal tissue that surrounds the epithelial enamel organ. The cells eventually migrate to the external surface of the newly formed root dentin and give rise to the cementoblasts that deposit cementum on the developing root, fibroblasts of the developing periodontal ligament, and osteoblasts of the developing alveolar bone.
The anteriorly located rigid section of the PALATE.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A continuous protein fiber consisting primarily of FIBROINS. It is synthesized by a variety of INSECTS and ARACHNIDS.
The curve formed by the row of TEETH in their normal position in the JAW. The inferior dental arch is formed by the mandibular teeth, and the superior dental arch by the maxillary teeth.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere.
Ocular disorders attendant upon non-ocular disease or injury.
Restoration of integrity to traumatized tissue.
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
Mice bearing mutant genes which are phenotypically expressed in the animals.
Congenital or postnatal overgrowth syndrome most often in height and occipitofrontal circumference with variable delayed motor and cognitive development. Other associated features include advanced bone age, seizures, NEONATAL JAUNDICE; HYPOTONIA; and SCOLIOSIS. It is also associated with increased risk of developing neoplasms in adulthood. Mutations in the NSD1 protein and its HAPLOINSUFFICIENCY are associated with the syndrome.
The developmental history of specific differentiated cell types as traced back to the original STEM CELLS in the embryo.
Basic glycoprotein members of the SERPIN SUPERFAMILY that function as COLLAGEN-specific MOLECULAR CHAPERONES in the ENDOPLASMIC RETICULUM.
The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve.
Artificial substitutes for body parts, and materials inserted into tissue for functional, cosmetic, or therapeutic purposes. Prostheses can be functional, as in the case of artificial arms and legs, or cosmetic, as in the case of an artificial eye. Implants, all surgically inserted or grafted into the body, tend to be used therapeutically. IMPLANTS, EXPERIMENTAL is available for those used experimentally.
A family of transcription factors that bind to the cofactor CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. Family members contain a highly conserved DNA-binding domain known as the runt domain. They can act as both activators and repressors of expression of GENES involved in CELL DIFFERENTIATION and CELL CYCLE progression.
Experimentation on, or using the organs or tissues from, a human or other mammalian conceptus in the postembryonic period, after the major structures have been outlined. In humans, this corresponds to the period from the third month after fertilization until birth.
An appreciable lateral deviation in the normally straight vertical line of the spine. (Dorland, 27th ed)
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Insertion of an implant into the bone of the mandible or maxilla. The implant has an exposed head which protrudes through the mucosa and is a prosthodontic abutment.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
A physical misalignment of the upper (maxilla) and lower (mandibular) jaw bones in which either or both recede relative to the frontal plane of the forehead.
A hydroxylated derivative of the amino acid LYSINE that is present in certain collagens.
The surgical removal of a tooth. (Dorland, 28th ed)
One of a pair of irregularly shaped bones that form the upper jaw. A maxillary bone provides tooth sockets for the superior teeth, forms part of the ORBIT, and contains the MAXILLARY SINUS.
The formation of dentin. Dentin first appears in the layer between the ameloblasts and odontoblasts and becomes calcified immediately. Formation progresses from the tip of the papilla over its slope to form a calcified cap becoming thicker by the apposition of new layers pulpward. A layer of uncalcified dentin intervenes between the calcified tissue and the odontoblast and its processes. (From Jablonski, Dictionary of Dentistry, 1992)
The maximum stress a material subjected to a stretching load can withstand without tearing. (McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed, p2001)
Biocompatible materials usually used in dental and bone implants that enhance biologic fixation, thereby increasing the bond strength between the coated material and bone, and minimize possible biological effects that may result from the implant itself.
Abnormal development of cartilage and bone.

The use of variable lactate/malic dehydrogenase ratios to distinguish between progenitor cells of cartilage and bone in the embryonic chick. (1/3582)

The activities of LDH and MDH have been studied, both in differentiated cartilage and bone from the embryonic chick, and in the pool of mixed osteogenic and chondrogenic stem cells found on the quadratojugal, a membrane bone. In confirmation of the model proposed by Reddi & Huggins (1971) we found that the LDH/MDH ratio was greater than 1 in cartilage and less than 1 in bone. Furthermore we established, for the first time, that ratios occurred in the chondrogenic and osteogenic stem cells, similar to the ratios in their differentiated counterparts. Alteration in LDH/MDH resulted from variations in the level of LDH/mug protein. MDH/mug protein remained constant, even when LDH/MDH was changing. We interpret these results in terms of adaptation of chondrogenic progenitor cells for anaerobic metabolism and anticipate that our model will be applicable to other skeletal systems where stem cells are being studied.  (+info)

Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand. (2/3582)

A receptor that mediates osteoprotegerin ligand (OPGL)-induced osteoclast differentiation and activation has been identified via genomic analysis of a primary osteoclast precursor cell cDNA library and is identical to the tumor necrosis factor receptor (TNFR) family member RANK. The RANK mRNA was highly expressed by isolated bone marrow-derived osteoclast progenitors and by mature osteoclasts in vivo. Recombinant OPGL binds specifically to RANK expressed by transfected cell lines and purified osteoclast progenitors. Transgenic mice expressing a soluble RANK-Fc fusion protein have severe osteopetrosis because of a reduction in osteoclasts, similar to OPG transgenic mice. Recombinant RANK-Fc binds with high affinity to OPGL in vitro and blocks osteoclast differentiation and activation in vitro and in vivo. Furthermore, polyclonal Ab against the RANK extracellular domain promotes osteoclastogenesis in bone marrow cultures suggesting that RANK activation mediates the effects of OPGL on the osteoclast pathway. These data indicate that OPGL-induced osteoclastogenesis is directly mediated through RANK on osteoclast precursor cells.  (+info)

Hindlimb patterning and mandible development require the Ptx1 gene. (3/3582)

The restricted expression of the Ptx1 (Pitx1) gene in the posterior half of the lateral plate mesoderm has suggested that it may play a role in specification of posterior structures, in particular, specification of hindlimb identity. Ptx1 is also expressed in the most anterior ectoderm, the stomodeum, and in the first branchial arch. Ptx1 expression overlaps with that of Ptx2 in stomodeum and in posterior left lateral plate mesoderm. We now show that targeted inactivation of the mouse Ptx1 gene severely impairs hindlimb development: the ilium and knee cartilage are absent and the long bones are underdeveloped. Greater reduction of the right femur size in Ptx1 null mice suggests partial compensation by Ptx2 on the left side. The similarly sized tibia and fibula of mutant hindlimbs may be taken to resemble forelimb bones: however, the mutant limb buds appear to have retained their molecular identity as assessed by forelimb expression of Tbx5 and by hindlimb expression of Tbx4, even though Tbx4 expression is decreased in Ptx1 null mice. The hindlimb defects appear to be, at least partly, due to abnormal chondrogenesis. Since the most affected structures derive from the dorsal side of hindlimb buds, the data suggest that Ptx1 is responsible for patterning of these dorsal structures and that as such it may control development of hindlimb-specific features. Ptx1 inactivation also leads to loss of bones derived from the proximal part of the mandibular mesenchyme. The dual role of Ptx1 revealed by the gene knockout may reflect features of the mammalian jaw and hindlimbs that were acquired at a similar time during tetrapod evolution.  (+info)

The development of the fetal sternum: a cross-sectional sonographic study. (4/3582)

OBJECTIVE: To assess the relationship between gestational age and sonographic appearance of the various sternal components and establish growth during human gestation. DESIGN: A prospective cross-sectional study. METHODS: The study was performed on 252 consecutive normal singleton pregnancies from 19 weeks of gestation until term, using transabdominal high-resolution ultrasound techniques. The sternal length, as well as the number of ossification centers at each gestational age, were recorded. RESULTS: The first occasion at which a fetal human sternum could be visualized with two to three ossification centers was at 19 weeks' gestational age. The fifth ossification center was first visualized at 29 weeks' gestation. The mean +/- SE of sternal length varied from 15 +/- 0.98 mm (95% confidence interval (CI) 12.79-17.21) at 19-20 weeks, to 36.50 +/- 0.29 mm (95% CI 35.58-37.42) at 37-38 weeks' gestation. Sternal length as a function of gestational age was expressed by the regression equation: sternal length (mm) = -11.06 + 1.39 x gestational age (weeks). The correlation coefficient, r = 0.924 for sternal length, was found to be highly statistically significant (p < 0.0001). CONCLUSIONS: The presented data offer normative measurements of the fetal sternum which may be helpful in the prenatal diagnosis of congenital syndromes that include, among other manifestations, abnormalities of sternal development.  (+info)

Effect of strontium on the epiphyseal cartilage plate of rat tibiae-histological and radiographic studies. (5/3582)

Following dietary administration of strontium carbonate, histological and radiographic changes in the epiphyseal cartilage plate of the rat tibiae were examined in the present study. The weight gain of the rat fed a strontium diet was less than that of the control rats. Longitudinal growth of tibiae and endochondral ossification were inhibited by strontium administration. The widths of both proximal and distal cartilage plates increased enormously as has also been shown by other investigators. Sizes of chondroblasts in columns of proximal cartilage plate in rats fed a strontium diet were smaller than those of the control rats and were not different between upper and lower parts. It is suggested that strontium inhibits bone growth through the inhibitory action on the maturation process of chondroblasts and the succeeding endochondral ossification.  (+info)

A quantitative assessment of the healing of intramembranous and endochondral autogenous bone grafts. (6/3582)

The aim of the study was to assess quantitatively the amount of new bone formed in the early stages of healing of intramembranous and endochondral autogenous bone grafts so as to gain further insight into their integration with host bone. Eighteen critical size defects were created in the parietal bone of nine New Zealand White rabbits. In the experimental group (five rabbits), each rabbit was grafted with intramembranous bone in one defect and with endochondral bone in the other. In the control group (four rabbits), one defect was left empty (passive control) and the other was grafted with rabbit skin collagen (active control). After 14 days, the rabbits were killed and the defects were prepared for histological analysis. Serial sections were made across the whole defect. Each defect was divided into five regions spaced 1500 microns apart. Two sections were randomly drawn from each region. Quantitative analysis was performed on 100 sections using an image analyser computer software system to assess the amount of new bone formed in each defect. No bone was detected across the defect in either the active or passive controls. One-hundred-and-sixty-six per cent more new bone was formed in defects grafted with intramembranous bone than those grafted with endochondral bone. This represented an extremely significant difference (P < 0.0001, unpaired t-test) between the two groups. The results show that intramembranous autogenous bone produced more bone than the endochondral bone when grafted in the skull. Clinically, it is recommended that intramembranous bone is used to replace lost membranous bone in the oral cavity, as well as in skull defects, whenever possible.  (+info)

Differential patterns of altered bone formation in different bone compartments in established osteoporosis. (7/3582)

AIM: To investigate the level of bone formation in the different bone compartments in cases of established osteoporosis, as previous work has concentrated on trabecular bone alone. METHODS: Bone formation rates were measured histomorphometrically, in the periosteal (P), cortical (C), subcortical (SC), and trabecular (T) compartments in iliac crest biopsies from 159 patients with established osteoporosis. The values were standardised using age and sex matched control data and patterns of differential change determined by analysis of parametric status (increased, normal, reduced). RESULTS: Mean bone formation was reduced in all four compartments. This was more marked (4.4/4.1 standard deviations below the mean in C/T, v 2.3/0.9 in P/SC) and more frequent (reduced in 81.5%/78.3% in T/C, v 43.3%/44% in P/SC) in the trabecular and cortical compartments than in the periosteal or subcortical bone. Parametric status was equal in trabecular and cortical bone in 85.4% of cases, and in periosteal and subcortical bone in 65.7%, but in all four compartments in only 35.1%, indicating differential alteration of bone formation in the two sets of compartments (T/C v P/SC). CONCLUSIONS: Altered trabecular bone formation is important in osteoporosis, but there are differential patterns of alteration in the other three compartments, emphasising the presence of different microenvironments in bone; thus the effect on the cortical compartment was similar to that on the trabecular, while the subcortical and periosteal compartments also showed linkage. The linkage between the two pairs was divergent, indicating different control of bone formation, with resultant different patterns of perturbation in osteoporosis.  (+info)

Effects of XT-44, a phosphodiesterase 4 inhibitor, in osteoblastgenesis and osteoclastgenesis in culture and its therapeutic effects in rat osteopenia models. (8/3582)

We have reported that denbufylline, a phosphodiesterase 4 (PDE4) inhibitor, inhibits bone loss in Walker256/S tumor-bearing rats, suggesting therapeutic potentiality of a PDE4 inhibitor in osteopenia. In the present study, effects of a new PDE4 inhibitor, 1-n-butyl-3-n-propylxanthine (XT-44), in bone were evaluated in cell cultures and animal experiments. In rat bone marrow culture, XT-44 stimulated mineralized-nodule formation, whereas it inhibited osteoclast-like cell formation in mouse bone marrow culture. In Walker256/S-bearing rats (6-week-old female Wistar Imamichi rats), rapid decrease in bone mineral density (BMD) was prominent, and oral administration of XT-44 (0.3 mg/kg, every 2 days) inhibited the decrease in BMD. In the second animal experiment, female Wistar rats (6-week-old) were sciatic neurectomized, and XT-44 was orally administered to these rats every 2 days for 4 weeks. XT-44 administration (0.3 mg/kg) recovered BMD in these neurectomized animals. Furthermore, 19-week-old, female Wistar rats were ovariectomized (OVX), and 15 weeks after surgery, these rats were orally administered XT-44 every 2 days for 8 weeks. XT-44 treatment (1 mg/kg) increased the BMD of OVX rats. These results indicate that XT-44 could be a candidate as a therapeutic drug for treating osteopenia including osteoporosis.  (+info)

Merck and Plasticell of London, UK, today announced the availability of OsteoMAX-XF™, the first fully defined, xeno-free human mesenchymal stem cell differentiation medium for the differentiation of mesenchymal stem cells into osteocytes.
Zhang, Z.-Y., Chong, M.S.K., Teoh, S.-H., Schantz, J.T., Fisk, N.M., Choolani, M.A., Chan, J. (2009). Superior osteogenic capacity for bone tissue engineering of fetal compared with perinatal and adult mesenchymal stem cells. Stem Cells 27 (1) : 126-137. [email protected] Repository. ...
TY - JOUR. T1 - Bioactive glass induced osteogenic differentiation of human adipose stem cells is dependent on cell attachment mechanism and mitogen-activated protein kinases. AU - Wang, Xiaoju. AU - Hyväri, L.. AU - Kellomäki, M.. AU - Hupa, Leena. AU - Vanhatupa, S.. AU - Miettinen, S.. N1 - oorganisk kemi. PY - 2018. Y1 - 2018. N2 - Bioactive glasses (BaGs) are widely utilised in bone tissue engineering (TE) but the molecular response of cells to BaGs is poorly understood. To elucidate the mechanisms of cell attachment to BaGs and BaG-induced early osteogenic differentiation, we cultured human adipose stem cells (hASCs) on discs of two silica-based BaGs S53P4 (23.0 Na2O - 20.0 CaO - 4.0 P2O5 - 53.0 SiO2 (wt-%)) and 1-06 (5.9 Na2O - 12.0 K2O - 5.3 MgO - 22.6 CaO - 4.0 P2O5 - 0.2 B2O3 - 50.0 SiO2) in the absence of osteogenic supplements. Both BaGs induced early osteogenic differentiation by increasing alkaline phosphatase activity (ALP) and the expression of osteogenic marker genes RUNX2a ...
The use of biomaterials to direct osteogenic differentiation of human mesenchymal stem cells (hMSCs) in. the absence of osteogenic supplements is thought to be part of the next generation of orthopedic. implants. We previously engineered surface-roughness gradients of average roughness (Ra) varying from. the sub-micron to the micrometer range (0.5-4.7 μm), and mean distance between peaks (RSm) gradually. varying from 214 μm to 33 μm. Here we have screened the ability of such surface-gradients of. polycaprolactone to influence the expression of alkaline phosphatase (ALP), collagen type 1 (COL1) and. mineralization by hMSCs cultured in dexamethasone (Dex)-deprived osteogenic induction medium. (OIM) and in basal growth medium (BGM). Ra 1.53 μm/RSm 79 μm in Dex-deprived OI medium,. and Ra 0.93 μm/RSm 135 μm in BGM consistently showed higher effectiveness at supporting the. expression of the osteogenic markers ALP, COL1 and mineralization, compared to the tissue culture polystyrene. (TCP) ...
When DArcy Wentworth Thompsons On Growth and Form was published 100 years ago, it raised the question of how biological forms arise during development and across evolution. In light of the advances in molecular and cellular biology since then, a succinct modern view of the question states: how do genes encode geometry? Our new special issue is packed with articles that use mathematical and physical approaches to gain insights into cell and tissue patterning, morphogenesis and dynamics, and that provide a physical framework to capture these processes operating across scales.. Read the Editorial by guest editors Thomas Lecuit and L. Mahadevan, as they provide a perspective on the influence of DArcy Thompsons work and an overview of the articles in this issue.. ...
Here, we aimed to investigate osteogenic differentiation of human adipose-derived stem cells (hASCs) in three-dimensional (3D) bioprinted tissue constructs in vitro and in vivo. A 3D Bio-plotter dispensing system was used for building 3D constructs. Cell viability was determined using live/dead cell staining. After 7 and 14 days of culture, real-time quantitative polymerase chain reaction (PCR) was performed to analyze the expression of osteogenesis-related genes (RUNX2, OSX, and OCN). Western blotting for RUNX2 and immunofluorescent staining for OCN and RUNX2 were also performed. At 8 weeks after surgery, osteoids secreted by osteogenically differentiated cells were assessed by hematoxylin-eosin (H&E) staining, Masson trichrome staining, and OCN immunohistochemical staining. Results from live/dead cell staining showed that most of the cells remained alive, with a cell viability of 89%, on day 1 after printing. In vitro osteogenic induction of the 3D construct showed that the expression levels ...
Supplementary Materials1. tumorigenesis. Previously, we set up a book system technology for inducing a quiescent stem cell-like stage only using an individual extracellular proteoglycan, fibromodulin (FMOD), circumventing gene transduction. In this scholarly study, we additional purified and considerably elevated the reprogramming price of the produce multipotent FMOD reprogrammed (FReP) cells. We also shown the molecular blueprint of FReP cell osteogenic differentiation by gene profiling. Radiographic evaluation demonstrated that implantation of FReP cells right into a critical-sized SCID mouse calvarial defect, added to the sturdy osteogenic capacity for FReP cells within a complicated medically relevant traumatic situation were verified by histological and immunohistochemical staining. Used together, weve provided a protracted potency, basic safety, and molecular profile of FReP cell-based bone tissue regeneration. As a result, FReP cells present a higher potential for mobile and gene ...
Estrogen receptor‐α (ERα) is crucial for the adaptive response of bone to loading but the role of endogenous estradiol (E2) for this response is unclear. To determine in vivo the ligand dependency and relative roles of different ERα domains for the osteogenic response to mechanical loading, gene‐targeted mouse models with (1) a complete ERα inactivation (ERα−/−), (2) specific inactivation of activation function 1 (AF‐1) in ERα (ERαAF‐10), or (3) specific inactivation of ERαAF‐2 (ERαAF‐20) were subjected to axial loading of tibia, in the presence or absence (ovariectomy [ovx]) of endogenous E2. Loading increased the cortical bone area in the tibia mainly as a result of an increased periosteal bone formation rate (BFR) and this osteogenic response was similar in gonadal intact and ovx mice, demonstrating that E2 (ligand) is not required for this response. Female ERα−/− mice displayed a severely reduced osteogenic response to loading with changes in cortical area ...
Stanford University Background: Stem cell-based bone engineering has shown great promise as an approach for treating patients with skeletal defects. FACS has identified CD90+ ASCs with enhanced osteogenesis. More recently, inhibition of Noggin (NOG) has been shown to leave endogenously produced BMPs relatively unopposed, also resulting in enhanced osteogenesis. The present study investigated the potential of a combinatorial approach, employing both an isolation of CD90+ ASCs via FACS and modulation of BMP signaling, to optimize bone regeneration.. Methods: Magnet assisted transfection was used to deliver minicircle (MC) NOG shRNA into CD90+ and unsorted cells. These cells were then treated with ODM in vitro. Alkaline phosphatase and quantification were performed on Day 7, alizarin red staining and quantification on Day 14. Osteogenic gene expression was examined by qRT-PCR. For evaluation of in vivo osteogenesis, critical-sized calvarial defects in nude mice were treated with a novel ...
In the present study, we investigated the effect of Notch signaling on BMP9-induced osteogenic differentiation in MSCs, and the possible mechanism underlying this process. Our findings suggested that Notch signaling can enhance the activity of BMP9 to induce osteogenic differentiation in MSCs, and this effect may be partly mediated by upregulation of ALK2.. BMP9, also called GDF-2, is one of the least studied BMPs (44). Numerous studies have indicated that BMP9 has pivotal biological functions in the areas of liver fibrosis, iron metabolism, cartilage formation and angiopoiesis, and recent studies have shown that BMP9 is the strongest inducer of osteogenic differentiation, which has been regarded as a potential factor in tissue engineering (45). The studies concerning BMP9-induced osteogenesis mechanism are conducive to its application in bone-related diseases. Previous research has indicated that fibroblast growth factor 2 (FGF2) inhibits BMP9-induced osteogenic differentiation by blocking ...
Addressing the problem of vascularization is of vital importance when engineering three-dimensional (3D) tissues. Endothelial cells are increasingly used in tissue-engineered constructs to obtain prevascularization and to enhance in vivo neovascularization. Rat bone marrow stromal cells were cultured in thermoresponsive dishes under osteogenic conditions with human umbilical vein endothelial cells (HUVECs) to obtain homotypic or heterotypic cell sheets (CSs). Cells were retrieved as sheets from the dishes after incubation at 20 °C. Monoculture osteogenic CSs were stacked on top of homotypic or heterotypic CSs, and subcutaneously implanted in the dorsal flap of nude mice for 7 days. The implants showed mineralized tissue formation under both conditions. Transplanted osteogenic cells were found at the new tissue site, demonstrating CS bone-inductive effect. Perfused vessels, positive for human CD31, confirmed the contribution of HUVECs for the neovascularization of coculture CS constructs. ...
Preclinical and clinical studies suggest a possible role for cyclooxygenases in bone repair and create concerns about the use of nonsteroidal antiinflammatory drugs in patients with skeletal injury. We utilized wild-type, COX-1-/-, and COX-2-/- mice to demonstrate that COX-2 plays an essential role in both endochondral and intramembranous bone formation during skeletal repair. The healing of stabilized tibia fractures was significantly delayed in COX-2-/- mice compared with COX-1-/- and wild-type controls. The histology was characterized by a persistence of undifferentiated mesenchyme and a marked reduction in osteoblastogenesis that resulted in a high incidence of fibrous nonunion in the COX-2-/- mice. Similarly, intramembranous bone formation on the calvaria was reduced 60% in COX-2-/- mice following in vivo injection of FGF-1 compared with either COX-1-/- or wild-type mice. To elucidate the mechanism involved in reduced bone formation, osteoblastogenesis was studied in bone marrow stromal ...
TY - JOUR. T1 - Circulating osteogenic cells. T2 - Implications for injury, repair, and regeneration. AU - Pignolo, Robert J.. AU - Kassem, Moustapha. PY - 2011/8/1. Y1 - 2011/8/1. N2 - The aim of this review is to provide a critical reading of recent literature pertaining to the presence of circulating, fluid-phase osteoblastic cells and their possible contribution to bone formation. We have termed this group of cells collectively as circulating osteogenic precursor (COP) cells. We present evidence for their existence, methods used for their isolation and identification, possible physiological and pathophysiological roles, cellular origins, and possible mechanisms for their migration to target tissues.. AB - The aim of this review is to provide a critical reading of recent literature pertaining to the presence of circulating, fluid-phase osteoblastic cells and their possible contribution to bone formation. We have termed this group of cells collectively as circulating osteogenic precursor (COP) ...
The most promising attempts to achieve bone regeneration artificially are based on the application of mediators such as bone morphogenetic proteins (BMPs) directly to the deficient tissue site. BMPs, as promoters of the regenerative process, have the ability to induce de novo bone formation in various tissues, and many animal models have demonstrated their high potential for ectopic and orthotopic bone formation. However, the biological activity of the soluble factors that promote bone formation in vivo is limited by diffusion and degradation, leading to a short half-life. Local delivery remains a problem in clinical applications. Several materials, including hydroxyapatite, tricalcium phosphate, demineralised bone matrices, poly-lactic acid homo- and heterodimers, and collagen have been tested as carriers and delivery systems for these factors in a sustained and appropriate manner. Unfortunately these delivery vehicles often have limitations in terms of biodegradability, inflammatory and immunological
Although numerous spinal biologics are commercially available, a cost-effective and safe bone graft substitute material for spine fusion has yet to be proven. In this study, 3D-Paints containing varying volumetric ratios of hydroxyapatite (HA) and human demineralized bone matrix (DBM) in a poly(lactide-co-glycolide) elastomer were three-dimensional (3D) printed into scaffolds to promote osteointegration in rats, with an end goal of spine fusion without the need for recombinant growth factor. Spine fusion was evaluated by manual palpation, and osteointegration and de novo bone formation within scaffold struts were evaluated by laboratory and synchrotron microcomputed tomography and histology. The 3:1 HA:DBM composite…. ...
In the present study, it was demonstrated that icariin promoted osteogenic differentiation by upregulating BMAL1 expression through BMP signaling in BMSCs. These findings suggested that BMAL1 plays a critical role in icariin-mediated osteogenic differentiation.. In fact, a circadian clock exists in every cell of the human body. The central players in these are BMAL1 encoded by the gene ARNTL and clock circadian regulator (CLOCK) by the gene CLOCK (19). BMSCs are stem cells with the ability to differentiate in vitro into adipocytes, osteoblasts and cartilage-forming chondroblasts (20). Regardless of its exact developmental origin, the function of the circadian clock gene is related to the behavior of various stem cells involved in homeostasis and repair of bone and adipose tissue (21). A recent report revealed impairment of osteogenic differentiation of BMSCs from BMAL1−/− mice (5). This finding was in line with our present study as well as an observational study that showed that the numbers ...
Previously reported that that FTO-knock out mice display postnatal growth retardation, which manifests as reduced body weight and bone mineral density (Guo et al., 2011); however, the molecular mechanism by which FTO stimulates osteogenic differentiation remains unknown. Here, we demonstrate for the first time that FTO stimulates osteogenic differentiation by inducing mild ER stress. The results of the current study illustrate one mechanism underlying the role of FTO in osteogenic differentiation. A relationship between FTO and AMPK has been previously reported (Pitman et al., 2013; Wu et al., 2017). One study demonstrated that AMPK decreases lipid accumulation in skeletal muscle cells by suppressing FTO expression (Wu et al., 2017). Another study revealed that knockdown of FTO reduces phosphorylation of AMPK in Alzheimers disease (Pitman et al., 2013). The current study demonstrated that activation of AMPK markedly increased expression of FTO and that a positive feedback loop existed between ...
Osteogenic lineage commitment is often evaluated by analyzing gene expression. However, many genes are transiently expressed during differentiation. The availability of genes for expression is influenced by epigenetic state, which affects the heterochromatin structure. DNA methylation, a form of epigenetic regulation, is stable and heritable. Therefore, analyzing methylation status may be less temporally dependent and more informative for evaluating lineage commitment. Here we analyzed the effect of mechanical stimulation on osteogenic differentiation by applying fluid shear stress for 24 hr to osteocytes and then applying the osteocyte-conditioned medium (CM) to progenitor cells. We analyzed gene expression and changes in DNA methylation after 24 hr of exposure to the CM using quantitative real-time polymerase chain reaction and bisulfite sequencing. With fluid shear stress stimulation, methylation decreased for both adipogenic and osteogenic markers, which typically increases availability of ...
Adult mesenchymal progenitor cells have enormous potential for use in regenerative medicine. However, the true identity of the progenitors in vivo and their progeny has not been precisely defined. We hypothesize that cells expressing a smooth muscle α-actin promoter (αSMA) directed Cre transgene represent mesenchymal progenitors of adult bone tissue. By combining complementary colors in combination with transgenes activating at mature stages of the lineage we characterized the phenotype and confirmed the ability of isolated αSMA+ cells to progress from a progenitor to fully mature state. In vivo lineage tracing experiments using a new bone formation model confirmed the osteogenic phenotype of αSMA+ cells. In vitro analysis of the in vivo labeled SMA9+ cells supported their differentiation potential into mesenchymal lineages. Utilizing a fracture-healing model, αSMA+ cells served as a pool of fibrocartilage and skeletal progenitors. Confirmation of the transition of αSMA+ progenitor cells to mature
There is an urgent need of synthetic bone grafts with enhanced osteogenic capacity. This can be achieved by combining biomaterials with exogenous growth factors, which however can have numerous undesired side effects, but also by tuning the intrinsic biomaterial properties. In a previous study, we showed the synergistic effect of nanostructure and pore architecture of biomimetic calcium deficient hydroxyapatite (CDHA) scaffolds in enhancing osteoinduction, i.e. fostering the differentiation of mesenchymal stem cells to bone forming cells. This was demonstrated by assessing bone formation after implanting the scaffolds intramuscularly. The present study goes one step forward, since it analyzes the effect of the geometrical features of the same CDHA scaffolds, obtained either by 3D-printing or by foaming, on the osteogenic potential and resorption behaviour in a bony environment. After 6 and 12 weeks of intraosseous implantation, both bone formation and material degradation had been drastically ...
Osterix, a zinc-finger transcription factor, is required for osteoblast differentiation and new bone formation during embryonic development. The c-Src of tyrosine kinase is involved in a variety of cellular signaling pathways, leading to the induction of DNA synthesis, cell proliferation, and cytoskeletal reorganization. Src activity is tightly regulated and its dysregulation leads to constitutive activation and cellular transformation. The function of Osterix can be also modulated by post-translational modification. But the precise molecular signaling mechanisms between Osterix and c-Src are not known. In this study we investigated the potential regulation of Osterix function by c-Src in osteoblast differentiation. We found that c-Src activation increases protein stability, osteogenic activity and transcriptional activity of Osterix. The siRNA-mediated knockdown of c-Src decreased the protein levels and transcriptional activity of Osterix. Conversely, Src specific inhibitor, SU6656, decreased ...
Knowledge of some of the fundamental biochemical factors that may influence the initiation and continued growth of bone-forming cell lines is presented. The discussion is limited to those factors shown experimentally to be present locally in bone tissue and synthesized in the environment of bone-forming cells. The current state of knowledge of basic research findings on osteogenic factors is given in detail. Cooperative actions of these locally produced and systemic factors are the primary stimuli that result in increased bone growth and volume.
Supplementary MaterialsS1 Fig: ARQ-197 will not affect trabecular bone tissue fraction in na?ve mice. the amount of osteoblasts per mm cortico-endosteal bone tissue (N.Ob/BS,mm) from naive mice (Na?ve) and na?ve mice treated with ARQ-197 (Na?ve + ARQ-197). (B) The percentage insurance of osteoblasts over the cortico-endosteal bone tissue (Ob.S/BS (%) from naive mice (Na?ve) and naive mice treated with ARQ-197 (Naive+ARQ-197). All data shown as indicate SD and analysed using an unpaired t-test.(TIF) pone.0199517.s003.tif (51K) GUID:?1B849EFE-9D95-4E80-B690-B9109372C217 S4 Fig: ARQ-197 does not have any effect on bone tissue formation over the cortico-endosteal surface area from the tibiae from na?ve mice. (A) Histomorphometric evaluation from the mineralising surface area (MS, %) (B) the nutrient apposition price (MAR, m/time) and (C) the bone tissue formation price (BFR/BS, mm2 X 10?3/mm/time) over the cortico-endosteal bone tissue surface area of tibiae from naive mice (Na?ve) and na?ve mice ...
Supplementary MaterialsS1 Fig: ARQ-197 will not affect trabecular bone tissue fraction in na?ve mice. the amount of osteoblasts per mm cortico-endosteal bone tissue (N.Ob/BS,mm) from naive mice (Na?ve) and na?ve mice treated with ARQ-197 (Na?ve + ARQ-197). (B) The percentage insurance of osteoblasts over the cortico-endosteal bone tissue (Ob.S/BS (%) from naive mice (Na?ve) and naive mice treated with ARQ-197 (Naive+ARQ-197). All data shown as indicate SD and analysed using an unpaired t-test.(TIF) pone.0199517.s003.tif (51K) GUID:?1B849EFE-9D95-4E80-B690-B9109372C217 S4 Fig: ARQ-197 does not have any effect on bone tissue formation over the cortico-endosteal surface area from the tibiae from na?ve mice. (A) Histomorphometric evaluation from the mineralising surface area (MS, %) (B) the nutrient apposition price (MAR, m/time) and (C) the bone tissue formation price (BFR/BS, mm2 X 10?3/mm/time) over the cortico-endosteal bone tissue surface area of tibiae from naive mice (Na?ve) and na?ve mice ...
Backround Microcalcifications may provoke plaque rupture leading to acute cardiovascular events. However, the mechanisms that initiate arterial calcification remain obscure.. Methods and Results We tested the hypothesis that inflammation promotes osteogenesis in atherosclerotic plaques using in vivo molecular imaging in apoE−/− mice (n=40). A bisphosphonate-derivatized near-infrared fluorescent (NIRF) imaging agent (750 nm) visualized osteogenic activity that was otherwise undetectable by X-ray computed tomography. Flow cytometry validated target cells as osteoblasts. A spectrally distinct NIRF nanoparticle (680 nm) was coinjected to simultaneously image macrophages. Fluorescence reflectance mapping associated osteogenic activity with inflammation in aortas of apoE−/− mice. Intravital dual-channel fluorescent microscopy further monitored osteogenic changes in carotid plaques at 20 and 30 weeks of age and revealed that both macrophage burden and osteogenesis concomitantly increased during ...
Gene silencing of noggin by small interfering RNA (siRNA) is a promising approach for the treatment of bone defects, because noggin deactivates bone morphogenetic protein-2 (BMP-2) and suppresses osteogenic differentiation. Here, we demonstrated the silencing of the noggin gene by siRNA polyplexes composed o
DICER1 RNAi inhibits osteogenic differentiation and proliferation of hADSCs. (a) DICER1 mRNA levels were determined in control-(si-cont) or DICER1 oligonucleoti
Intramembranous ossification is the process by which flat bones are created in mammalian fetuses, and also how broken bones are...
Mechanical cues are employed to promote stem cell differentiation and functional tissue formation in tissue engineering and regenerative medicine. We have developed a Magnetic Force Bioreactor (MFB) that delivers highly targeted local forces to cells at a pico-newton level, utilizing magnetic micro- and nano-particles to target cell surface receptors. In this study, we investigated the effects of magnetically targeting and actuating specific two mechanical-sensitive cell membrane receptors-platelet-derived growth factor receptor α (PDGFRα) and integrin ανβ3. It was found that a higher mineral-to-matrix ratio was obtained after three weeks of magneto-mechanical stimulation coupled with osteogenic medium culture by initially targeting PDGFRα compared with targeting integrin ανβ3 and non-treated controls. Moreover, different initiation sites caused a differentiated response profile when using a 2-day-lagged magneto-mechanical stimulation over culture periods of 7 and 12 days). However, both
Adipose derived stem cells (ASCs) with osteogenic differentiation potential have been documented as an alternative cell source for bone regeneration. However, most of previous in vivo studies were carried out on small animals along with relatively short-term follow-up. In this study, we investigated …
Growing vertebrae in the cervical (neck) region of a fetus. At this stage the tissue is mostly cartilage (blue) that is being replaced by the laying down of new bone tissue (pink strips) at the mid-point of each vertebral body. Note formation of early bone marrow spaces at the waist of each vertebra. This type of skeletal development is called endochondral ossification. Magnification x70 when printed at 10cm height. - Stock Image C026/4041
Folia Histochemica et Cytobiologica (FHC) is an international,English-language journal devoted to the developing fields of histochemistry,cytochemistry,cell biology,cell and tissue biology.It is source of the recent research in fields of and cell biology
J:103164 Minina E, Schneider S, Rosowski M, Lauster R, Vortkamp A, Expression of Fgf and Tgfbeta signaling related genes during embryonic endochondral ossification. Gene Expr Patterns. 2005 Dec;6(1):102-109 ...
The natural pure compound obtusilactone A (OA) was identified in Cinnamomum kotoense Kanehira & Sasaki, and shows effective anti-cancer activity. We studied the effect of OA on osteogenesis of bone marrow-derived mesenchymal stem cells (BMSCs). OA possesses biocompatibility, stimulates Alkaline Phosphatase (ALP) activity and facilitates mineralization of BMSCs. Expression of osteogenesis markers BMP2, Runx2, Collagen I, and Osteocalcin was enhanced in OA-treated BMSCs. An in vivo rat model with local administration of OA via needle implantation to bone marrow-residing BMSCs revealed that OA increased the new bone formation and trabecular bone volume in tibias. Micro-CT images and H&E staining showed more trabecular bone at the needle-implanted site in the OA group than the normal saline group. Thus, OA confers an osteoinductive effect on BMSCs via induction of osteogenic marker gene expression, such as BMP2 and Runx2 expression and subsequently elevates ALP activity and mineralization, followed
Title:In Vitro Osteogenesis of Human Stem Cells by Using a Three-Dimensional Perfusion Bioreactor Culture System: A Review. VOLUME: 7 ISSUE: 1. Author(s):Gabriele Ceccarelli, Nora Bloise, Marco Vercellino, Rosalia Battaglia, Lucia Morgante, Maria Gabriella Cusella De Angelis, Marcello Imbriani and Livia Visai. Affiliation:Dep. of Molecular Medicine, University of Pavia, Viale Taramelli 3/B, 27100 Pavia, Italy.. Keywords:Biomaterials, extracellular matrix, induced pluripotent stem cells (iPSCs), mesenchymal stem cells (MSC), osteogenesis, perfusion bioreactor, scaffolds, tissue engineering. Abstract:Tissue engineering (by culturing cells on appropriate scaffolds, and using bioreactors to drive the correct bone structure formation) is an attractive alternative to bone grafting or implantation of bone substitutes. Osteogenesis is a biological process that involves many molecular intracellular pathways organized to optimize bone modeling. The use of bioreactor systems and especially the perfusion ...
Adipose-derived stem cells (ASC) are multipotent stem cells that show great potential as a cell source for osteogenic tissue replacements and it is critical to understand the underlying mechanisms of lineage specification. Here we explore the role of primary cilia in human ASC (hASC) differentiation. This study focuses on the chemosensitivity of the primary cilium and the action of its associated proteins: polycystin-1 (PC1), polycystin-2 (PC2) and intraflagellar transport protein-88 (IFT88), in hASC osteogenesis. To elucidate cilia-mediated mechanisms of hASC differentiation, siRNA knockdown of PC1, PC2 and IFT88 was performed to disrupt cilia-associated protein function. Immunostaining of the primary cilium structure indicated phenotypic-dependent changes in cilia morphology. hASC cultured in osteogenic differentiation media yielded cilia of a more elongated conformation than those cultured in expansion media, indicating cilia-sensitivity to the chemical environment and a relationship between the
BACKGROUND: Growth hormone (GH) is a potent regulator of bone formation. The proposed mechanism of GH action is through the stimulation of osteogenic precursor cell proliferation and, following clonal expansion of these cells, promotion of differentiation along the osteogenic lineage. OBJECTIVES: We tested this hypothesis by studying the effects of GH on primary cell populations of human periodontal ligament cells (PLC) and alveolar bone cells (ABC), which contain a spectrum of osteogenic precursors. METHODS: The cell populations were assessed for mineralization potential after long-term culture in media containing beta-glycerophosphate and ascorbic acid, by the demonstration of mineral deposition by Von Kossa staining. The proliferative response of the cells to GH was determined over a 48-h period using a crystal violet dye-binding assay. The profile of the cells in terms of osteogenic marker expression was established using quantitative reverse transcriptase polymerase chain reaction (RT-PCR) ...
Osteogenic differentiation of mesenchymal stem cells has been extensively investigated with regards to different aspects, including the analysis of cell intracellular and extracellular proteome, cell gene expression pattern, and morphology. During the osteogenic differentiation, osteoblasts produce and release specific proteins, like osteocalcin and osteopontin. Simultaneously, cells produce the extracellular matrix (ECM) that resembles the bone ECM, with high quantity of calcium and phosphorus. We focused on the ultrastructural changes occurring during the osteogenic differentiation of MSC cultured in alginate hydrogel. The analysis revealed that during the osteogenic differentiation the most of cells become dead, and these dead cells contain large quantities of calcium and deposition is strictly connected with the cellular death and small membrane vesicles released by cells. Cell organelles were not present within differentiated cells, while in cells from non-osteogenic group the cellular
Ex vivo regional gene therapy strategies using animal mesenchymal stem cells genetically modified to overexpress osteoinductive growth factors has been successfully used in a variety of animal models to induce both heterotopic and orthotopic bone formation. However, in order to adapt regional gene therapy for clinical applications it is essential to assess the osteogenic capacity of transduced human cells and choose the cell type that demonstrates the best clinical potential. Bone marrow stem cells (BMSC) and adipose-derived stem cells (ASC) were selected in our study for in vitro evaluation, before and after transduction with a lentiviral two-step transcriptional amplification system (TSTA) overexpressing BMP-2 (LV-TSTA-BMP-2) or GFP (LV-TSTA-GFP); cell growth, transduction efficiency, BMP-2 production and osteogenic capacity were assessed ...
Background: Improved understanding of the interactions between bone cells and endothelial cells involved in osteogenesis should aid the development of new strategies for bone tissue engineering. The aim of the present study was to determine whether direct communication between bone marrow stromal cells (MSC) and human umbilical vein endothelial cells (EC) could influence the osteogenic potential of MSC in osteogenic factor-free medium. Methods: After adding EC to MSC in a direct-contact system, cell viability and morphology were investigated with the WST assay and immnostaining. The effects on osteogenic differentiation of adding EC to MSC was systematically tested by the using Superarray assay and results were confirmed with real-time PCR. Results: Five days after the addition of EC to MSC in a ratio of 1:5 (EC/MSC) significant increases in cell proliferation and cellular bridges between the two cell types were detected, as well as increased mRNA expression of alkaline phosphatase (ALP). This ...
There has been an explosion of research publications in the field of mesenchymal stem cells (MSCs) in the past 10 yr. Many researchers have sought to exploit their potential as a source of reparative cells for clinical use in a variety of contexts [1]. Adult stem cells are multipotent, undifferentiated, self-renewing capable of healing and regeneration of injured tissues [2-4]. Adult MSCs were initially identified in bone marrow (BM) and since then have been isolated and characterized from different human and animal adult tissues, peripheral blood, adipose, muscle, skin, dental pulp and other tissues [5-10].. Adult stem cells can be conveniently sampled from an extensive array of sources bypassing the ethical controversy associated with the embryonic stem cells, which is increasingly affecting the use of stem cell research and therapy. Even though, MSCs can be isolated from a variety of tissues and species, there is significant variation in their biological properties (morphological and ...
The long-term success of arthroplastic joints is dependent on the stabilization of the implant within the skeletal site. Movement of the arthroplastic implant within the bone can stimulate osteolysis, and therefore methods which promote rigid fixation or bone growth are expected to enhance implant stability and the long-term success of joint arthroplasty. In the present study, we used a simple bilateral bone defect model to analyze the osteogenic activity of three small-molecule drug implants via microcomputerized tomography (micro-CT) and histomorphometry. In this study, we show that local delivery of alendronate, but not lovastatin or omeprazole, led to significant new bone formation at the defect site. Since alendronate impedes osteoclast-development, it is theorized that alendronate treatment results in a net increase in bone formation by preventing osteoclast mediated remodeling of the newly formed bone and upregulating osteoblasts.
Cyclooxygenase (COX)-2 participates essentially in bone healing, demonstrated by COX-2 knockout mice that showed delayed fracture repair. Considerable controversy still exists on inhibitory effects of COX-2 inhibitors on bone healing in clinical case
Exogenous bone morphogenetic proteins (Bmp) are well known to induce ectopic bone formation, but the physiological effect of Bmp signaling on normal bone is not completely understood. By deleting the receptor Bmpr1a in osteoblast-lineage cells with Dmp1-Cre, we observed a dramatic increase in trabecular bone mass in postnatal mice, due to a marked increase in osteoblast number likely driven by hyperproliferation of Sp7+ preosteoblasts. Similarly, inducible deletion of Bmpr1a in Sp7-positive cells specifically in postnatal mice increased trabecular bone mass. However, deletion of Smad4 by the same approaches had only a minor effect, indicating that Bmpr1a signaling suppresses trabecular bone formation through effectors beyond Smad4. Besides increasing osteoblast number in the trabecular bone, deletion of Bmpr1a by Dmp1-Cre also notably reduced osteoblast activity, resulting in attenuation of periosteal growth. The impairment in osteoblast activity correlated with reduced mTORC1 signaling in vivo, ...
Effects of silica-gentamicin nanohybrids on osteogenic differentiation of human osteoblast-like SaOS-2 cells Wei He,1 Dina A Mosselhy,2,3 Yudong Zheng,1 Qingling Feng,4 Xiaoning Li,4 Xing Yang,4 Lina Yue,1 Simo-Pekka Hannula2 1School of Materials Science and Engineering, University of Science and Technology Beijing, Beijing, Peopleâ s Republic of China; 2Department of Chemistry and Materials Science, School of Chemical Engineering, Aalto University, Espoo, Finland; 3Microbiological Unit, Fish Diseases Department, Animal Health Research Institute, Giza, Egypt; 4State Key Laboratory of New Ceramics and Fine Processing, School of Materials Science and Engineering, Tsinghua University, Beijing, Peopleâ s Republic of China Introduction: In recent years, there has been an increasing interest in silica (SiO2) nanoparticles (NPs) as drug delivery systems. This interest is mainly attributed to the ease of their surface functionalization for drug loading. In orthopedic applications, gentamicin-loaded SiO2
Definition of osteoprogenitor cells in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is osteoprogenitor cells? Meaning of osteoprogenitor cells as a legal term. What does osteoprogenitor cells mean in law?
To explore the influence of inflammatory processes on bone formation, we applied a new in vivo screening model. Confined biological pockets were first created in rabbits as a response to implanted bone cement discs. These biomembrane pockets were subsequently used to study the effects of inflammatory stimuli on ectopic bone ... read more formation within biphasic calcium phosphate (BCP) constructs loaded with TNF-α, lipopolysaccharide (LPS) or lipoteichoic acid (LTA), all with or without bone morphogenetic protein (BMP)-2. Analysis of bone formation after 12 weeks demonstrated that the inflammatory mediators were not bone-inductive in combination with the BCP alone, but inhibited or enhanced BMP-induced bone formation. LPS was associated with a strong inhibition of bone formation by BMP-2, while LTA and TNF-α showed a positive interaction with BMP-2. Since the biomembrane pockets did not interfere with bone formation and prevented the leakage of pro-inflammatory compounds to the surrounding ...
Recent studies have suggested the existence of osteoblastic cells in the circulation, but the origin and role of these cells in vivo are not clear. Here, we examined how these cells contribute to osteogenesis in a bone morphogenetic protein (BMP)-induced model of ectopic bone formation. Following lethal dose-irradiation and subsequent green fluorescent protein-transgenic bone marrow cell-transplantation (GFP-BMT) in mice, a BMP-2-containing collagen pellet was implanted into muscle. Three weeks later, a significant number of GFP-positive osteoblastic cells were present in the newly generated ectopic bone. Moreover, peripheral blood mononuclear cells (PBMNCs) from the BMP-2-implanted mouse were then shown to include osteoblast progenitor cells (OPCs) in culture. Passive transfer of the PBMNCs isolated from the BMP-2-implanted GFP-mouse to the BMP-2-implanted nude mouse led to GFP-positive osteoblast accumulation in the ectopic bone. These data provide new insight into the mechanism of ectopic ...
Fingerprint Dive into the research topics of Order versus Disorder: In vivo bone formation within osteoconductive scaffolds. Together they form a unique fingerprint. ...
Objectives: This work aims to establish Platelet Lysates (PL) as optimal source1 of growth factors and other molecules that are vital for promoting cell proliferation and differentiation pathways, eventually allowing the substitution FBS and/or osteogenic supplements in culture media in bone tissue engineering strategies. Furthermore we intent to design new approaches to incorporate PLs in a scaffold material, as a hydrogel encapsulating the cells or as a coating for 3D porous structures, thus developing a tissue engineered construct with enhanced/multiple functionalities.. Methods: Starch-polycaprolactone (SPCL) meshes were obtained by a fiber bonding method as previously described2. PL gels were obtained by activation of platelets coagulation cascade using thrombin dissolved in a calcium chloride solution. Human adipose stem cells (hASCs) were obtained by enzymatic digestion of lipoaspirates samples. hASCs were either seeded directly into the SPCL scaffolds (control group) or into the ...
Osteoporosis results from the imbalance between bone resorption and bone formation, and restoring the normal balance of bone remodeling is highly desirable for identification of better treatment. In this study, using a cell-based high-throughput screening model representing Runt-related transcription factor 2 (RUNX2) transcriptional activity, we identified a novel small-molecular-weight compound, T63, as an efficient up-regulator of osteogenesis. T63 increased the alkaline phosphatase (ALPL) activity and mineralization as well as gene expression of Alpl and other osteogenic marker genes in mouse osteoblasts and mesenchymal stem cell-like cells. Upon induction of osteoblast differentiation, T63 inhibited adipogenic differentiation in the pluripotent mesenchymal cells. Consistently, T63 up-regulated RUNX2 mRNA and protein levels, and knockdown of RUNX2 reduced the osteogenic role of T63. Mechanistically, T63 activated both BMPs and WNT/β-catenin signaling pathways. Inhibition of either signaling pathway
Our study suggests that the number of connective-tissue progenitor cells is increased in traumatized tissue. Furthermore, wounds in which heterotopic ossification eventually forms have a higher percentage of connective-tissue progenitor cells committed to osteogenic differentiation than do wounds in …
PURPOSE:To evaluate the role of transforming growth factor beta 1 (TGF-β1) on the induced osteogenic differentiation of human dermal fibroblasts.METHODS:We performed four groups with cultured dermal fibroblasts according to the culture medium: CONTROL (DMEM culture medium); TGF-β1 (DMEM culture medium with 10 ng/ml of TGF-β1); OSTEOG (DMEM culture medium with 0.5 µg/ml of ascorbic acid, 10 mmol/l of β-glycerophosphate and 10 nmol/L of dexamethasone); and OSTEOG/TGF-β1 (osteogenic medium with 10 ng/ml of TGF-β1). Alkaline phosphatase (ALP) activity and the amount of osteocalcin (OC) in the supernatant, as well as the capability to form calcium phosphate deposits, were analysed for 28 dayRESULTS:There were significant differences (p,0.05) between CONTROL and TGF-β1 groups in comparison with OSTEOG and OSTEOG/TGF-β1 groups in the ALP activity and OC amount. Although, both osteogenic groups had the same behavior with regard the expression curve during the experimental time, the ...
Regulating and reverting the adipo-osteogenic lineage decision of trabecular human bone marrow stromal cells (hBMSCs) represents a promising approach for osteoporosis therapy and prevention. Fibroblast growth factor 1 (FGF1) and its subfamily member FGF2 were scored as lead candidates to exercise control over lineage switching processes (conversion) in favor of osteogenesis previously. However, their impact on differentiation events is controversially discussed in literature. Hence, the present study aimed to investigate the effects of these FGFs on the adipogenic and osteogenic differentiation and conversion of primary hBMSCs. Moreover, involved downstream signaling mechanisms should be elucidated and, finally, the results should be evaluated with regard to the possible therapeutic approach. This study clearly revealed that culture in the presence of FGF1 strongly prevented the adipogenic differentiation of hBMSCs as well as the adipogenic conversion of pre-differentiated osteoblastic cells. Lipid
Connective Tissue Gene Tests offers five panel options for osteogenesis imperfecta (OI) testing utilizing NextGen sequencing technology, an OI COL1A1 & COL1A2 panel, an OI core panel, a dominant OI panel, a recessive OI panel and a combined dominant and recessive OI panel. In addition to genes associated with the autosomal dominant and autosomal recessive forms of OI, the panels also contain genes for disorders included in the differential diagnosis of OI. The Osteogenesis imperfecta core NGS panel consists of three genes: COL1A1, COL1A2 and IFITM5.. Copy number variation (CNV) analysis of the Osteogenesis imperfecta core genes is also offered as a panel. Additionally, CTGT offers a comprehensive test (both NGS and CNV panels) for these genes. Panel genes are also offered as individual sequencing and deletion/duplication tests unless otherwise indicated.. Osteogenesis imperfecta core panel. ...
myo-Inositol (MI) plays an essential role in several important processes of cell physiology, is involved in the neural system, and provides an effective treatment for some psychiatric disorders. Its role in osteogenesis and bone formation nonetheless is unclear. Sodium/MI cotransporter 1 (SMIT1, the major cotransporter of MI) knockout (SMIT1(-/-)) mice with markedly reduced tissue MI levels were used to characterize the essential roles of MI and SMIT1 in osteogenesis. SMIT1(-/-) embryos had a dramatic delay in prenatal mineralization and died soon after birth owing to respiratory failure, but this could be rescued by maternal MI supplementation. The rescued SMIT1(-/-) mice had shorter limbs, decreased bone density, and abnormal bone architecture in adulthood. Deletion of SMIT1 resulted in retarded postnatal osteoblastic differentiation and bone formation in vivo and in vitro. Continuous MI supplementation partially restored the abnormal bone phenotypes in adult SMIT1(-/-) mice and strengthened ...
Purpose: The roles of angiogenesis and osteogenesis in autologous and allogenic bone grafts and the use of platelet-rich plasma (PRP) as a modifier were investigated. Materials and Methods: Forty rabbit mandibles received onlay grafts of fresh autologous and frozen allogeneic bone. PRP was added on the right side. After intervals of 3, 7, 14, 28, and 56 days, the animals were euthanized. Hematoxylin and eosin staining was used to measure the quantity and area of osteoblasts. Sections stained with toluidine blue showed newly formed bone area. In sections with Weigert-van Gieson staining, the number of vessels and their lumens was quantified. The quantity and area of cellular arrangements expressing CD31 and the area of vessels were obtained. Results: Quantities of osteoblasts and their areas, newly formed matrices, and vessels and their lumen areas were obtained and identified by immunomarking with CD31. In general, values for these were higher in rabbits with allogeneic bone grafts and on the ...
TY - JOUR. T1 - Sclerostin vaccination mitigates estrogen deficiency induction of bone mass loss and microstructure deterioration. AU - Wang, Feng Sheng. AU - Wu, Re Wen. AU - Lain, Wei Shiung. AU - Tsai, Tsai Chen. AU - Chen, Yu Shan. AU - Sun, Yi Chih. AU - Ke, Huei Jing. AU - Li, Jui Chen. AU - Hwang, Jaulang. AU - Ko, Jih Yang. PY - 2018/7/1. Y1 - 2018/7/1. N2 - Sclerostin (SOST) is a Wnt signaling inhibitor detrimental to osteogenic differentiation and bone mineral acquisition. While control of SOST action delays the pathogenesis of skeletal disorders, the effects of SOST vaccination on the estrogen deficiency-induced bone deterioration remain elusive. In this study, we generated a SOST-Fc fusion protein which was composed of a SOST peptide Pro-Asn-Ala-Ile-Gly along with an IgG Fc fragment. SOST-Fc vaccination increased serum anti-SOST antibody levels and reduced serum SOST concentrations in mice. In vitro, anti-SOST serum attenuated the SOST-induced inhibition of osteogenic gene expression ...
Both the topographic surface and chemical composition modification can enhance rapid osteogenic differentiation and bone formation. Till now, the synergetic effects of topography and chemistry cues guiding biological responses have been rarely reported. Herein, the ordered micro-patterned topography and classically
Osteogenesis imperfecta (OI), also known as brittle bone disease, is a genetic disorder of connective tissue characterized by fragile bones...
Costa-Pinto A. R., Vargel I., Tuzlakoglu K., Correlo V. M., Sol P. C., Faria S., Piskin E., Reis R. L., and Neves N. M., Influence of scaffold composition over in vitro osteogenic differentiation of hBMSCs and in vivo inflammatory response., Journal of Biomaterials Applications, vol. 28, issue 9, pp. 1430-1442, 2013. ...
In a new study presented at RSNA 2011, growth hormone replacement for six months was found to increase bone formation in abdominally obese women.
A biomedical implant is disclosed with osteogenic factors and a solid impermeable membrane occluding a portion of its surface for the generation of new bone growth at the target site of the implant. The implant is porous, bioresorbable, and forms a three dimensional architectural scaffold for the formation of new bone tissue. The implant is formed with a polymer or collagen, bone morphogenetic protein and ceramic particles.
The objective of the presented prospective clinical trial was the investigation of the behavior of implants with chemically modified surface using an early loading protocol in bone with reduced density. It was found that in most cases (89%) even in D3 and D4 bone an early loading protocol with prosthetic rehabilitation of hydrophilic implants after 8 weeks could be successfully performed.. The chemical modification of the used implants is based on conditioning of the surface with OH-ions. Hydroxylated titanium surfaces possess higher surface free energy and hydrophilicity [20] leading to increased production of osteogenic factors such as osteocalcin and growth factors [10]. In a pilot study in dogs, Schwarz et al. [21] found a significantly stronger proliferation of vascular structures as well as an increased osteocalcin activity and improved bone building processes for chemically modified, hydroxylated surfaces as compared to conventional surfaces.. A faster bone apposition rate was found ...
Skeletal muscle-derived stem cells (MDSCs) can undergo osteogenesis when treated with bone morphogenetic proteins (BMPs), making them a potential cell source for bone tissue engineering. pathway in the osteogenic differentiation of MDSCs. Inhibition of the ERK1/2 pathway increased ALP activity and mineralization, whereas inhibition of the p38 MAPK pathway decreased osteogenesis, suggesting opposing roles of these pathways in the BMP4-induced osteogenesis of MDSCs. Inhibition of the PI3K pathway significantly increased mineralization by MDSCs. These findings highlight the involvement of the ERK1/2, p38 MAPK, and PI3K pathways in opposing capacities in MDSC differentiation and warrant further investigation, as it may identify novel therapeutic targets for the development of stem buy Liquiritin cell-based therapies for bone tissue engineering. Introduction Control cells play a crucial function in embryonic advancement, organogenesis, and tissues regeneration in adults.1 Because of their ...
Physical interaction of skeletal precursors with multiple myeloma cells has been shown to suppress their osteogenic potential while favoring their tumor-promoting features. Although several transcriptome analyses of myeloma patient-derived mesenchymal stem cells have displayed differences compared to their healthy counterparts, these analyses insufficiently reflect the signatures mediated by tumor cell contact, vary due to different methodologies, and lack results in lineage-committed precursors. To determine tumor cell contact-mediated changes on skeletal precursors, we performed transcriptome analyses of mesenchymal stem cells and osteogenic precursor cells cultured in contact with the myeloma cell line INA-6. Comparative analyses confirmed dysregulation of genes which code for known disease-relevant factors and additionally revealed upregulation of genes that are associated with plasma cell homing, adhesion, osteoclastogenesis, and angiogenesis. Osteoclast-derived coupling factors, a ...
Elevated osteogenic potential of stem cells from inflammatory dental pulp tissues by Wnt4 overexpression for treating bone defect in rats
Tissue engineering provides unique opportunities for regenerating diseased or damaged tissues using cells obtained from tissue biopsies. Tissue engineered grafts can also be used as high fidelity models to probe cellular and molecular interactions underlying developmental processes. In this study, we co-cultured human umbilical vein endothelial cells (HUVECs) and human mesenchymal stem cells (MSCs) under various environmental conditions to elicit synergistic interactions leading to the colocalized development of capillary-like and bone-like tissues. Cells were encapsulated at the 1:1 ratio in fibrin gel to screen compositions of endothelial growth medium (EGM) and osteogenic medium (OM). It was determined that, to form both tissues, co-cultures should first be supplied with EGM followed by a 1:1 cocktail of the two media types containing bone morphogenetic protein-2. Subsequent studies of HUVECs and MSCs cultured in decellularized, trabecular bone scaffolds for 6 weeks assessed the effects on ...
Osteogenesis imperfecta, as the name suggests, refers to the impaired bone formation ascribed to defective genes encoding collagen. Individuals with osteogenesis
Osteogenesis imperfecta (OI) refers to a heterogeneous group of congenital, non-sex-linked, genetic disorders of collagen type I production, involving connective tissues and bones. The hallmark feature of osteogenesis imperfecta is osteoporosis...
Bone morphogenetic protein 2 (BMP2) is one of the key chondrogenic growth factors involved in the cartilage regeneration. However, it also exhibits osteogenic abilities and triggers endochondral...
Symptoms of osteogenesis imperfecta include short stature, weak muscles, and bones that fracture easily. This eMedTV Web page lists some of the potential osteogenesis imperfecta symptoms for each type of the disorder.
View Notes - biology4 from BIO 4432 at Texas State. Proteins Functions of Proteins: -Control the rate of reactions -Regulate cell processes -Used to form bones and muscles -Transport substances into
Bioactive PLGA-BG scaffolds have impact on human BMSC {\em in vitro} osteogenesis with and without osteogenic inducers - {\em in vitro} results and preliminary clinical approaches : [abstract] / Anna M. Osyczka, Joanna Filipowska, Tadeusz Niedzwiedzki, Grzegorz Tylko, Justyna KOKOSZKA, Katarzyna CHOLEWA-KOWALSKA, Elżbieta PAMUŁA, Maria ŁĄCZKA // W: RMSC-2012 : BITs 5\textsuperscript{th} annual world congress of Regenerative Medicine & Stem Cell : Guangzhou, China, [December 2-4, 2012]. - [China : s. n.], [2012]. - S. 166. - Justyna Kokoszka, Katarzyna Cholewa-Kowalska, Maria Łączka - afiliacja: Department of Faculty of Materials Science and Ceramics Biomaterials, University of Science and Technology, Poland ; Elżbieta Pamuła - afiliacja: Department of Biomaterials, University of Science and Technology, Poland ...
Bioactive PLGA-BG scaffolds have impact on human BMSC {\em in vitro} osteogenesis with and without osteogenic inducers - {\em in vitro} results and preliminary clinical approaches : [abstract] / Anna M. Osyczka, Joanna Filipowska, Tadeusz Niedzwiedzki, Grzegorz Tylko, Justyna KOKOSZKA, Katarzyna CHOLEWA-KOWALSKA, Elżbieta PAMUŁA, Maria ŁĄCZKA // W: RMSC-2012 : BITs 5\textsuperscript{th} annual world congress of Regenerative Medicine & Stem Cell : Guangzhou, China, [December 2-4, 2012]. - [China : s. n.], [2012]. - S. 166. - Justyna Kokoszka, Katarzyna Cholewa-Kowalska, Maria Łączka - afiliacja: Department of Faculty of Materials Science and Ceramics Biomaterials, University of Science and Technology, Poland ; Elżbieta Pamuła - afiliacja: Department of Biomaterials, University of Science and Technology, Poland ...
Osteogenesis imperfecta (OI) is an inherited (genetic) bone disorder that is present at birth. It is also known as brittle bone disease. A child born with OI may have soft bones that break (fracture) easily, bones that are not formed normally, and other problems. Signs and symptoms may range from mild to severe.
Your child has been diagnosed with osteogenesis imperfecta (OI). This is a rare condition that causes bones to be very thin and delicate. So they break (fracture) easily. OI is sometimes called brittle bone disease. There are four types of OI that range from mild to severe. A child with OI will be referred to a pediatric orthopedist.
Osteogenesis imperfecta, type II: Many different types of mutations in the COL1A1 gene can cause osteogenesis imperfecta type ... Osteogenesis imperfecta, type IV: Several different types of mutations in the COL1A1 gene cause osteogenesis imperfecta type IV ... Osteogenesis imperfecta, type I: Osteogenesis imperfecta is the most common disorder caused by mutations in this gene. ... type II osteogenesis imperfecta. Osteogenesis imperfecta, type III: Mutations in the COL1A1 gene may result in the production ...
Hypermobility spectrum disorder Osteogenesis imperfecta (brittle bone disease) - caused by poor quality collagen, or ... "Osteogenesis imperfecta". Genetics Home Reference. Retrieved 2019-11-19. Reference, Genetics Home. "Stickler syndrome". ...
Type I occurs as part of osteogenesis imperfecta. Preventive and restorative care are important as well as esthetics as a ... Occurs in people without other inherited disorders (i.e. Osteogenesis imperfecta). It is an autosomal dominant trait. A few ... Type I: DI associated with Osteogenesis Imperfecta (OI). Type of DI with similar dental abnormalities usually an autosomal ... Bisphosphonates have recently been introduced to treat several bone disorders, which include osteogenesis imperfecta. A ...
Osteogenesis imperfecta, known as brittle bone disease, is an incurable genetic bone disorder which can be lethal. Those with ... Gautieri A, Uzel S, Vesentini S, Redaelli A, Buehler MJ (2009). "Molecular and mesoscale disease mechanisms of Osteogenesis ... Rauch F, Glorieux FH (2004). "Osteogenesis imperfecta". Lancet. 363 (9418): 1377-85. doi:10.1016/S0140-6736(04)16051-0. PMID ...
He has osteogenesis imperfecta. He worked for almost 20 years in the voluntary sector, serving in various public affairs roles ...
He had osteogenesis imperfecta. Disability in Twentieth-century German Culture by Carol Poore, pg 220 German National Ethics ...
He has osteogenesis imperfecta. Guss has a brother named Sean and two sisters named Amy and Lena. He has one son, Caleb Guss ( ... "I have a bone-disease (osteogenesis imperfecta), so I've broken a lot of bones, and I'm really small and physically weaker than ...
He has Osteogenesis Imperfecta. He played Trick in Lost Girl, which played for five seasons. Additionally, Howland played Harry ...
The term childhood disease refers to disease that is contracted or becomes symptomatic before the age of 18 years old. Many of these diseases can also be contracted by adults. Some childhood diseases include: ...
ACAN Osteogenesis imperfecta, type I; 166200; COL1A1 Osteogenesis imperfecta, type II; 166210; COL1A2 Osteogenesis imperfecta, ... COL1A2 Osteogenesis imperfecta, type IV; 166220; COL1A2 Osteogenesis imperfecta, type IX; 259440; PPIB Osteogenesis imperfecta ... type VI; 610698; FKBP10 Osteogenesis imperfecta, type VII; 610682; CRTAP Osteogenesis imperfecta, type VIII; 610915; LEPRE1 ... type IIB; 610854; CRTAP Osteogenesis imperfecta, type III; 259420; ...
... and osteogenesis (e.g., RUNX2). The beta subunit is a non-DNA binding regulatory subunit; it allosterically enhances DNA ...
Dymecki, S. M.; Black, J.; Nord, D. S.; Jones, S. B.; Baranowski, T. J.; Brighton, C. T. (1985). "Medullary osteogenesis with ... she worked in the lab of Carl Theodore Brighton exploring the use of electrical current in stimulating osteogenesis. After ...
... created the first classification system for Osteogenesis Imperfecta that he later developed further to be the ... Sillence DO, Senn A, Danks DM (1979). "Genetic heterogeneity in osteogenesis imperfecta". J. Med. Genet. 16 (2): 101-16. doi: ...
Steiner, R. D., & Basel, D. (December 12, 2019). "COL1A1/2 Osteogenesis Imperfecta" (PDF). GeneReviews: 1-29. Retrieved ... osteogenesis imperfecta, trauma, radiation myelopathy, vitamin B12 deficiency (subacute combined degeneration), compression of ...
In classic non-deforming osteogenesis Imperfecta with blue sclerae or common variable osteogenesis Imperfecta with normal ... COL1A1/2-related osteogenesis Imperfecta is inherited in an autosomal dominant manner. The proportion of cases caused by a De ... COL1A1/2-related osteogenesis Imperfecta is identified by repeated fractures with trivial trauma, defective dentinogenesis ... Accordingly, COL1A1/2-related osteogenesis Imperfecta has been classified into four sub-types (I, II, III, and IV) built upon ...
Shapiro JR, Sponsellor PD (December 2009). "Osteogenesis imperfecta: questions and answers". Current Opinion in Pediatrics. 21 ... osteogenesis imperfecta, fibrous dysplasia, and other conditions that exhibit bone fragility. Bisphosphonates are used to treat ... Bisphosphonates have been used to reduce fracture rates in children with the disease osteogenesis imperfecta and to treat ...
Julie Fernandez - actress with osteogenesis imperfecta; founded The Disability Foundation; active on presentation of the ...
For example, mutations in SERPINF1 cause osteogenesis imperfecta type VI in humans. In the absence of a required serpin, the ... Marini JC, Reich A, Smith SM (August 2014). "Osteogenesis imperfecta due to mutations in non-collagenous genes: lessons in the ... Byers PH, Pyott SM (1 January 2012). "Recessively inherited forms of osteogenesis imperfecta". Annual Review of Genetics. 46: ... "Mutations in SERPINF1 cause osteogenesis imperfecta type VI". Journal of Bone and Mineral Research. 26 (12): 2798-803. doi: ...
"Entrez Gene: COL1A2 collagen, type I, alpha 2". Byers PH, Wallis GA, Willing MC (1991). "Osteogenesis imperfecta: translation ... Mutations in this gene are associated with osteogenesis imperfecta, Cardiac-valvular, and Arthrochlasia type Ehlers-Danlos ... GeneReviews/NCBI/NIH/UW entry on Osteogenesis Imperfecta v t e. ... produces the osteogenesis imperfecta type IV phenotype". J Biol ...
"OMIM Entry - # 616507 - OSTEOGENESIS IMPERFECTA, TYPE XVII; OI17". Aho, S; Uitto J (March 1999). "180-kD bullous ... which in turn causes a type of osteogenesis imperfecta. Collagen, type XVII, alpha 1 has been shown to interact with Keratin 18 ...
Activins are involved in embryogenesis and osteogenesis. They also regulate many hormones including pituitary, gonadal and ... Bone morphogenetic proteins cause the transcription of mRNAs involved in osteogenesis, neurogenesis, and ventral mesoderm ... They are involved in a multitude of cellular functions including osteogenesis, cell differentiation, anterior/posterior axis ...
"The role of soft tissues in osteogenesis. An experimental study of canine spine fusions". The Journal of Bone and Joint Surgery ...
Ingram has a form of osteogenesis imperfecta; having regularly fractured her bones, she requires periodic infusions to increase ...
BMP8A may be involved in epithelial osteogenesis. It also plays a role in bone homeostasis. It is a disulfide-linked homodimer ...
She has osteogenesis imperfecta (Brittle Bone Disease). She has long "apricot" (red) hair, pale skin and dark eyes. She is ...
Distraction osteogenesis - bone lengthening by gradual distraction. This involves cutting bone and moving ends apart ... Kloukos, Dimitrios; Fudalej, Piotr; Sequeira-Byron, Patrick; Katsaros, Christos (2018). "Maxillary distraction osteogenesis ...
Van Dijk FS, Sillence DO (June 2014). "Osteogenesis imperfecta: clinical diagnosis, nomenclature and severity assessment". ... For instance, it has been associated with retinitis pigmentosa, hypertrophic cardiomyopathy, osteogenesis imperfecta, and ...
Mutations in the CRTAP gene are associated with osteogenesis imperfecta, types VII and IIB, a connective tissue disorder ... Marini JC, Cabral WA, Barnes AM (2010). "Null mutations in LEPRE1 and CRTAP cause severe recessive osteogenesis imperfecta". ... December 2006). "Deficiency of cartilage-associated protein in recessive lethal osteogenesis imperfecta". N. Engl. J. Med. 355 ... December 2008). "CRTAP and LEPRE1 mutations in recessive osteogenesis imperfecta". Hum. Mutat. 29 (12): 1435-42. doi:10.1002/ ...
Cremin B, Goodman H, Spranger J, Beighton P (1982). "Wormian bones in osteogenesis imperfecta and other disorders". Skeletal ...
Li M, Zhang C, Yang Y (January 2019). "Effects of mechanical forces on osteogenesis and osteoclastogenesis in human periodontal ... Glowacki J, Schulten AJ, Perrott D, Kaban LB (February 2008). "Nicotine impairs distraction osteogenesis in the rat mandible". ...
Shapiro, Jay R. (2014), "Clinical and Genetic Classification of Osteogenesis Imperfecta and Epidemiology", Osteogenesis ... "Osteogenesis imperfecta". Retrieved 2018-04-17.. *^ Grond-Ginsbach, C; Debette, S; Pezzini, A (2005 ... Osteogenesis imperfecta (OI), also known as brittle bone disease, is a group of genetic disorders that mainly affect the bones. ... "Is Osteogenesis Imperfecta Inherited?". 4 April 2014. Retrieved 7 November 2018.. *^ Glorieux FH, Bishop NJ, Plotkin H, Chabot ...
Osteogenesis imperfecta (OI) is a group of genetic disorders that mainly affect the bones. Explore symptoms, inheritance, ... Osteogenesis imperfecta (OI) is a group of genetic disorders that mainly affect the bones. The term "osteogenesis imperfecta" ... Genetic Testing Registry: Osteogenesis imperfecta type III *Genetic Testing Registry: Osteogenesis imperfecta with normal ... Type I (also known as classic non-deforming osteogenesis imperfecta with blue sclerae) is the mildest form of osteogenesis ...
Osteogenesis imperfecta (OI), rare hereditary disease of connective tissue characterized by brittle bones that fracture easily ... osteogenesis imperfectaX-ray of an adult affected by osteogenesis imperfecta.. Reddicharla. ... Osteogenesis imperfecta (OI), also called brittle bone disease, rare hereditary disease of connective tissue characterized by ... Osteogenesis imperfecta is a disorder of connective tissue characterized by thin-walled, extremely fracture-prone bones… ...
Craniofacial surgeons at Seattle Childrens are leaders in using distraction osteogenesis for craniofacial syndromes. ... Distraction osteogenesis makes a longer bone out of a short one. ... Distraction osteogenesis is a way to make a longer bone out of ... How does distraction osteogenesis work?. In both distraction osteogenesis and traditional procedures, surgeons make a cut in a ... What types of distraction osteogenesis are done at Seattle Childrens?. Distraction osteogenesis is an option for many ...
... makes a longer bone out of a short one. After surgeons cut a bone, a distractor device pulls the 2 ... What is distraction osteogenesis?. Distraction osteogenesis is a way to make a longer bone out of a shorter one. ... How does distraction osteogenesis work?. In both distraction osteogenesis and traditional procedures, surgeons make a cut in a ... What types of distraction osteogenesis are done at Seattle Childrens?. Distraction osteogenesis is an option for many ...
Distraction osteogenesis (DO) is used in orthopedic surgery, and oral and maxillofacial surgery to repair skeletal deformities ... Distraction osteogenesis (DO), also called callus distraction, callotasis and osteodistraction, is a process used in orthopedic ... Patel PK, Zhao L, Ellis MF (January 6, 2015). de la Torre JI (ed.). "Distraction Osteogenesis: Background, History of the ... ISBN 978-3-642-23499-6. Baur DA, Helman J, Rodriguez JC, Altay MA (March 8, 2016). Meyers AD (ed.). "Distraction Osteogenesis ...
Child abuse and osteogenesis imperfecta. Br Med J (Clin Res Ed) 1987; 295 :1561 doi:10.1136/bmj.295.6612.1561-b ... Child abuse and osteogenesis imperfecta.. Br Med J (Clin Res Ed) 1987; 295 doi: ( ...
Osteogenesis imperfecta (OI, or Brittle Bone Disease) is a clinically and genetically heterogeneous group of heritable ... Review COL1A1/2 Osteogenesis Imperfecta[GeneReviews®. 1993]. Review COL1A1/2 Osteogenesis Imperfecta. Steiner RD, Basel D. ... Review Osteogenesis imperfecta: practical treatment guidelines.[Paediatr Drugs. 2000]. Review Osteogenesis imperfecta: ... Osteogenesis imperfecta type I is commonly due to a COL1A1 null allele of type I collagen. Am J Hum Genet. 1992;51(3):508-15. [ ...
Osteogenesis imperfecta (OI), also known as brittle bone disease, is an inherited disorder of the connective tissue. A child ... Osteogenesis Imperfecta. Facebook Twitter Linkedin Pinterest Print. What You Need to Know *Osteogenesis imperfecta (OI) is an ... What is osteogenesis imperfecta in children?. Osteogenesis imperfecta (OI) is an inherited (genetic) bone disorder that is ... Osteogenesis Imperfecta , Natalies Story By the age of 10, Natalie Brosh had already broken 19 bones and undergone seven ...
An autosomal dominant form of osteogenesis imperfecta, a connective tissue disorder characterized by low bone mass, bone ...
Osteogenesis imperfecta (or brittle bone disease) prevents the body from building strong bones. People with OI have bones that ... What Causes Osteogenesis Imperfecta (OI)?. Osteogenesis imperfecta (os-tee-oh-JEN-uh-sis im-pur-FEK-tuh) happens because of a ... What Is Osteogenesis Imperfecta (OI)?. Osteogenesis imperfecta (OI) is a genetic disorder that prevents the body from building ... How Is Osteogenesis Imperfecta (OI) Treated?. Theres no cure for osteogenesis imperfecta. Treatment is based on a childs ...
17, Evenings with Genetics will highlight the current research and resources available to those living with osteogenesis ... Osteogenesis imperfecta is a genetic disorder that affects the bodys connective tissues and often leaves people with fragile ... V. Reid Sutton, professor of molecular and human genetics at Baylor, will discuss the causes of osteogenesis imperfecta, the ... "One of the important things is that osteogenesis imperfecta can affect everyone differently. So its important that treatment ...
Osteogenesis RT2 Profiler PCR Array The Rat Osteogenesis RT² Profiler PCR Array profiles the expression of 84 genes related to ... Osteogenesis RT2 Profiler PCR Array The Human Osteogenesis RT² Profiler PCR Array profiles the expression of 84 genes related ... Osteogenesis RT2 Profiler PCR Array The Mouse Osteogenesis RT² Profiler PCR Array profiles the expression of 84 genes related ... Solutions optimized for osteogenesis studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP ...
Distraction Osteogenesis. Many facial reconstruction patients are children, so there is a great incentive to develop techniques ... Microscopic changes in the condyle and disc in response to distraction osteogenesis of the minipig mandible. J Oral Maxillofac ... Excellence in OMS Research - Distraction Osteogenesis. According to Dr. Leonard Kaban, chief of oral and maxillofacial surgery ... One of the most promising new techniques in mandibular reconstruction is distraction osteogenesis (DO), the gradual lengthening ...
In 1835, Lobstein coined the term osteogenesis imperfecta and was one of the first to correctly understand the etiology of the ... The earliest known case of osteogenesis imperfecta (OI) is in a partially mummified infants skeleton from ancient Egypt now ... encoded search term (Osteogenesis Imperfecta (OI)) and Osteogenesis Imperfecta (OI) What to Read Next on Medscape. Related ... Osteogenesis Imperfecta (OI). Updated: Nov 29, 2018 * Author: Manoj Ramachandran, MBBS, MRCS, FRCS; Chief Editor: Harris ...
Your company will receive signage at the registration table noting your company as provider of the evenings Specialty Cocktail, Red Carpet Photo Station or Music. along with your Corporate logo featured on Strong Bones Gala: Houston "Thank You" signage and website.. Silver sponsorship includes four free admissions to the Strong Bones Gala: Houston.. Silver Sponsor tickets cost $1,000.00, of which $500.00 is tax deductible.. ...
Your Company logo and web link on web pages and e- announcements for Strong Bones Gala: Houston and your Company logo featured on a table sign and "Thank You" signage and website at Strong Bones Gala: Houston.. Gold sponsorship includes a reserved table and eight free admissions to Strong Bones Gala: Houston.. Gold Sponsor tickets cost $2,500.00, of which $1,500.00 is tax deductible.. ...
Roy Morello and Paul W. Esposito (February 10th 2012). Osteogenesis Imperfecta, Osteogenesis Yunfeng Lin, IntechOpen, DOI: ... Roy Morello and Paul W. Esposito (February 10th 2012). Osteogenesis Imperfecta, Osteogenesis Yunfeng Lin, IntechOpen, DOI: ... /,. Embed this code snippet in the HTML of your website to show ... Osteogenesis Imperfecta. By Roy Morello and Paul W. Esposito. Submitted: May 5th 2011Reviewed: November 3rd 2011Published: ...
Methods and devices for distraction osteogenesis are disclosed employing an energy storage device and a controlled release of ... A kit for distraction osteogenesis comprising; a plurality of base elements adapted to be attached to a first segment of bone, ... 1. A device for distraction osteogenesis comprising; a first anchor element adapted to be attached to a first segment of bone, ... However, a new approach is distraction osteogenesis, a technique which employs the bodys bone regeneration ability to fill a ...
A Study in Adult Patients With Type I, III or IV Osteogenesis Imperfecta Treated With BPS804. *Osteogenesis Imperfecta, Type I ... An Exploratory Study of BPS804 Treatment in Adult Patients With Type I, III or IV Osteogenesis Imperfecta. *Osteogenesis ... Osteogenesis Imperfecta (OI) Quality of Life Survey Pilot Project 2. *Osteogenesis Imperfecta ... Efficacy and Safety of Alendronate in Chinese Children or Adolescents With Osteogenesis Imperfecta. *Osteogenesis Imperfecta ...
Keywords: MACRODONTIA; MANDIBULAR DISTRACTION OSTEOGENESIS; PEDIATRIC DENTISTRY; PIERRE ROBIN SEQUENCE Document Type: Case ... In severe cases of obstruction, mandibular distraction osteogenesis (MDO) can alleviate the airway blockage through elongation ...
Endothelial Notch activity promotes angiogenesis and osteogenesis in bone.. Ramasamy SK#1, Kusumbe AP#1, Wang L1, Adams RH1. ... Blood vessel growth in the skeletal system and osteogenesis seem to be coupled, suggesting the existence of molecular crosstalk ... Organisation and role of growing vessels in the regulation of osteogenesis in postnatal long bone. Endothelial columns, which ... These findings establish a molecular framework coupling angiogenesis, angiocrine signals and osteogenesis, which may prove ...
Make research projects and school reports about Osteogenesis imperfecta easy with credible articles from our FREE, online ... and pictures about Osteogenesis imperfecta at ... Osteogenesis Imperfecta Gale Encyclopedia of Medicine, 3rd ed. ... Osteogenesis imperfecta. Definition. Osteogenesis imperfecta (OI) is a group of genetic diseases in which the bones are formed ... Osteogenesis Imperfecta. Definition. Osteogenesis imperfecta (OI) is a group of genetic diseases of collagen in which the bones ...
V. Osteogenesis imperfecta," Journal of Chronic Diseases, vol. 3, no. 2, pp. 180-202, 1956. View at Google Scholar · View at ... Osteogenesis imperfecta (OI) is the most common of the heritable disorders of bone as first defined by McKusick in 1956 [1]. ... E. P. Homan, F. Rauch, I. Grafe et al., "Mutations in SERPINF1 cause osteogenesis imperfecta type VI," Journal of Bone and ... D. Sillence, "Osteogenesis imperfecta: an expanding panorama of variants," Clinical Orthopaedics and Related Research, vol. 159 ...
In 1835, Lobstein coined the term osteogenesis imperfecta and was one of the first to correctly understand the etiology of the ... The earliest known case of osteogenesis imperfecta (OI) is in a partially mummified infants skeleton from ancient Egypt now ... encoded search term (Osteogenesis Imperfecta (OI)) and Osteogenesis Imperfecta (OI) What to Read Next on Medscape ... Osteogenesis Imperfecta (OI) Clinical Presentation. Updated: Feb 24, 2020 * Author: Manoj Ramachandran, MBBS, MRCS, FRCS; Chief ...
G. R. Kirkhamand and S. H. Cartmell, "Genes and proteins involved in the regulation of osteogenesis," in Topics in Tissue ... Potential Role of Activating Transcription Factor 5 during Osteogenesis. Luisa Vicari,1 Giovanna Calabrese,1 Stefano Forte,1 ... Osteogenesis is a complex process comprising various stages, including proliferation, condensation, differentiation, and ... These findings suggest that activating transcription factor 5 could play an interesting regulatory role during osteogenesis, ...
Childrens Hospital Zurich have discovered the first X-chromosome-inherited type of the congenital disease osteogenesis ... In both families, this new form of osteogenesis imperfecta was caused by two different mutations of the same gene (MBTPS2) in ... Scientists discover X-chromosome-inherited type of osteogenesis imperfecta. *Download PDF Copy ... Surprisingly, mutations in the gene MBTPS2 also cause a completely different disease, namely osteogenesis imperfecta, explains ...
A definition of the medical terms "osteogenesis" and "osteogeny" is presented. The terms refer to the formation and development ...
Jojo, who suffers from type I osteogenesis imperfecta, has begun treatment with pamidronate, a bisphosphonate proven to reduce ...
  • Osteogenesis imperfecta ( OI ), also known as brittle bone disease , is a group of genetic disorders that mainly affect the bones . (
  • Osteogenesis imperfecta (OI) , also called brittle bone disease , rare hereditary disease of connective tissue characterized by brittle bones that fracture easily. (
  • Osteogenesis imperfecta (OI, or Brittle Bone Disease) is a clinically and genetically heterogeneous group of heritable disorders of connective tissue. (
  • Genetic diseases such as osteogenesis imperfecta, or "brittle bone disease" also present with weakened bones. (
  • Researchers from the University of Zurich and University Children's Hospital Zurich have discovered the first X-chromosome-inherited type of the congenital disease osteogenesis imperfecta, also known as brittle-bone disease. (
  • Osteogenesis imperfecta (OI), also known as brittle-bone disease, is a genetic (inherited) disorder characterized by bones that break easily without a specific cause. (
  • Osteogenesis imperfecta (OI) or "brittle bone disease" is a congenital disorder in which a person is born with very brittle bones, usually due to either a complete lack of or incorrectly formed type I collagen. (
  • How is Osteogenesis imperfecta (Brittle bone disease) Treated? (
  • Type V osteogenesis imperfecta: a new form of brittle bone disease. (
  • What is distraction osteogenesis? (
  • Distraction osteogenesis is a way to make a longer bone out of a shorter one. (
  • Distraction osteogenesis allows for bigger corrections in bone position than is possible in a single traditional surgery. (
  • Seattle Children's is a leader in distraction osteogenesis for craniofacial syndromes. (
  • How does distraction osteogenesis work? (
  • In both distraction osteogenesis and traditional procedures, surgeons make a cut in a bone. (
  • In distraction osteogenesis, a surgeon attaches a device called a distractor to the cut bone. (
  • What is Seattle Children's experience with distraction osteogenesis? (
  • We are experienced in treating children of all ages with distraction osteogenesis. (
  • Distraction osteogenesis (DO), also called callus distraction, callotasis and osteodistraction, is a process used in orthopedic surgery, podiatric surgery, and oral and maxillofacial surgery to repair skeletal deformities and in reconstructive surgery. (
  • One of the most promising new techniques in mandibular reconstruction is distraction osteogenesis (DO), the gradual lengthening of bone using a specialized appliance (a "distractor") to place tension forces across an osteotomy. (
  • Magill J, Goldwaser B, Troulis MJ, Kaban LB. Automating skeletal expansion: An implant for distraction osteogenesis of the mandible. (
  • Mandibular advancement by distraction osteogenesis for tracheostomy-dependant children with severe micrognathia. (
  • Analysis of skeletal movements in mandibular distraction osteogenesis. (
  • Thurmueller P, Troulis MJ, Rosenberg A, Chuang SK, Kaban LB. Microscopic changes in the condyle and disc in response to distraction osteogenesis of the minipig mandible. (
  • Yeshwant K, Seldin EB, Kikinis R, Kaban LB. A computer-assisted approach to planning multidimensional distraction osteogenesis. (
  • Methods and devices for distraction osteogenesis are disclosed employing an energy storage device and a controlled release of energy to provide a separating force. (
  • In severe cases of obstruction, mandibular distraction osteogenesis (MDO) can alleviate the airway blockage through elongation of the mandible and subsequent anterior placement of the tongue. (
  • Distraction osteogenesis after acute limb-shortening for segmental tibial defects. (
  • Distraction osteogenesis is a useful technique to correct severe mandibular brachygnathia in pediatric human patients. (
  • Distraction osteogenesis of the alveolar ridge: a review of the literature. (
  • The downside of distraction osteogenesis is that there must be a minimum quantity of bone about 5 mm of the transport and anchorage segment in order to have adequate strength to with- stand force of mobilization and transport. (
  • Distraction osteogenesis may be a viable alternative to MMA or, more likely, can be used in conjunction with MMA. (
  • A retrospective chart review was carried out for all infants who had mandibular distraction osteogenesis for severe airway obstruction over a four-year period, commencing when this surgery was first performed in our hospital. (
  • Use of virtual "cutting tools" and "collision tools" to plan out surgery on the 3D images, means that orthognathic surgery as well as distraction osteogenesis can be carried out with a far greater degree of precision, leading to more predictable results. (
  • Distraction osteogenesis is a procedure that helps lengthen a bone. (
  • Distraction osteogenesis is a surgical technique that gradually lengthens the jaw bone. (
  • Distraction osteogenesis is a new surgical technique in jaw surgery. (
  • Distraction osteogenesis seems to be a technique with less risk of relapse after large advancements (10mm or more) but it all depends on the surgical skill and experience of the surgeon. (
  • Successful application of proper preoperative planning, good surgical technique and good patient compliance will ensure the success of distraction osteogenesis. (
  • The alveolar distraction osteogenesis device may be affixed to small and thin bone segments. (
  • An alveolar distraction osteogenesis device according to the first embodiment includes a submergible first and second members. (
  • An alveolar distraction osteogenesis device according to a second embodiment includes an osseointegrated cylindrical member along with an adaptable threaded rod which may be used with a stabilizing plate. (
  • The alveolar distraction osteogenesis device is activated using a hexagonal drive wrench or a slot screw driver. (
  • 2. The osteogenesis distraction apparatus of claim 1, further comprising an activating means coupled to the base of the rod for transferring a force. (
  • 3. The osteogenesis distraction apparatus of claim 2, wherein the rod is removed by rotating the base clockwise. (
  • 6. The osteogenesis distraction apparatus of claim 1, wherein said cylindrical member is covered with a coating for enhancing an osseointegration process. (
  • 7. The osteogenesis distraction apparatus of claim 6, wherein said coating is a bondable titanium plasma. (
  • At the age of 4, hastened distraction osteogenesis resulted in a tapered bony segment of the middle proximal phalanx. (
  • Prior osteogenesis distraction had left the middle proximal phalanx of the affected hand elongated and tapered, complicating bony fixation. (
  • Proliferation of masseter myocytes after distraction osteogenesis of the porcine mandible. (
  • PURPOSE: Long-term success of distraction osteogenesis depends on the ability of the surrounding soft tissues to tolerate distraction forces and to adapt to the resulting increase in skeletal length and volume. (
  • A proliferative response may contribute to improved long-term stability of mandibular expansion by distraction osteogenesis. (
  • Several treatments for the correction of the dento-facial deformity have been described, among them distraction osteogenesis is one that shows promising results. (
  • Distraction osteogenesis is the process of bone formation that occurs during slow separation of the segments of bone after an osteotomy and it has been used to alleviate facial asymmetry. (
  • Mandibular distraction osteogenesis has been applied for many years, but long-term reports present controversial results. (
  • The purpose of the case report is to describe the immediate and long-term effects of distraction osteogenesis used to treat mandible asymmetry in a 5-year-old boy with Goldenhar syndrome. (
  • The preferred method for treatment of hemifacial microsomia in children is distraction osteogenesis that consists on bone development through osteotomy and sequential stretching of the healing callus (2-5). (
  • The aim of this paper is to describe a case of a child with Goldenhar syndrome in which distraction osteogenesis was used to treat the mandibular asymmetry and to discuss its follow-up. (
  • The patient was submitted to a distraction osteogenesis when he was 5 years old. (
  • To investigate the effects of inferior alveolar nerve on new bone formation in rabbit mandibular distraction osteogenesis. (
  • 20 New Zealand White rabbits underwent bilateral distraction osteogenesis with a rate of 1 mm/day. (
  • The loss of the sensory nerves could result in a decrease of the new bone quality during the mandibular distraction osteogenesis. (
  • However, it remains unclear whether the peripheral nerve ingrowth is crucial to the new bone formation in the scenario of endogenous or exogenous bone regeneration, such as distraction osteogenesis and bone tissue engineering respectively. (
  • Distraction osteogenesis (DO) has been widely applied in the treatment of bone defects and deformities in orthopedics and craniomaxillofacial surgery 5 . (
  • Skeletal and dental effects of tooth-borne versus hybrid devices for mandibular symphyseal distraction osteogenesis. (
  • Authors: Niculescu JA, King JW, Lindauer SJ Abstract Abstract Objective: To evaluate and compare, retrospectively, the skeletal and dental effects of mandibular symphyseal distraction osteogenesis (MSDO) achieved through the use of tooth-borne versus hybrid distractors. (
  • Distraction osteogenesis is a surgical dental procedure performed to initiate new bone growth in the maxillofacial region. (
  • The goal of this research was to analyze the regionalized awareness of distraction osteogenesis. (
  • A survey was conducted among dentists in Kentucky and Tennessee with multiple questions to determine their knowledge and use of distraction osteogenesis. (
  • The survey sent to dentists in Tennessee and Kentucky provided vital information on the awareness of distraction osteogenesis. (
  • Type I (also known as classic non-deforming osteogenesis imperfecta with blue sclerae) is the mildest form of osteogenesis imperfecta. (
  • An autosomal dominant form of osteogenesis imperfecta, a connective tissue disorder characterized by low bone mass, bone fragility and susceptibility to fractures after minimal trauma. (
  • In both families, this new form of osteogenesis imperfecta was caused by two different mutations of the same gene (MBTPS2) in the X chromosome. (
  • Chu ML, Williams CJ, Pepe G, Hirsch JL, Prockop DJ, Ramirez F. Internal deletion in a collagen gene in a perinatal lethal form of osteogenesis imperfecta. (
  • Type III is the most severe nonlethal form of osteogenesis imperfecta. (
  • On Tuesday, Sept. 17, Evenings with Genetics , a monthly speaker series hosted by Baylor College of Medicine and Texas Children's Hospital, will highlight the current research and resources available to those living with osteogenesis imperfecta. (
  • osteogenesis imperfecta X-ray of an adult affected by osteogenesis imperfecta. (
  • We provide comprehensive, family-centered and coordinated care for children, adults and families affected by osteogenesis imperfecta (OI). (
  • Other types of this condition, including types III (progressively deforming osteogenesis imperfecta) and IV (common variable osteogenesis imperfecta with normal sclerae), have signs and symptoms that fall somewhere between these two extremes. (
  • Other types of osteogenesis imperfecta are more severe, causing frequent bone fractures that are present at birth and result from little or no trauma. (
  • A defect in the structure of type I collagen weakens connective tissues, particularly bone, resulting in the characteristic features of these more severe types of osteogenesis imperfecta. (
  • What Are the Types of Osteogenesis Imperfecta (OI)? (
  • Four types of osteogenesis imperfecta were originally described by Sillence in 1979 and are now used broadly as the Sillence criteria. (
  • Osteogenesis imperfecta is a genetic disorder that causes increased bone fractures and collagen defects. (
  • The milder forms of osteogenesis imperfecta, including type I, are characterized by bone fractures during childhood and adolescence that often result from minor trauma, such as falling while learning to walk. (
  • Type II osteogenesis imperfecta - babies with type II OI usually are born with many fractures, are very small, and have severe breathing problems. (
  • Type IV osteogenesis imperfecta - people with type IV OI can have mild to serious bone deformities, short stature, frequent fractures (which may lessen after puberty), and a curved spine. (
  • People with type three of Osteogenesis Imperfecta may have more than 100 fractures before puberty. (
  • Osteogenesis imperfecta - oral implications Osteogenesis imperfecta (OI) is an inherited, rare connective tissue disorder leading to bone fragility and hence an increased risk of bone fractures and a number of other symptoms related to the connective tissue, including risk of dentinogenesis imperfecta (DI). (
  • Osteogenesis imperfecta (os-tee-oh-JEN-uh-sis im-pur-FEK-tuh) happens because of a defect in the gene that makes the protein collagen . (
  • Type I osteogenesis imperfecta - people with type I OI have less collagen than normal. (
  • In osteogenesis imperfecta, the collagen produced is abnormal and disorganized, which results in a number of abnormalities throughout the body, the most notable being fragile, easily broken bones. (
  • Osteogenesis imperfecta refers to genetic conditions which alter the integrity of a specific type of collagen. (
  • Osteogenesis imperfecta (OI) is a systemic connective tissue disorder most often caused by mutations in collagen type 1 related genes. (
  • A collagen-targeted biomimetic RGD peptide to promote osteogenesis. (
  • These results indicate that the combination of this biomimetic peptide with the currently used collagen+BMP system might be a promising approach to improve osteogenesis and to reduce the doses of BMPs needed in clinical orthopedics. (
  • Osteopenia due to deficient extracellular matrix synthesis is a hallmark of osteogenesis imperfecta (OI), Previous studies carried out within 72 h of osteoblast subculture, at an early stage of matrix synthesis, indicated that for osteoblasts derived from human OI patients the total amounts of collagen, osteonectin, and three proteoglycans were significantly reduced, while total amounts of thrombospondin, fibronectin, and matrix hyaluronan were elevated compared with age-matched controls. (
  • Osteogenesis imperfecta (OI) is a rare, heritable systemic disorder of bone and connective tissue, which in almost 90% of cases is due to mutations affecting the normal synthesis of type I collagen. (
  • Genotype-phenotype correlations in nonlethal osteogenesis imperfecta caused by mutations in the helical domain of collagen type I. Eur J Hum Genet. (
  • Bone collagen: new clues to its mineralization mechanism from recessive osteogenesis imperfecta. (
  • Osteogenesis imperfecta (OI) is a hereditary bone disorder caused by defects of type I collagen. (
  • Osteogenesis imperfecta (OI) is a genetic disease in which the most common mutations result in substitutions for glycine residues in the triple helical domain of the chains of type I collagen. (
  • Clinically, mutations in type I collagen genes are associated with osteogenesis imperfecta (OI) 1 and some forms of Ehlers-Danlos syndrome. (
  • Osteogenesis imperfecta is a hereditary collagen disorder causing diffuse abnormal fragility of bone and is sometimes accompanied by sensorineural hearing loss, blue sclerae, dentinogenesis imperfecta, and joint hypermobility. (
  • Osteogenesis imperfecta is a rare hereditary disease mostly caused by mutations impairing collagen synthesis and modification. (
  • In addition to a complete medical history and physical examination, diagnostic procedures for osteogenesis imperfecta may include a skin biopsy to evaluate the amount and structure of collagen. (
  • Moreover, the emergence of special drug designations by various regulatory authorities related to osteogenesis imperfecta is another factor boosting the market growth. (
  • What is the long-term outlook for a child with osteogenesis imperfecta? (
  • There are many families that have adopted a child with Osteogenesis Imperfecta, club foot , or other orthopedic differences. (
  • Crutches, splints, and other ambulatory aids can help a child with osteogenesis imperfecta to walk better. (
  • For children with osteogenesis imperfecta, an injury does not have to occur for a bone to fracture. (
  • Infection in the bones is a concern for children with osteogenesis imperfecta, and doctors prescribe antibiotics to treat or prevent infections. (
  • Behavior of scoliosis during growth in children with osteogenesis imperfecta. (
  • Effect of intravenous pamidronate therapy on functional abilities and level of ambulation in children with osteogenesis imperfecta. (
  • Intravenous neridronate in children with osteogenesis imperfecta: a randomized controlled study. (
  • Risedronate in children with osteogenesis imperfecta: a randomised, double-blind, placebo-controlled trial. (
  • Two years experience with denosumab for children with Osteogenesis imperfecta type VI. (
  • Do Bisphosphonates Alter the Skeletal Response to Mechanical Stimulation in Children With Osteogenesis Imperfecta? (
  • In vitro models of osteogenesis are essential for investigating bone biology and the effects of pharmaceutical, chemical, and physical cues on bone formation. (
  • Existing in vitro models of osteogenesis include two-dimensional (2D) single type cell monolayers and 3D cultures. (
  • However, an in vitro scaffold-free multicellular 3D model of osteogenesis is missing. (
  • We hypothesized that the self-inductive ossification capacity of bone marrow tissue can be harnessed in vitro and employed as a scaffold-free multicellular 3D model of osteogenesis. (
  • Therefore, this platform holds significant potential to be used as a model of osteogenesis, offering an alternative to in vitro monolayer cultures and in vivo animal models. (
  • Gurkan UA, Krueger A, Akkus O (2010) Ossifying bone marrow explant culture as a three-dimensional mechanoresponsive in vitro model of osteogenesis. (
  • CHEMICON's In Vitro Osteogenesis Assay Kit contains all reagents necessary to efficiently differentiate MC3T3-E1cells to a mature osteoblastic lineage, as determined by staining for mineralization. (
  • Mesenchymal stem cells derived from mouse or human iPS cells (iPS-MSCs) have been reported by several groups 10 , 11 and used for osteogenesis both in vitro and in vivo 12 , which makes iPS-MSCs a promising cell source for studying orthopedic diseases, regenerative orthopedic therapy and patient-specific cell therapy. (
  • While soluble supplementation strategies have been identified to enhance osteogenesis, they are subject to significant diffusive loss in vivo or the need for frequent re-addition in vitro . (
  • This study investigated the potential of NAC as an osteogenesis-enhancing molecule in vitro and in vivo. (
  • Osteogenesis imperfecta is a genetic disorder that affects the body's connective tissues and often leaves people with fragile or brittle bones. (
  • Osteogenesis imperfecta (OI) is the most common heritable disorder of connective tissue. (
  • Osteogenesis imperfecta (OI) is a rare clinically and genetically heterogeneous systemic disorder of bone and connective tissue characterized by bone fragility and physical findings related to the underlying connective tissue disorder. (
  • Osteogenesis Imperfecta (OI) is an hereditary disease of connective tissue, characterised clinically by frequent fracture following minimal trauma. (
  • Osteogenesis imperfecta (OI) is an extremely heterogeneous group of heritable connective tissue disorders. (
  • Osteogenesis imperfecta (OI) is an inherited disorder of the tissue that holds the body together (connective tissue). (
  • Osteogenesis imperfecta (OI) is a heritable connective tissue disorder with a predominately autosomal-dominant inheritance pattern. (
  • 2002) Acetabular protrusion in osteogenesis imperfecta. (
  • In many cases Osteogenesis Imperfecta can have unidentified mutations and lead to a more serious type of OI such as Type V and VI. (
  • Osteogenesis imperfecta can be caused by mutations in one of several genes. (
  • Osteogenesis imperfecta type I is caused by mutations in the COL1A1 gene or, less commonly, the COL1A2 gene. (
  • The mutations that cause osteogenesis imperfecta types II, III, and IV occur in either the COL1A1 or COL1A2 gene. (
  • Mutations in other genes cause rare forms of osteogenesis imperfecta. (
  • When caused by mutations in the COL1A1 or COL1A2 gene, osteogenesis imperfecta has an autosomal dominant pattern of inheritance, which means one copy of the altered gene in each cell is sufficient to cause the condition. (
  • Osteogenesis imperfecta (OI) is a disorder of bone fragility chiefly caused by mutations in the COL1A1 and COL1A2 genes that encode type I procollagen. (
  • Patients often have a family history of osteogenesis imperfecta (OI), but most cases are due to new mutations. (
  • Surprisingly, mutations in the gene MBTPS2 also cause a completely different disease, namely osteogenesis imperfecta,' explains Marianne Rohrbach. (
  • Exome sequencing identifies truncating mutations in human SERPINF1 in autosomal-recessive osteogenesis imperfecta. (
  • The company's aim behind this collaboration was to advance OI research by developing the first-ever swine models of osteogenesis imperfecta. (
  • Currently, most individuals with osteogenesis imperfecta are treated with intravenous medications to increase their bone density and in some cases with orthopedic surgery. (
  • Correlation of ocular rigidity and blue sclerae in osteogenesis imperfecta. (
  • Hearing loss has been associated with Osteogenesis leading to ultimately deformities within the ossicle and inner ear bones. (
  • Osteogenesis imperfecta (OI) is a genetic disorder that prevents the body from building strong bones. (
  • Endothelial-cell-specific and inducible genetic disruption of Notch signalling in mice not only impaired bone vessel morphology and growth, but also led to reduced osteogenesis, shortening of long bones, chondrocyte defects, loss of trabeculae and decreased bone mass. (
  • Osteogenesis imperfecta (OI) is a group of genetic diseases in which the bones are formed improperly, making them fragile and prone to breaking. (
  • Osteogenesis Imperfecta is a disease that occurs when someone has weak bones, and it is a genetic disorder. (
  • Semler O, Cheung MS, Glorieux FH, Rauch F. Wormian bones in osteogenesis imperfecta: correlation to clinical findings and genotype. (
  • Osteogenesis imperfecta tarda (medical condition): A genetic condition characterized mainly by fragile bones that fracture. (
  • Osteogenesis Imperfecta(OI) is an inherited disorder characterised by extreme fragility of the bones. (
  • Jessica Minor, a program coordinator with Kaiser Permanente's Mid-Atlantic States Region, was diagnosed with osteogenesis imperfecta (known as brittle bones disease) at 9 months. (
  • van Dijk FS, Sillence DO (2014) Osteogenesis imperfecta: clinical diagnosis, nomenclature and severity assessment. (
  • Osteogenesis imperfecta: clinical diagnosis, nomenclature and severity assessment. (
  • Diagnosis of osteogenesis imperfecta is usually clinical, but there are no standardized criteria. (
  • Findings are consistent with the known diagnosis of osteogenesis imperfecta . (
  • Osteogenesis imperfecta (OI) is the most common of the heritable disorders of bone as first defined by McKusick in 1956 [ 1 ]. (
  • Osteogenesis imperfecta is a heritable bone fragility disease with a heterogenic genetic origin. (
  • If you know the author of Pamidronate Treatment of Severe Osteogenesis Imperfecta in Children under 3 Years of Age , please help us out by filling out the form below and clicking Send. (
  • Severe osteogenesis imperfecta can be detected in utero by level II ultrasonography. (
  • Cyclic administration of pamidronate in children with severe osteogenesis imperfecta. (
  • This photo shows a person with severe osteogenesis imperfecta who has a barrel chest, curving of the spine, severe bone deformities, loose joints, and poor muscle development. (
  • Analyzing the expression, regulation, and sequence of osteogenesis genes can help determine their relative importance to the biology of the cellular or disease processes under study. (
  • Makareeva E, Aviles NA, Leikin S. Chaperoning osteogenesis: new protein-folding disease paradigms. (
  • We identified a novel COL1A2 gene mutation in a Czech patient, born to unaffected parents, who was diagnosed according to clinical and anthropometric findings and radiographic features as having type 3 osteogenesis imperfecta, which is a severe form of this disease. (
  • Osteogenesis imperfecta tarda is listed as a " rare disease " by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). (
  • Glorieux FH (2008) Osteogenesis imperfecta. (
  • Rauch F, Glorieux FH (2004) Osteogenesis imperfecta. (
  • The primary aim is to elucidate whether there are differences in osteogenesis and in the characteristics of the newly formed bone between patients following different post-operative NSAID chronotherapeutic protocols. (
  • 1995) Gastrointestinal problems in patients who have type-III osteogenesis imperfecta. (
  • Hearing loss is present in 50 to 65% of all patients with osteogenesis imperfecta and may occur in any of the 4 types. (
  • Karbowski A, Schwitalle M, Eckardt A. [Scoliosis in patients with osteogenesis imperfecta: a federal nation-wide cross-sectional study]. (
  • Overall Objective: To test the hypothesis that oral vitamin D supplementation at higher than currently prescribed doses has a beneficial effect on the skeleton of young patients with osteogenesis imperfecta (OI). (
  • This will provide a reliable preclinical model to establish the efficacy and safety of new therapies required for the patients with osteogenesis imperfecta. (
  • Dr. V. Reid Sutton , professor of molecular and human genetics at Baylor, will discuss the causes of osteogenesis imperfecta, the prognosis for those living with the disorder and the newest treatments being tested in clinical trials. (
  • Pontz BF, Stoss H, Spranger J. Heterogeneity in osteogenesis imperfecta: clinical and morphological findings. (
  • Germain-Lee EL , Brennen FS, Stern D, Kantipuly A, Melvin P, Terkowitz MS, Shapiro JR. Cross-sectional and longitudinal growth patterns in osteogenesis imperfecta: implications for clinical care. (
  • [12] The term "osteogenesis imperfecta" came into use in 1895 and means imperfect bone formation. (
  • The term "osteogenesis imperfecta" means imperfect bone formation. (
  • Shapiro JR , Thompson CB, Wu Y, Nunes M, Gillen C. Bone mineral density and fracture rate in response to intravenous and oral biphosphonates in adult osteogenesis imperfecta. (
  • 1988) Obstruction of the colon due to protrusio acetabuli in osteogenesis imperfecta: Treatment by pelvic osteotomy: Report of a case. (
  • What are the symptoms of osteogenesis imperfecta in a child? (
  • The symptoms of osteogenesis imperfecta may look like other medical conditions. (
  • What Are the Signs & Symptoms of Osteogenesis Imperfecta (OI)? (
  • MK149) is a quantitative assay that measures bone osteogenesis via the specific and highly sensitive detection of ucOC released from porcine bone tissues by osteoclasts or inactive ucOC produced by osteoblasts. (
  • Bone osteogenesis is often detected through osteocalcin (OC), a bone-specific protein that is synthesized only by bone-forming osteoblasts. (
  • Because of osteocalcin's exclusivity to osteoblasts, it is often used as a marker specific to bone osteogenesis. (
  • A novel IFITM5 mutation in severe atypical osteogenesis imperfecta type VI impairs osteoblast production of pigment epithelium-derived factor. (
  • A mutation in the 5ʹ-UTR of IFITM5 creates an in-frame start codon and causes autosomal-dominant osteogenesis imperfecta type V with hyperplastic callus. (
  • Osteogenesis imperfecta is a genetic disorder . (
  • Osteogenesis imperfecta type III is a rare, but highly debilitating, genetic disorder that is marked by fairly severe bone defects. (
  • Blood vessel growth in the skeletal system and osteogenesis seem to be coupled, suggesting the existence of molecular crosstalk between endothelial and osteoblastic cells. (
  • So it's important that treatment or management decisions be individualized to the person with osteogenesis imperfecta and what they're experiencing at that particular point in their life," Sutton said. (
  • This material gives the reader information about Pamidronate treatment for osteogenesis imperfecta in children younger than three years old. (
  • To date, there is no known treatment, medicine, or surgery that will cure osteogenesis imperfecta (OI). (
  • The rise in funding for research & development to develop novel treatment and therapies is a major factor propelling growth of the global osteogenesis imperfecta treatment market. (
  • For instance, in November 2017, the Europe Medicines Agency (EMA) expanded all the indications for the first drug setrusumab for osteogenesis imperfect treatment. (