Osteogenesis. Medical search

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 3.1.3.1.

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 3.4.24.14.

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.

Agents that inhibit BONE RESORPTION and/or favor BONE MINERALIZATION and BONE REGENERATION. They are used to heal BONE FRACTURES and to treat METABOLIC BONE DISEASES such as 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)

1. Bone fractures: The most common symptom of OI is an increased risk of fractures, which can occur with minimal trauma or even without any apparent cause.
2. Dental problems: People with OI may have poorly formed teeth, tooth decay, and gum disease.
3. Short stature: Many individuals with OI are short in stature, due to the effects of chronic fractures and pain on growth and development.
4. Muscle weakness: Some people with OI may experience muscle weakness, particularly in the limbs.
5. Joint problems: OI can cause issues with joint mobility and stability, leading to arthritis and other degenerative conditions.
6. Scoliosis: Curvature of the spine is common in people with OI, which can lead to back pain and respiratory problems.
7. Blue sclerae: A distinctive feature of OI is the presence of blue-colored sclerae (the white part of the eye).
8. Other symptoms: Some people with OI may experience hearing loss, vision problems, and delayed development.

There are several types of OI, each caused by a mutation in a specific gene. The most common forms of OI are type I, type II, and type III. Type I is the mildest form and type III is the most severe. There is no cure for OI, but treatment focuses on managing symptoms and preventing complications. This may include:

1. Bracing and orthotics: To support weakened bones and improve posture.
2. Physical therapy: To maintain muscle strength and flexibility.
3. Pain management: To reduce the risk of chronic pain and improve quality of life.
4. Dental care: Regular dental check-ups and appropriate treatment to prevent tooth decay and gum disease.
5. Respiratory care: To manage breathing problems and prevent respiratory infections.
6. Monitoring for hearing loss: Regular hearing tests to detect any hearing loss and provide appropriate intervention.
7. Early intervention: To help children with OI develop skills and abilities to their full potential.
8. Genetic counseling: For families with a history of OI, to understand the risks and implications for future pregnancies.

It's important for people with OI to work closely with their healthcare provider to manage their condition and prevent complications. With proper care and support, many people with OI can lead active and fulfilling lives.

What is Dentinogenesis Imperfecta?
Dentinogenesis imperfecta (DI) is a group of rare genetic disorders that affect the development of dentin, the hard tissue beneath the enamel of the tooth. It is characterized by fragile teeth that are prone to decay and fracture, as well as other oral and skeletal abnormalities. There are several types of DI, each with different symptoms and causes.

What are the Symptoms of Dentinogenesis Imperfecta?
The symptoms of dentinogenesis imperfecta (DI) can vary depending on the type and severity of the disorder. Common symptoms include:
Fragile teeth that break or decay easily
Tooth sensitivity to heat, sweetness, or cold
Greyish-yellow or brown discoloration of the teeth
Small, peg-shaped teeth
Crowded or misaligned teeth
Abnormal eruption of teeth (teeth coming in crooked or not at all)
Gum recession or exposure of the roots of the teeth
Poor enamel formation leading to yellow or brown spots on the teeth
Bone malformations such as short stature, bowed legs, or scoliosis
Other skeletal abnormalities such as clubfoot or missing joints
Frequent ear infections or hearing loss

What are the Causes of Dentinogenesis Imperfecta?
Dentinogenesis imperfecta (DI) is caused by mutations in genes that control the development and formation of dentin. The specific genes affected vary depending on the type of DI, but they all play a role in the production or structure of dentin. Some of the known causes of DI include:
Autosomal dominant inheritance – This means that if one parent has the condition, each child has a 50% chance of inheriting it.
Autosomal recessive inheritance – This means that if both parents carry the gene for DI, each child has a 25% chance of inheriting the condition. If only one parent carries the gene, each child has a 50% chance of inheriting the normal version of the gene and a 50% chance of being a carrier.
Chromosomal abnormalities – Some cases of DI have been linked to chromosomal changes such as an extra or missing copy of a specific chromosome.
Environmental factors – There is no evidence that any environmental factors cause dentinogenesis imperfecta, but exposure to certain chemicals or viruses during pregnancy may increase the risk of developing the condition.

What are the Treatment Options for Dentinogenesis Imperfecta?
There is no cure for dentinogenesis imperfecta, but there are several treatment options available to manage the symptoms and prevent complications. Some of these treatment options include:

1. Regular dental care – Regular dental check-ups can help identify and treat any oral health problems early on. This may involve fluoride applications, sealants, and fillings to protect the teeth from decay.
2. Restorative dentistry – If a tooth is damaged or decayed, restorative procedures such as crowns or fillings can help repair it. In some cases, teeth may need to be extracted if they are too badly damaged to be saved.
3. Orthodontic treatment – DI can cause teeth to become crooked or misaligned, so orthodontic treatment may be necessary to straighten the teeth and improve their alignment.
4. Pain management – People with DI may experience pain or discomfort due to sensitive teeth or exposed dentin. Over-the-counter pain relievers such as ibuprofen or acetaminophen can help manage this pain.
5. Preventive measures – To prevent further damage to the teeth, people with DI should avoid chewing on hard objects, use a soft-bristled toothbrush, and avoid acidic foods and drinks. They may also need to take antibiotics to prevent infection if they have a dental procedure or experience any oral trauma.
6. Root canal treatment – If the pulp of a tooth becomes damaged or infected, root canal treatment may be necessary to remove the infected tissue and save the tooth.
7. Dental implants – If a tooth cannot be saved and needs to be extracted, dental implants may be an option to replace it. These are artificial teeth that are surgically implanted into the jawbone to provide a natural-looking and functioning replacement for missing teeth.
8. Gum grafting – People with DI may experience receding gums, which can expose the roots of the teeth and make them more sensitive. Gum grafting can help cover the exposed roots and protect the teeth from further damage.
9. Bone grafting – In some cases, people with DI may need bone grafting to repair damaged bone in the jawbone. This can help support dental implants or other restorative procedures.
10. Orthodontic treatment – People with DI may benefit from orthodontic treatment to correct misaligned teeth and improve chewing and biting function.

Overall, it is important for people with DI to work closely with their dentist to develop a personalized treatment plan that addresses their specific needs and helps them maintain good oral health.

Heterotopic ossification can cause a range of symptoms depending on its location and severity, including pain, stiffness, limited mobility, and difficulty moving the affected limb or joint. Treatment options for heterotopic ossification include medications to reduce inflammation and pain, physical therapy to maintain range of motion, and in severe cases, surgical removal of the abnormal bone growth.

In medical imaging, heterotopic ossification is often diagnosed using X-rays or other imaging techniques such as CT or MRI scans. These tests can help identify the presence of bone growth in an abnormal location and determine the extent of the condition.

Overall, heterotopic ossification is a relatively rare condition that can have a significant impact on a person's quality of life if left untreated. Prompt medical attention and appropriate treatment can help manage symptoms and prevent long-term complications.

Micrognathism can lead to several oral health issues, including difficulty chewing, speaking, and breathing. It can also cause aesthetic concerns, as the smaller lower jaw can give the appearance of a "weak" or "receding" chin.

Treatment options for micrognathism depend on the underlying cause and severity of the condition. In mild cases, orthodontic treatment may be sufficient to correct the bite and improve oral function. In more severe cases, surgical intervention may be necessary to lengthen the lower jaw and achieve proper alignment of the teeth and jaws.

In addition to oral health issues, micrognathism can also impact an individual's overall quality of life, as it can affect their self-esteem and confidence. Therefore, it is important for individuals with micrognathism to receive proper diagnosis and treatment from a team of specialists, including orthodontists, oral surgeons, and other healthcare professionals.

Word origin:

Micrognathism comes from the Greek words "mikros," meaning small, and "gnathos," meaning jaw.

Example sentence:

"The patient was diagnosed with micrognathism, which was causing difficulty chewing and speaking, as well as aesthetic concerns."

Mandibular fractures can be classified into different types based on their location and severity. Some common types of mandibular fractures include:

1. Symphyseal fracture: This type of fracture occurs in the joint portion of the mandible, where the two bone parts meet.
2. Body fracture: This type of fracture occurs in the main body of the mandible.
3. Condylar fracture: This type of fracture occurs in the part of the mandible that forms the jaw joint, called the condyle.
4. Angle fracture: This type of fracture occurs near the angle of the mandible, where it meets the maxilla (the bone of the upper jaw).
5. Subcondylar fracture: This type of fracture occurs below the condyle, in the lower part of the mandible.

The symptoms of mandibular fractures can vary depending on the severity of the injury, but may include:

* Pain and tenderness in the jaw and facial area
* Swelling and bruising around the affected eye
* Difficulty opening or closing the mouth
* Numbness or tingling in the lower jaw and tongue
* Difficulty speaking or eating

Treatment for mandibular fractures usually involves immobilizing the jaw with a splint or brace to allow the bone to heal properly. In some cases, surgery may be required to realign the bones and secure them in place with plates, screws, or wires.

Complications of mandibular fractures can include:

* Infection
* Nerve damage
* Facial asymmetry
* Difficulty speaking or eating
* Temporomandibular joint (TMJ) dysfunction

It is important to seek medical attention immediately if you suspect that you have a mandibular fracture, as prompt treatment can help prevent complications and improve outcomes.

Some common types of bone diseases include:

1. Osteoporosis: A condition characterized by brittle, porous bones that are prone to fracture.
2. Osteoarthritis: A degenerative joint disease that causes pain and stiffness in the joints.
3. Rheumatoid arthritis: An autoimmune disorder that causes inflammation and pain in the joints.
4. Bone cancer: A malignant tumor that develops in the bones.
5. Paget's disease of bone: A condition characterized by abnormal bone growth and deformity.
6. Osteogenesis imperfecta: A genetic disorder that affects the formation of bone and can cause brittle bones and other skeletal deformities.
7. Fibrous dysplasia: A rare condition characterized by abnormal growth and development of bone tissue.
8. Multiple myeloma: A type of cancer that affects the plasma cells in the bone marrow.
9. Bone cysts: Fluid-filled cavities that can form in the bones and cause pain, weakness, and deformity.
10. Bone spurs: Abnormal growths of bone that can form along the edges of joints and cause pain and stiffness.

Bone diseases can be diagnosed through a variety of tests, including X-rays, CT scans, MRI scans, and bone biopsies. Treatment options vary depending on the specific disease and can include medication, surgery, or a combination of both.

Open fracture: The bone breaks through the skin, exposing the bone to the outside environment.

Closed fracture: The bone breaks, but does not penetrate the skin.

Comminuted fracture: The bone is broken into many pieces.

Hairline fracture: A thin crack in the bone that does not fully break it.

Non-displaced fracture: The bone is broken, but remains in its normal position.

Displaced fracture: The bone is broken and out of its normal position.

Stress fracture: A small crack in the bone caused by repetitive stress or overuse.

Examples of spontaneous fractures include:

1. Pathological fractures: Fractures that occur in the presence of a bone-weakening condition such as osteoporosis, Paget's disease, or bone cancer.
2. Stress fractures: Small cracks in the bone that occur due to repetitive stress or overuse, often seen in athletes or individuals engaged in high-impact activities.
3. Osteogenesis imperfecta: A genetic disorder characterized by brittle bones and an increased risk of fractures.
4. Osteoporotic fractures: Fractures that occur due to bone loss and weakening associated with osteoporosis.
5. Frailty fractures: Fractures that occur in individuals who are frail or have a low bone mineral density, often seen in older adults.

Symptoms of spontaneous fractures may include pain, swelling, and difficulty moving the affected limb. Treatment for these fractures depends on the underlying cause and may involve immobilization, medication, or surgery.

Types of Scleral Diseases:

1. Scleritis: This is an inflammatory condition that affects the sclera, causing redness, pain, and swelling. It can be caused by infection, autoimmune disorders, or other factors.
2. Sclerochoroidal detachment: This is a condition where the sclera pulls away from the choroid, a layer of blood vessels beneath the retina. It can cause vision loss and is often seen in patients with uveitis or other inflammatory conditions.
3. Scleral rupture: This is a rare condition where the sclera tears or ruptures, causing sudden vision loss. It is often caused by trauma or inflammation.
4. Scleroconjunctivitis: This is an inflammatory condition that affects the sclera and conjunctiva, causing redness, discharge, and sensitivity to light.
5. Sclerodermia: This is a rare genetic disorder that affects the skin and eyes, including the sclera. It can cause thinning of the skin and abnormal growth of tissue.

Symptoms of Scleral Diseases:

The symptoms of scleral diseases can vary depending on the specific condition, but may include:

* Redness and inflammation in the eye
* Pain or discomfort in the eye
* Blurred vision or vision loss
* Sensitivity to light
* Discharge or tearing
* Swelling of the eye
* Bulging of the eye
* Abnormal growth of tissue

Diagnosis and Treatment of Scleral Diseases:

Diagnosis of scleral diseases is typically made through a combination of physical examination, imaging tests such as ultrasound or MRI, and laboratory tests to rule out other conditions. Treatment depends on the specific condition and may include:

* Medications such as anti-inflammatory drugs or antibiotics
* Surgery to remove abnormal tissue or correct structural problems
* Laser therapy to improve vision or reduce inflammation
* Injections of medication into the eye
* Oral medications to treat underlying conditions such as autoimmune disorders or infections.

Prognosis:

The prognosis for scleral diseases varies depending on the specific condition and the severity of the symptoms. In general, early diagnosis and treatment can improve the outlook for many of these conditions. However, some scleral diseases may have a poor prognosis if left untreated or if they are not properly managed. It is important to seek medical attention if you experience any symptoms of scleral disease.

Prevention:

While some scleral diseases may be genetic and cannot be prevented, there are steps you can take to reduce your risk of developing certain conditions. For example:

* Avoid exposure to harmful substances such as chemicals or radiation
* Wear protective eyewear when performing activities that could potentially damage the eyes
* Maintain a healthy diet and exercise regularly to reduce your risk of developing underlying conditions such as diabetes or high blood pressure.

It is important to note that some scleral diseases may not have any noticeable symptoms until they are advanced, so it is important to receive regular eye exams to detect any potential issues early on.

In conclusion, scleral diseases can cause a wide range of symptoms and can be challenging to diagnose and treat. However, with proper medical attention and self-care, many people with scleral diseases are able to manage their symptoms and improve their quality of life. It is important to seek medical attention if you experience any symptoms of scleral disease, and to maintain regular eye exams to detect any potential issues early on.

The condition is caused by a variety of genetic mutations that can affect the development of the nervous system, muscles, or connective tissue. The symptoms of arthrogryposis can vary widely depending on the specific type and severity of the condition. They may include:

* Joint contractures: The joints become stiff and fixed in place, which can limit movement and cause deformities.
* Muscle weakness: The muscles may be weak or paralyzed, leading to difficulty moving the affected limbs.
* Delayed motor development: Children with arthrogryposis may experience delays in reaching developmental milestones such as sitting, standing, and walking.
* Limited range of motion: The joints may have a limited range of motion, making it difficult to move the affected limbs through their full range of motion.
* Muscle wasting: The muscles may waste away due to lack of use, leading to a weakened appearance.

There is no cure for arthrogryposis, but treatment options are available to help manage the symptoms and improve quality of life. These may include:

* Physical therapy: To maintain or improve muscle strength and range of motion.
* Occupational therapy: To assist with daily activities and fine motor skills.
* Surgery: To release contracted joints and improve mobility.
* Bracing and orthotics: To support weakened joints and improve posture.
* Medications: To manage pain and spasticity.

It is important to note that arthrogryposis is a complex condition, and the specific treatment plan will depend on the type and severity of the condition, as well as the individual needs of the patient. Early diagnosis and intervention are key to improving outcomes for individuals with arthrogryposis.

The term "leg length inequality" is used in the medical field to describe a condition where one leg is shorter than the other, resulting in an imbalance and potential discomfort or pain. The condition can be caused by various factors, such as genetics, injury, or uneven muscle development.

There are several different types of leg length inequality, including:

1. Congenital leg length inequality: This is a condition that is present at birth and is caused by genetic or environmental factors during fetal development.
2. Acquired leg length inequality: This type of inequality is caused by an injury or condition that affects the bones or muscles in one leg, such as a fracture or tendonitis.
3. Neurological leg length inequality: This type of inequality is caused by a neurological condition, such as cerebral palsy, that affects the development of the muscles and bones in one leg.

The symptoms of leg length inequality can vary depending on the severity of the condition, but may include:

1. Pain or discomfort in the lower back, hips, or legs
2. Difficulty walking or standing for long periods of time
3. A noticeable difference in the length of the legs
4. Muscle spasms or cramps in the legs
5. Difficulty maintaining balance or stability

Treatment options for leg length inequality will depend on the severity of the condition and may include:

1. Shoe lifts or inserts to raise the shorter leg
2. Orthotics or braces to support the affected leg
3. Physical therapy to strengthen the muscles and improve balance and coordination
4. Surgery to lengthen the shorter leg, either by cutting the bone and inserting a device to lengthen it or by fusion of the vertebrae to realign the spine.
5. In some cases, a combination of these treatments may be necessary to effectively address the condition.

It is important to note that early diagnosis and treatment of leg length inequality can help prevent further progression of the condition and reduce the risk of complications. If you suspect you or your child may have leg length inequality, it is important to consult with a healthcare professional for proper evaluation and treatment.

The term "chondrodysplasia" refers to a group of disorders that affect the development of cartilage and bone, while "punctata" means "spotted" or "speckled" in Latin. This refers to the characteristic punctate (small, dark spots) appearance of the skin and other tissues in individuals with CDP.

CDP is caused by mutations in genes that are involved in the formation and maintenance of cartilage and bone. The disorder typically affects both males and females equally, and the age of onset and severity of symptoms can vary widely. In addition to the characteristic physical features of CDP, individuals with this condition may also experience joint pain, hearing loss, and other health problems.

There is no cure for chondrodysplasia punctata, but treatment options are available to manage the associated symptoms and improve quality of life. These may include physical therapy, medication, and surgery. With appropriate care and support, individuals with CDP can lead fulfilling lives despite their condition.

There are several subtypes of EDS, each with different symptoms and characteristics. The most common forms of EDS include:

1. Classical EDS: This is the most common form of EDS and is characterized by skin that is highly elastic and stretchy, as well as joint hypermobility (loose joints) and tissue fragility.
2. Hypermobile EDS: This subtype is similar to classical EDS but has a milder form of joint hypermobility.
3. Hypermobility Spectrum Disorder (HSD): This is a newer term that encompasses individuals with hypermobile joints and musculoskeletal pain, without the typical skin features of EDS.
4. Vascular EDS: This rare subtype is characterized by fragile blood vessels that can rupture easily, leading to life-threatening complications such as organ failure or death.
5. Arthrochalasia EDS: This subtype is characterized by joint hypermobility and dislocations, as well as other features such as scoliosis and pectus excavatum (a depression in the chest wall).

EDS can affect people of all ages and genders, and it is estimated that one in 2,500 to 5,000 individuals have some form of EDS. The symptoms of EDS can vary widely depending on the subtype and severity of the condition, but common symptoms include:

* Skin that is highly elastic and stretchy
* Joint hypermobility (loose joints)
* Tissue fragility
* Muscle weakness
* Chronic pain
* Fatigue
* GI issues
* Sleep disturbances
* Neurological problems such as headaches, seizures, and poor coordination

EDS is caused by mutations in genes that code for collagen or other proteins that provide structure and strength to connective tissue. These mutations can be inherited from one's parents or can occur spontaneously. There is currently no cure for EDS, but various treatments can help manage the symptoms. These may include:

* Pain management medication
* Physical therapy
* Bracing or orthotics to support weakened joints
* Surgery to repair damaged tissues or correct physical deformities
* Lifestyle modifications such as regular exercise, a healthy diet, and stress reduction techniques.

It's important to note that EDS can be difficult to diagnose, as the symptoms can be subtle and may not be immediately apparent. A thorough medical history and physical examination, along with specialized testing such as genetic analysis or imaging studies, may be necessary to confirm the diagnosis.

Tibial fractures can range in severity from minor cracks or hairline breaks to more severe breaks that extend into the bone's shaft or even the joint. Treatment for these injuries often involves immobilization of the affected leg with a cast, brace, or walking boot, as well as pain management with medication and physical therapy. In some cases, surgery may be necessary to realign and stabilize the bone fragments.

1. Osteogenesis imperfecta (OI): This is a genetic disorder that affects the formation of collagen, which is essential for bone strength and density. People with OI have brittle bones that are prone to fractures, often from minimal trauma.
2. Achondroplasia: This is the most common form of short-limbed dwarfism, caused by a genetic mutation that affects the development of cartilage and bone. People with achondroplasia have short stature, short limbs, and characteristic facial features.
3. Cleidocranial dysostosis: This is a rare genetic disorder that affects the development of the skull and collarbones. People with cleidocranial dysostosis may have misshapen or absent collarbones, as well as other skeletal abnormalities.
4. Fibrous dysplasia: This is a benign bone tumor that can affect any bone in the body. It is caused by a genetic mutation that causes an overgrowth of fibrous tissue in the bone, leading to deformity and weakness.
5. Multiple epiphyseal dysplasia (MED): This is a group of disorders that affect the growth plates at the ends of long bones, leading to irregular bone growth and deformity. MED can be caused by genetic mutations or environmental factors.

These are just a few examples of developmental bone diseases. There are many other conditions that can affect the formation and development of bones during fetal life or childhood, each with its own unique set of symptoms and characteristics.

Some examples of musculoskeletal abnormalities include:

- Carpal tunnel syndrome: Compression of the median nerve in the wrist that can cause numbness, tingling, and weakness in the hand and arm.

- Kyphosis: An exaggerated curvature of the spine, often resulting from osteoporosis or other conditions that affect the bones.

- Osteoarthritis: Wear and tear on the joints, leading to pain, stiffness, and limited mobility.

- Clubfoot: A congenital deformity in which the foot is turned inward or outward.

- Scoliosis: An abnormal curvature of the spine that can be caused by genetics, injury, or other factors.

Musculoskeletal abnormalities can be diagnosed through physical examination, imaging tests such as X-rays and MRIs, and other diagnostic procedures. Treatment options vary depending on the specific condition but may include medication, physical therapy, braces or orthotics, or surgery in severe cases.

The symptoms of a femoral fracture may include:

* Severe pain in the thigh or groin area
* Swelling and bruising around the affected area
* Difficulty moving or straightening the leg
* A visible deformity or bone protrusion

Femoral fractures are typically diagnosed through X-rays, CT scans, or MRIs. Treatment for these types of fractures may involve immobilization with a cast or brace, surgery to realign and stabilize the bone, or in some cases, surgical plate and screws or rods may be used to hold the bone in place as it heals.

In addition to surgical intervention, patients may also require physical therapy to regain strength and mobility in the affected leg after a femoral fracture.

There are several types of osteoporosis, including:

1. Postmenopausal osteoporosis: This type of osteoporosis is caused by hormonal changes that occur during menopause. It is the most common form of osteoporosis and affects women more than men.
2. Senile osteoporosis: This type of osteoporosis is caused by aging and is the most common form of osteoporosis in older adults.
3. Juvenile osteoporosis: This type of osteoporosis affects children and young adults and can be caused by a variety of genetic disorders or other medical conditions.
4. secondary osteoporosis: This type of osteoporosis is caused by other medical conditions, such as rheumatoid arthritis, Crohn's disease, or ulcerative colitis.

The symptoms of osteoporosis can be subtle and may not appear until a fracture has occurred. They can include:

1. Back pain or loss of height
2. A stooped posture
3. Fractures, especially in the spine, hips, or wrists
4. Loss of bone density, as determined by a bone density test

The diagnosis of osteoporosis is typically made through a combination of physical examination, medical history, and imaging tests, such as X-rays or bone density tests. Treatment for osteoporosis can include medications, such as bisphosphonates, hormone therapy, or rANK ligand inhibitors, as well as lifestyle changes, such as regular exercise and a balanced diet.

Preventing osteoporosis is important, as it can help to reduce the risk of fractures and other complications. To prevent osteoporosis, individuals can:

1. Get enough calcium and vitamin D throughout their lives
2. Exercise regularly, especially weight-bearing activities such as walking or running
3. Avoid smoking and excessive alcohol consumption
4. Maintain a healthy body weight
5. Consider taking medications to prevent osteoporosis, such as bisphosphonates, if recommended by a healthcare provider.

Types of Jaw Abnormalities:

1. Malocclusion: This is a misalignment of the teeth, which can cause problems with biting and chewing, as well as difficulty opening and closing the mouth.
2. Temporomandibular joint (TMJ) disorders: These are conditions that affect the joint that connects the jawbone to the skull, leading to pain, limited movement, and clicking or locking of the jaw.
3. Osteogenesis imperfecta: This is a genetic disorder that affects the development of the jaw bones, causing them to be weak and brittle.
4. Cleft lip and palate: A congenital deformity that can affect the jaw bones, teeth, and soft tissues of the face and mouth.
5. Orthognathic anomalies: These are abnormalities in the position or shape of the jaw bones, such as a receding chin or a protruding jaw.
6. Tumors: Benign or malignant growths can occur in the jaw bones or soft tissues, causing pain, swelling, and other symptoms.
7. Trauma: Injuries to the jaw can result from accidents, sports injuries, or other forms of trauma.
8. Infection: Bacterial, viral, or fungal infections can affect the jaw bones, muscles, or other tissues, causing pain, swelling, and other symptoms.
9. Degenerative conditions: Conditions such as osteoarthritis, rheumatoid arthritis, and temporomandibular joint disease can cause degeneration of the jaw bones and surrounding tissues.
10. Genetic syndromes: Certain genetic syndromes, such as Down syndrome, can increase the risk of jaw abnormalities.

Causes of Jaw Pain in Children:

1. Teething: Teething can cause discomfort and pain in the jaw, especially during the eruption of the first and second molars.
2. Ear infections: Middle ear infections can cause pain in the jaw, as well as fever and other symptoms.
3. Sinusitis: Inflammation of the sinuses can cause pain in the jaw and face.
4. Dental problems: Tooth decay, gum disease, or other dental issues can cause pain in the jaw.
5. Orthodontic problems: Issues with braces or other orthodontic appliances can cause discomfort and pain in the jaw.
6. Jaw injuries: Injuries to the jaw bones or soft tissues, such as from sports or falls, can cause pain and swelling.
7. TMJ disorders: Disorders of the temporomandibular joint can cause pain and dysfunction in the jaw.
8. Genetic conditions: Certain genetic conditions, such as Down syndrome, can increase the risk of jaw pain in children.
9. Osteogenesis imperfecta: A rare genetic disorder that affects the development of bones, including the jaw.
10. Juvenile idiopathic arthritis: An autoimmune condition that affects the joints, including the temporomandibular joint.

It's important to note that jaw pain in children can be a symptom of a more serious underlying condition, so it's always best to consult with a healthcare professional for proper evaluation and treatment.

Also known as nonunion or malunion.

Note: This term is not intended to be used as a substitute for proper medical advice. Do you have a specific question about your condition? Please ask your healthcare provider for more information.

1. Abnormal development of the skull and facial bones, resulting in a distinctive "golden" color to the face and head.
2. Deformities of the ears and eyes, such as Microtia (small or missing ear) and Anotia (absence of the external ear).
3. Cervical spine abnormalities, including a short or missing neck.
4. Heart defects, such as atrial septal defects or ventricular septal defects.
5. Bone deformities, such as scoliosis or clubfoot.
6. Limb abnormalities, such as micromelia (small limbs) or dysmelia (abnormal limb development).
7. Intellectual disability and developmental delays.
8. Other health problems, such as gastrointestinal issues, hearing loss, and vision loss.

Goldenhar Syndrome is a complex condition, and its exact cause is not fully understood. However, it is thought to be due to genetic mutations that affect the development of the embryo during early pregnancy. The syndrome can be diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and genetic testing.

There is no cure for Goldenhar Syndrome, but treatment may include surgery to correct physical deformities, management of associated health problems, and supportive care to help with developmental delays and intellectual disability. With proper management and support, many individuals with Goldenhar Syndrome can lead fulfilling lives.

TD is caused by mutations in the foxh1 gene, which plays a crucial role in regulating the expression of genes involved in embryonic development. The disorder is usually diagnosed during the second trimester of pregnancy, and it affects approximately 1 in 20,000 to 1 in 50,000 births worldwide.

Characteristic features of TD include:

* Severe growth restriction
* Microcephaly (a small head)
* Limb deformities
* Spina bifida (a type of neural tube defect)
* Cleft palate and other facial abnormalities
* Hydrocephalus (fluid accumulation in the brain)
* Respiratory and gastrointestinal problems

There is no cure for TD, and treatment is focused on managing symptoms and supporting the family. The condition is often fatal before or shortly after birth, with survival rates ranging from 10% to 30%. However, some individuals with TD may live into their teenage years or even longer if they receive appropriate medical care and support.

The diagnosis of TD is based on a combination of prenatal ultrasound findings, fetal MRI, and genetic testing. Prenatal testing for TD is typically offered to families who have a known family history of the condition or who are at increased risk due to other factors such as advanced maternal age or a previous child with a genetic disorder.

There are several support organizations and resources available for families affected by TD, including the Thanatophoric Dysplasia Family Foundation and the National Organization for Rare Disorders (NORD). These organizations can provide information, support, and advocacy for individuals and families affected by the condition.

Soft tissue injuries can cause pain, swelling, bruising, and limited mobility, and can impact an individual's ability to perform daily activities. Treatment for soft tissue injuries may include rest, ice, compression, and elevation (RICE), as well as physical therapy, medication, or surgery, depending on the severity of the injury.

Some common examples of soft tissue injuries include:

* Sprains: stretching or tearing of ligaments, which connect bones to other bones and provide stability to joints.
* Strains: stretching or tearing of muscles or tendons, which connect muscles to bones.
* Contusions: bruises that occur when blood collects in soft tissues as a result of trauma.
* Tendinitis: inflammation of tendons, which connect muscles to bones.
* Bursitis: inflammation of bursae, small fluid-filled sacs that cushion joints and reduce friction between tendons and bones.
* Fasciitis: inflammation of the fascia, a thin layer of tissue that surrounds muscles and other organs.

The symptoms of ankylosis may include pain, stiffness, limited range of motion, and difficulty moving the affected joint. In severe cases, ankylosis can lead to a complete loss of mobility and flexibility in the affected joint, causing significant disability and impacting daily activities.

Treatment for ankylosis depends on the underlying cause and the severity of the condition. Conservative management may include physical therapy, pain medication, and lifestyle modifications, while surgical intervention may be necessary in severe cases to relieve pressure on nerves or realign the bones. In some cases, ankylosis may be a chronic condition that requires ongoing management and monitoring to manage symptoms and prevent complications.

Femoral neoplasms refer to abnormal growths or tumors that occur in the femur, which is the longest bone in the human body and runs from the hip joint to the knee joint. These tumors can be benign (non-cancerous) or malignant (cancerous), and their impact on the affected individual can range from minimal to severe.

Types of Femoral Neoplasms:

There are several types of femoral neoplasms, including:

1. Osteosarcoma: This is a type of primary bone cancer that originates in the femur. It is rare and tends to affect children and young adults.
2. Chondrosarcoma: This is another type of primary bone cancer that arises in the cartilage cells of the femur. It is more common than osteosarcoma and affects mostly older adults.
3. Ewing's Sarcoma: This is a rare type of bone cancer that can occur in any bone, including the femur. It typically affects children and young adults.
4. Giant Cell Tumor: This is a benign tumor that occurs in the bones, including the femur. While it is not cancerous, it can cause significant symptoms and may require surgical treatment.

Symptoms of Femoral Neoplasms:

The symptoms of femoral neoplasms can vary depending on the type and location of the tumor. Common symptoms include:

1. Pain: Patients with femoral neoplasms may experience pain in the affected leg, which can be worse with activity or weight-bearing.
2. Swelling: The affected limb may become swollen due to fluid accumulation or the growth of the tumor.
3. Limited mobility: Patients may experience limited mobility or stiffness in the affected joint due to pain or swelling.
4. Fracture: In some cases, femoral neoplasms can cause a fracture or weakening of the bone, which can lead to further complications.

Diagnosis and Treatment of Femoral Neoplasms:

The diagnosis of femoral neoplasms typically involves a combination of imaging studies and biopsy. Imaging studies, such as X-rays, CT scans, or MRI scans, can help identify the location and extent of the tumor. A biopsy may be performed to confirm the diagnosis and determine the type of tumor.

Treatment for femoral neoplasms depends on the type and location of the tumor, as well as the patient's age and overall health. Treatment options may include:

1. Observation: Small, benign tumors may not require immediate treatment and can be monitored with regular imaging studies to ensure that they do not grow or change over time.
2. Surgery: Many femoral neoplasms can be treated with surgery to remove the tumor and any affected bone tissue. In some cases, this may involve removing a portion of the femur or replacing it with a prosthetic implant.
3. Radiation therapy: This may be used in combination with surgery to treat more aggressive tumors or those that have spread to other areas of the body.
4. Chemotherapy: This may also be used in combination with surgery and radiation therapy to treat more aggressive tumors or those that have spread to other areas of the body.
5. Targeted therapy: This is a type of chemotherapy that targets specific molecules involved in the growth and progression of the tumor. Examples include denintuzumab mafodotin, which targets a protein called B-cell CD19, and olaratumab, which targets a protein called platelet-derived growth factor receptor alpha (PDGFR-alpha).
6. Immunotherapy: This is a type of treatment that uses the body's own immune system to fight cancer. Examples include pembrolizumab and nivolumab, which are checkpoint inhibitors that work by blocking proteins on T cells that prevent them from attacking cancer cells.

The prognosis for patients with femoral neoplasms depends on the type and location of the tumor, as well as the patient's age and overall health. In general, the prognosis is better for patients with benign tumors than those with malignant ones. However, even for patients with malignant tumors, there are many treatment options available, and the prognosis can vary depending on the specifics of the case.

It's important to note that these are general treatment options and the best course of treatment will depend on the specifics of each individual case. Patients should discuss their diagnosis and treatment options with their healthcare provider to determine the most appropriate course of action for their specific situation.

There are several factors that can contribute to bone resorption, including:

1. Hormonal changes: Hormones such as parathyroid hormone (PTH) and calcitonin can regulate bone resorption. Imbalances in these hormones can lead to excessive bone resorption.
2. Aging: As we age, our bones undergo remodeling more frequently, leading to increased bone resorption.
3. Nutrient deficiencies: Deficiencies in calcium, vitamin D, and other nutrients can impair bone health and lead to excessive bone resorption.
4. Inflammation: Chronic inflammation can increase bone resorption, leading to bone loss and weakening.
5. Genetics: Some genetic disorders can affect bone metabolism and lead to abnormal bone resorption.
6. Medications: Certain medications, such as glucocorticoids and anticonvulsants, can increase bone resorption.
7. Diseases: Conditions such as osteoporosis, Paget's disease of bone, and bone cancer can lead to abnormal bone resorption.

Bone resorption can be diagnosed through a range of tests, including:

1. Bone mineral density (BMD) testing: This test measures the density of bone in specific areas of the body. Low BMD can indicate bone loss and excessive bone resorption.
2. X-rays and imaging studies: These tests can help identify abnormal bone growth or other signs of bone resorption.
3. Blood tests: Blood tests can measure levels of certain hormones and nutrients that are involved in bone metabolism.
4. Bone biopsy: A bone biopsy can provide a direct view of the bone tissue and help diagnose conditions such as Paget's disease or bone cancer.

Treatment for bone resorption depends on the underlying cause and may include:

1. Medications: Bisphosphonates, hormone therapy, and other medications can help slow or stop bone resorption.
2. Diet and exercise: A healthy diet rich in calcium and vitamin D, along with regular exercise, can help maintain strong bones.
3. Physical therapy: In some cases, physical therapy may be recommended to improve bone strength and mobility.
4. Surgery: In severe cases of bone resorption, surgery may be necessary to repair or replace damaged bone tissue.

* Genetic mutations or variations
+ Examples: craniofacial syndromes, such as Turner syndrome
+ Other examples: asymmetrical facial features due to genetic mutations or variations
* Trauma or injuries
+ Examples: facial injuries from accidents or assaults
+ Other examples: facial paralysis or nerve damage due to trauma
* Neurological conditions
+ Examples: Bell's palsy, Moebius syndrome
+ Other examples: other neurological conditions that affect facial muscles or nerves
* Congenital conditions
+ Examples: cleft lip and palate, Down syndrome
+ Other examples: other congenital conditions that affect facial development

Note: The causes of facial asymmetry can be complex and multifactorial, and may involve a combination of genetic and environmental factors.

Slide 4: Symptoms of Facial Asymmetry

* Visible unevenness or disproportion of the face
+ May be more noticeable when viewed from the side or front
* Difficulty closing the eyes completely due to uneven eyelids
* Difficulty smiling or expressing emotions due to uneven facial muscles
* Headaches or eye strain due to misalignment of the bones or soft tissues of the face
* Self-esteem issues or body dissatisfaction due to the appearance of the face

Note: The symptoms of facial asymmetry can vary in severity and may not be immediately noticeable to others. However, they can have a significant impact on an individual's quality of life and self-esteem.

Slide 5: Diagnosis of Facial Asymmetry

* Physical examination and observation of the face and facial features
+ Measurement of the distance between facial landmarks, such as the eyes, nose, and mouth
+ Assessment of the symmetry of the eyebrows, eyelids, and facial muscles
* Imaging studies, such as CT or MRI scans, may be ordered to evaluate the bones and soft tissues of the face
* 3D imaging technology may be used to create a detailed model of the face and assess its symmetry

Note: A thorough diagnosis of facial asymmetry is important to identify any underlying causes or associated conditions that may need to be addressed.

Slide 6: Treatment of Facial Asymmetry

* Treatment options for facial asymmetry depend on the underlying cause and severity of the condition
+ Surgical procedures, such as orthodontic surgery or facial reconstructive surgery, may be necessary to correct any underlying bone or soft tissue abnormalities
+ Non-surgical treatments, such as injectable fillers or Botox, may be used to address unevenness or disproportion of the face
* Treatment may also involve addressing any associated conditions, such as TMJ dysfunction or nasal airway obstruction
* Regular follow-up appointments with a healthcare professional are important to monitor progress and adjust treatment as needed

Note: The most appropriate treatment approach for facial asymmetry will depend on the individual case and may involve a combination of surgical and non-surgical techniques.

Slide 7: Facial Asymmetry in Children

* Facial asymmetry can be present at birth or develop later in childhood due to various causes
+ Genetic conditions, such as craniosynostosis or hemifacial spasm, may cause facial asymmetry in children
+ Trauma or injury to the face can also lead to facial asymmetry
* Diagnosis and treatment of facial asymmetry in children is important to ensure proper development and self-esteem
* Treatment options for children may include surgery, orthodontic care, and other interventions depending on the underlying cause and severity of the condition

Note: Early diagnosis and appropriate treatment can help ensure proper development and self-esteem in children with facial asymmetry.

Slide 8: Facial Asymmetry in Adults

* Facial asymmetry can occur at any age, but is more common in adults due to various factors such as injury, trauma, or surgery
* Adults may experience facial asymmetry due to conditions such as Bell's palsy, tumors, or craniofacial injuries
* Treatment options for adults may include surgery, physical therapy, and other interventions depending on the underlying cause and severity of the condition
* Adults with facial asymmetry may also experience psychological effects such as lowered self-esteem and social anxiety

Note: Facial asymmetry in adults can have a significant impact on quality of life, and early diagnosis and appropriate treatment is important to address both physical and psychological symptoms.

Slide 9: Non-Surgical Treatment Options

* Non-surgical treatment options for facial asymmetry may include:
+ Orthodontic care to align teeth and improve bite
+ Facial exercises to strengthen muscles and improve symmetry
+ Botulinum toxin injections to relax facial muscles and improve symmetry
+ Fillers or injectables to correct facial asymmetry caused by volume loss or tissue deficiency
+ Physical therapy to improve facial muscle function and reduce asymmetry

Note: Non-surgical treatment options can be effective in mild to moderate cases of facial asymmetry, but may not be sufficient for more severe cases.

Slide 10: Surgical Treatment Options

* Surgical treatment options for facial asymmetry may include:
+ Osteotomy (cutting and repositioning of bone) to correct skeletal asymmetry
+ Soft tissue surgery to correct soft tissue asymmetry
+ Facial implants to improve symmetry
+ Fat transfer to augment or restore facial tissues
+ Bone grafting to correct defects or deformities

Note: Surgical treatment options can be effective in severe cases of facial asymmetry, but may be associated with risks such as infection and scarring.

Slide 11: Psychological Impact of Facial Asymmetry

* Facial asymmetry can have a significant psychological impact on individuals, including:
+ Lowered self-esteem and confidence
+ Increased anxiety and stress
+ Difficulty forming relationships or finding employment
+ Feelings of isolation and stigma

Note: The psychological impact of facial asymmetry can be significant, but can be mitigated with appropriate treatment and support.

Slide 12: Conclusion

* Facial asymmetry is a common condition that can have a significant impact on an individual's quality of life
* Both surgical and non-surgical treatment options are available for facial asymmetry, depending on the severity of the condition
* A comprehensive evaluation by a healthcare professional is necessary to determine the appropriate course of treatment for each individual case.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Some common examples of eye manifestations include:

1. Redness or inflammation of the conjunctiva (the thin membrane that covers the white part of the eye): This can be a sign of an infection, allergy, or other condition.
2. Discharge or crusting around the eyes: This can be a sign of an infection or allergies.
3. Swelling of the eyelids or eye socket: This can be a sign of an infection, injury, or other condition.
4. Bulging of one or both eyes (proptosis): This can be a sign of a tumor or other condition that is putting pressure on the eye socket.
5. Abnormal alignment of the eyes (strabismus): This can be a sign of a neurological disorder or other condition.
6. Blurring or distortion of vision: This can be a sign of a variety of conditions, including refractive errors, cataracts, glaucoma, or retinal detachment.
7. Abnormal pupillary reaction to light (photophobia): This can be a sign of a neurological disorder or other condition.
8. Eye twitching or spasms: This can be a sign of a neurological disorder or other condition.
9. Blind spots in the field of vision: This can be a sign of a retinal detachment or other condition.
10. Abnormal color vision (color blindness): This can be a sign of a genetic disorder or other condition.

Healthcare professionals may use a variety of tests and procedures to evaluate eye manifestations, including visual acuity tests, refraction tests, retinoscopy, and imaging studies such as ultrasound or MRI. Treatment of eye manifestations depends on the underlying cause and can range from glasses or contact lenses for refractive errors to surgery for cataracts or retinal detachment. In some cases, treatment of the underlying condition can help resolve the eye manifestations.

Sotos syndrome is usually diagnosed during infancy or early childhood, based on a combination of clinical features and genetic testing. Treatment is focused on managing the symptoms and addressing any associated medical conditions, such as seizures or heart defects. With appropriate support and care, individuals with Sotos syndrome can lead fulfilling lives and achieve their full potential.

This definition of Sotos syndrome is based on common usage in the medical community and may vary slightly depending on context and individual perspectives. It is important to note that medical knowledge and understanding of this condition are constantly evolving, and the definition and diagnostic criteria for Sotos syndrome may be refined over time as new research and clinical experience become available.

Some common types of mandibular diseases include:

1. Temporomandibular joint (TMJ) disorders: These are conditions that affect the joint that connects the mandible to the skull, causing pain and limited mobility in the jaw.
2. Osteomyelitis: This is a bone infection that can occur in the mandible, often as a result of trauma or infection.
3. Bone cancer: This is a malignant tumor that can develop in the mandible, often affecting the jawbone and surrounding tissues.
4. Osteogenic sarcoma: This is a type of bone cancer that typically occurs in the mandible of young adults.
5. Fibrous dysplasia: This is a developmental disorder where abnormal fibrous tissue develops in the mandible, leading to bone deformity and pain.
6. Non-odontogenic mandibular keratocyst: This is a benign cyst that can occur in the mandible, often causing pain and swelling.
7. Mandibular fracture: This is a break in the mandible that can be caused by trauma, such as a fall or a blow to the face.
8. Ameloblastoma: This is a rare benign tumor that develops in the mandible, often causing pain and swelling.
9. Pyogenic granuloma: This is a type of bacterial infection that can occur in the mandible, often causing pain and swelling.
10. Osteochondroma: This is a benign cartilage-capped bone tumor that can occur in the mandible, often causing pain and limited mobility in the jaw.

These are just a few examples of mandibular diseases, and there are many other conditions that can affect the mandible as well. If you are experiencing any symptoms or pain in your jaw, it is important to see a dentist or oral surgeon for proper diagnosis and treatment.

* Thoracic scoliosis: affects the upper back (thoracic spine)
* Cervical scoliosis: affects the neck (cervical spine)
* Lumbar scoliosis: affects the lower back (lumbar spine)

Scoliosis can be caused by a variety of factors, including:

* Genetics: inherited conditions that affect the development of the spine
* Birth defects: conditions that are present at birth and affect the spine
* Infections: infections that affect the spine, such as meningitis or tuberculosis
* Injuries: injuries to the spine, such as those caused by car accidents or falls
* Degenerative diseases: conditions that affect the spine over time, such as osteoporosis or arthritis

Symptoms of scoliosis can include:

* An uneven appearance of the shoulders or hips
* A difference in the height of the shoulders or hips
* Pain or discomfort in the back or legs
* Difficulty standing up straight or maintaining balance

Scoliosis can be diagnosed through a variety of tests, including:

* X-rays: images of the spine that show the curvature
* Magnetic resonance imaging (MRI): images of the spine and surrounding tissues
* Computed tomography (CT) scans: detailed images of the spine and surrounding tissues

Treatment for scoliosis depends on the severity of the condition and can include:

* Observation: monitoring the condition regularly to see if it progresses
* Bracing: wearing a brace to support the spine and help straighten it
* Surgery: surgical procedures to correct the curvature, such as fusing vertebrae together or implanting a metal rod.

It is important for individuals with scoliosis to receive regular monitoring and treatment to prevent complications and maintain proper spinal alignment.

Example Sentence: "The patient was diagnosed with retrognathia and required orthodontic treatment to correct the issue."

The term "Osteochondrodysplasias" comes from the Greek words "osteo," meaning bone; "chondro," meaning cartilage; and "dysplasia," meaning abnormal growth or development. These disorders can affect people of all ages, but are most commonly seen in children and young adults.

There are many different types of OCDs, each with its own unique set of symptoms and characteristics. Some of the most common types include:

* Brittle bone disease (osteogenesis imperfecta): This is a condition in which the bones are prone to fractures, often without any obvious cause.
* Camptodactyly-arthropathy-coxa vara-pericarditis (CACP) syndrome: This is a rare condition that affects the hands, feet, and joints, causing stiffness, pain, and limited mobility.
* Diaphyseal dysplasia: This is a condition in which the bones in the arms and legs are abnormally short and brittle.
* Epiphyseal dysplasia: This is a condition in which the growth plates at the ends of the long bones are abnormal, leading to short stature and other skeletal deformities.

There is no cure for OCDs, but treatment options are available to manage symptoms and improve quality of life. These may include physical therapy, braces or orthotics, medications to manage pain and inflammation, and in some cases, surgery. Early diagnosis and intervention are important to help manage the condition and prevent complications.

... (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 ...

https://en.wikipedia.org/wiki/Distraction_osteogenesis

"osteogenesis imperfecta". Merriam-Webster Dictionary. Retrieved 23 August 2021. Rowe DW (2008). "Osteogenesis imperfecta". ... Donohoe M (2020). "Therapy, Orthotics and Assistive Devices for Osteogenesis Imperfecta". In Kruse RW (ed.). Osteogenesis ... Wikimedia Commons has media related to Osteogenesis imperfecta. "Osteogenesis Imperfecta Overview". NIH Osteoporosis and ... Shapiro JR (2014). "Clinical and Genetic Classification of Osteogenesis Imperfecta and Epidemiology". Osteogenesis Imperfecta. ...

https://en.wikipedia.org/wiki/Osteogenesis_imperfecta

"Osteogenesis Imperfecta Federation of Europe". Gregory, Ted (May 5, 2009). "Osteogenesis Imperfecta: Motivational Speaker Sean ... V.C. Andrews's character Vera from the 1982 book and 2015 film My Sweet Audrina had osteogenesis imperfecta. As a child, she ... This is a list of cases of people who have osteogenesis imperfecta. Raul Krauthausen - German/Colombian activist and recipient ... Ivana Baquero's character Mandy from the 2005 film Fragile had osteogenesis imperfecta. Her nurse becomes obsessed with her and ...

https://en.wikipedia.org/wiki/List_of_people_with_osteogenesis_imperfecta

"Osteogenesis Imperfecta". The Lecturio Medical Concept Library. Retrieved 27 August 2021. "Osteomalacia and Rickets". The ... Osteogenesis imperfecta Osteomalacia Osteomyelitis Osteopenia Osteopetrosis Osteoporosis Porotic hyperostosis Primary ...

https://en.wikipedia.org/wiki/Bone_disease

Osteogenesis imperfecta Osteochondritis dissecans Ankylosing spondylitis Skeletal fluorosis is a bone disease caused by an ... "Osteogenesis Imperfecta". The Lecturio Medical Concept Library. Retrieved 26 August 2021. "Osteochondritis Dissecans". The ... magnification Structure detail of an animal bone Artificial bone Bone health Distraction osteogenesis National Bone Health ...

https://en.wikipedia.org/wiki/Bone

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 ...

https://en.wikipedia.org/wiki/Collagen,_type_I,_alpha_1

Osteogenesis imperfecta (brittle bone disease) - caused by poor quality collagen, or insufficient amounts of normal collagen ( ... "Osteogenesis imperfecta". Genetics Home Reference. Retrieved 2019-11-19. Reference, Genetics Home. "Stickler syndrome". ...

https://en.wikipedia.org/wiki/Connective_tissue_disease

Occurs in people without other inherited disorders (i.e. Osteogenesis imperfecta). It is an autosomal dominant trait. A few ... Waltimo-Sirén J, Kolkka M, Pynnönen S, Kuurila K, Kaitila I, Kovero O (March 2005). "Craniofacial features in osteogenesis ... Malmgren B, Norgren S (March 2002). "Dental aberrations in children and adolescents with osteogenesis imperfecta". Acta ... Jensen BL, Lund AM (1997-07-01). "Osteogenesis imperfecta: clinical, cephalometric, and biochemical investigations of OI types ...

https://en.wikipedia.org/wiki/Dentinogenesis_imperfecta

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 ...

https://en.wikipedia.org/wiki/Folding@home

He has osteogenesis imperfecta.[citation needed] He worked for almost 20 years in the voluntary sector, serving in various ... People with osteogenesis imperfecta, British politicians with disabilities). ...

https://en.wikipedia.org/wiki/Kevin_Shinkwin,_Baron_Shinkwin

He had osteogenesis imperfecta. Disability in Twentieth-century German Culture by Carol Poore, pg 220 German National Ethics ... People with osteogenesis imperfecta, Officers Crosses of the Order of Merit of the Federal Republic of Germany, All stub ...

https://en.wikipedia.org/wiki/Peter_Radtke

He has osteogenesis imperfecta. Guss has a brother named Sean and two sisters named Amy and Lena. He has one son, Caleb Guss ( ... The primary reason for his departure is that he was unable to tour due to the progression of his osteogenesis imperfecta. Josh ... "I have a bone-disease (osteogenesis imperfecta), so I've broken a lot of bones, and I'm really small and physically weaker than ...

https://en.wikipedia.org/wiki/Randy_Guss

Distraction osteogenesis "Антропометрическая Хирургия". Publications About Anthropometrical Cosmetology prostosportsman [Screen ...

https://en.wikipedia.org/wiki/Anthropometric_cosmetology

In classic non-deforming osteogenesis imperfecta with blue sclerae or common variable osteogenesis imperfecta with normal ... Steiner, RD; Adsit, J; Basel, D (14 February 2013). "COL1A1/2 Osteogenesis Imperfecta". COL1A1/2-Related Osteogenesis ... 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 ...

https://en.wikipedia.org/wiki/Osteochondrodysplasia

He has Osteogenesis Imperfecta. He played Trick in Lost Girl, which played for five seasons. Additionally, Howland played Harry ...

https://en.wikipedia.org/wiki/Rick_Howland

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; ...

https://en.wikipedia.org/wiki/List_of_OMIM_disorder_codes

... osteogenesis imperfecta); cerebral palsy (CP); cleft palate or lip; club foot (talipes); dissociative identity disorder (DID); ...

https://en.wikipedia.org/wiki/Kupenda_for_the_Children

... and osteogenesis (e.g., RUNX2). The beta subunit is a non-DNA binding regulatory subunit; it allosterically enhances DNA ...

https://en.wikipedia.org/wiki/CBFB

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 electric current in stimulating osteogenesis. After ...

https://en.wikipedia.org/wiki/Susan_Dymecki

In osteogenesis imperfecta, popcorn calcifications are often seen around the knees and ankles in radiological imaging, and are ... "Popcorn Calcification in Osteogenesis Imperfecta". American Journal of Medical Genetics. Part A. 146A (21): 2725-2732. doi: ... a prognostic sign in osteogenesis imperfecta". Radiology. 136 (2): 351-358. doi:10.1148/radiology.136.2.7403509. PMID 7403509. ...

https://en.wikipedia.org/wiki/Popcorn_calcification

Sillence created the standard four-type system of osteogenesis imperfecta in 1979. It enabled progress into the molecular ... Sillence DO, Senn A, Danks DM (April 1979). "Genetic heterogeneity in osteogenesis imperfecta". Journal of Medical Genetics. 16 ...

https://en.wikipedia.org/wiki/David_Sillence

"Expertise in Osteogenesis Imperfecta: Worldwide". "CBC Toronto - Shriners in Ontario drop plan to fight for hospital". Archived ... along with McGill University was named number 1 in the world in expertise in Osteogenesis Imperfecta (OI) with researchers ... Frank Rauch ranked #1 and Francis H. Glorieux #3 in global expertise in Osteogenesis Imperfecta (OI). Following years of ...

https://en.wikipedia.org/wiki/Shriners_Hospital_for_Children_–_Canada

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 ...

https://en.wikipedia.org/wiki/Lhermitte's_sign

... may be used for treatment of osteogenesis imperfecta. A single 5 mg dose of zoledronic acid is used for the ... Dwan, K; Phillipi, CA; Steiner, RD; Basel, D (19 October 2016). "Bisphosphonate therapy for osteogenesis imperfecta". The ...

https://en.wikipedia.org/wiki/Zoledronic_acid

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 ...

https://en.wikipedia.org/wiki/Bisphosphonate

She was born with osteogenesis imperfecta. Schaeffer graduated from Daniel Boone High School in 2002 and, as of September 2021 ... People with osteogenesis imperfecta, Living people, American television actresses, 20th-century American actresses, American ...

https://en.wikipedia.org/wiki/Tarah_Lynne_Schaeffer

Distraction osteogenesis Distraction osteogenesis is based on creating more cranial space for the brain by gradually moving the ... Distraction osteogenesis and minimal invasive endoscopic surgery are yet in experimental phase. Trigonocephaly seems to be the ... Over the past few years[when?] distraction osteogenesis has been gradually acknowledged since it has a positive effect on ... Akai, Takuya; Iizuka, Hideaki; Kawakami, Shigehiko (2006). "Treatment of craniosynostosis by distraction osteogenesis". ...

https://en.wikipedia.org/wiki/Trigonocephaly

Julie Fernandez - actress with osteogenesis imperfecta; founded The Disability Foundation; active on presentation of disabled ...

https://en.wikipedia.org/wiki/List_of_disability_rights_activists

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 ... December 2011). "Mutations in SERPINF1 cause osteogenesis imperfecta type VI". Journal of Bone and Mineral Research. 26 (12): ... Byers PH, Pyott SM (1 January 2012). "Recessively inherited forms of osteogenesis imperfecta". Annual Review of Genetics. 46: ...

https://en.wikipedia.org/wiki/Serpin

Distraction Osteogenesis of the Facial Skeleton. Hamilton, Ontario, Canada: Decker; 2007:38-48. Abduljabbar MH, Basendwh MA. ...

https://en.wikipedia.org/wiki/Hyaluronic_acid

Organization: Osteogenesis Imperfecta Foundation. About:. The OI Foundations mission is to educate, build public awareness, ...

https://askjan.org/organizations/Osteogenesis-Imperfecta-Foundation.cfm

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 ...

https://medlineplus.gov/genetics/condition/osteogenesis-imperfecta/

NICHD conducts and supports a variety of clinical research projects related to osteogenesis imperfecta. ... Select one of the following links to view ClinicalTrials.gov search results for studies on osteogenesis imperfecta. ... How many people are affected by or at risk of osteogenesis imperfecta (OI)? ... How many people are affected by or at risk of osteogenesis imperfecta (OI)? ...

https://www.nichd.nih.gov/health/topics/osteogenesisimp/clinicaltrials

Osteogenesis imperfecta type 3 in Golden Retrievers. Osteogenesis imperfecta type 3 (OI) is a connective tissue disease ... Combination Golden Retriever 2 vWDI + Epidermolysis bullosa + Osteogenesis imperfecta + DM. ... collagen Gly208Ala mutation in a severe case of canine osteogenesis imperfecta Archives of Biochemistry & Biophysics 384:37-46 ...

https://www.genomia.cz/en/test/oi-gr/

Mesenchymal stromal cell-derived small extracellular vesicles modulate macrophage polarization and enhance angio-osteogenesis ... Mesenchymal stromal cell-derived small extracellular vesicles modulate macrophage polarization and enhance angio-osteogenesis ...

https://scholarbank.nus.edu.sg/handle/10635/241026

BeagleCOL1A2Beendergestel

https://www.combibreed.be/osteogenesis-imperfecta/

Osteogenesis imperfecta.. Antonella Forlino, Joan C Marini. Lancet 2016 April 17. Osteogenesis imperfecta is a phenotypically ... In this Seminar, together with diagnosis, management, and treatment, we describe the defects causing osteogenesis imperfecta ... have been described in patients with osteogenesis imperfecta. Knowledge of the specific molecular basis of each form of the ...

https://read.qxmd.com/read/26542481/osteogenesis-imperfecta?redirected=slug

To improve the quality of life of people living with OI in Ghana through education awareness creation, treatments and Mutual support. Read more. ...

https://www.oifghana.org/calendar/action~agenda/time_limit~1698451200/request_format~json/

We report a new case of osteogenesis imperfecta ( OI ) type II which is a perinatal lethal form. Definition: An osteogenesis ... Patients with type III or type IV osteogenesis imperfecta.. COMPASSIONATE ALLOWANCE INFORMATION. OSTEOGENESIS IMPERFECTA ( OI ... Az osteogenesis imperfecta egy ritka öröklődő betegség, amely. II -es típusban szenvedők 1 éves korukig meghalnak. OI Type II ... Osteogenesis Imperfecta Congenita. The severity of the abnormality varies enormously - from Type II OI, which is. Type II, the ...

http://haz.ritlen.ru/osteogenesis-imperfecta-ii/

Hydrogen Sulfide Promotes Osteogenesis by Modulating Macrophage Polarization. Hydrogen Sulfide Promotes Osteogenesis by ... However, whether hydrogen sulfide mediates osteogenesis by influencing macrophages is unknown. Here, we aimed to investigate ...

https://pesquisa.bvsalud.org/portal/resource/pt/mdl-36571916

The diagnosis of osteogenesis imperfecta type III was performed based on clinical and radiographic findings along with the ... Introduction: Osteogenesis imperfecta is a rare genetic condition, which the main clinical manifestation is bone fragility with ... This study was conducted in order to familiarize health professionals with possible systemic manifestations of osteogenesis ... Osteogenesis imperfecta associated with dentinogenesis imperfecta: case report. RFO UPF []. 2012, 17, 3, pp. 336-341. ISSN 1413 ...

http://revodonto.bvsalud.org/scielo.php?script=sci_abstract&pid=S1413-40122012000300016&lng=es&nrm=iso&tlng=en

Lazar, T., deHaan, J.J., Peck, J.N., Campbell, B.G., Ginn, P.E., Phillips, L., Suero, A., Chase, J. : Osteogenesis imperfecta ...

https://dogwellnet.com/ctp/phenes/258-osteogenesis-imperfecta-type-iii-col1a1-related/?breeds=213

New uses of bisphosphonates: osteogenesis imperfecta. Title. New uses of bisphosphonates: osteogenesis imperfecta ... Osteogenesis imperfecta is a heterogeneous group of inherited disorders chiefly affecting type I collagen, resulting in bone ... The role of growth hormone and bone marrow transplantation in the treatment of osteogenesis imperfecta is still unresolved. ... Devogelaer JP, "New uses of bisphosphonates: osteogenesis imperfecta," Pediatric Palliative Care Library, accessed June 5, 2023 ...

https://pedpalascnetlibrary.omeka.net/items/show/12989

What is osteogenesis imperfecta? Osteogenesis imperfecta (OI) is a disease that causes your bones to break (fracture) easily. ... Osteogenesis Imperfecta https://www.niams.nih.gov/health-topics/osteogenesis-imperfecta ...

https://www.niams.nih.gov/search?search=What%20is%20Raynaud%E2%80%99s%20Phenomenon%3F&type=All&media=All&f%5B0%5D=archived%3A0&f%5B1%5D=audience%3A50&f%5B2%5D=diseases_and_conditions%3A180&f%5B3%5D=diseases_and_conditions%3A185&f%5B4%5D=diseases_and_conditions%3A191&f%5B5%5D=diseases_and_conditions%3A235&f%5B6%5D=diseases_and_conditions%3A248&f%5B7%5D=diseases_and_conditions%3A252&f%5B8%5D=diseases_and_conditions%3A307&f%5B9%5D=language%3Aen

Park, J. S., Yang, H. N., Woo, D. G., Jeon, S. Y. & Park, K. H. The promotion of chondrogenesis, osteogenesis and adipogenesis ... Contact osteogenesis by biodegradable 3D-printed poly(lactide-co-trimethylene carbonate) *Mohamad Nageeb Hassan ... Inclusion of calcium phosphate does not further improve in vitro and in vivo osteogenesis in a novel, highly biocompatible, ... VK staining can help detect osteogenesis. PLGC scaffold alone showed little brown nodules between the defective area and the ...

https://www.nature.com/articles/srep12721?error=cookies_not_supported&code=bca46b44-c0ca-47ee-8337-293c41bb7f44

Orthopedic Surgery Grand Rounds Zoom Attendance Only

https://cpd.education.bcm.edu/bcm-052-ay22/content/mechanisms-joint-dysfunction-osteogenesis-imperfecta

... dosage of ERF causes complex craniosynostosis in humans and mice and links ERK1/2 signaling to regulation of osteogenesis ... dosage of ERF causes complex craniosynostosis in humans and mice and links ERK1/2 signaling to regulation of osteogenesis ...

https://www.well.ox.ac.uk/publications/375699

Osteogenesis imperfecta Disorders of biotinidase Biotinidase deficiency. Sources: Raghuveer TS, Garg U, Graf WD. Inborn errors ...

https://www.cdc.gov/mmwr/preview/mmwrhtml/rr6102a1.htm

IFITM1 increases osteogenesis through Runx2 in human alveolar-derived bone marrow stromal cells. In: Bone. 2012 ; Vol. 51, No. ... IFITM1 increases osteogenesis through Runx2 in human alveolar-derived bone marrow stromal cells. Bone. 2012 Sep;51(3):506-514. ... IFITM1 increases osteogenesis through Runx2 in human alveolar-derived bone marrow stromal cells. / Kim, Beom Su; Kim, Hyung Jin ... title = "IFITM1 increases osteogenesis through Runx2 in human alveolar-derived bone marrow stromal cells", ...

https://pure.ewha.ac.kr/en/publications/ifitm1-increases-osteogenesis-through-runx2-in-human-alveolar-der

Pulse wave (PW) PBM significantly stimulated viability and cell proliferation of healthy BMMSCs compared to those of control-OVX, OVX-alendronate, OVX-LASER, and LASER+alendronate-OVX. In addition stimulatory effect of LASER+alendronate on viability and cell proliferation of OVX-BMMSCs compared to t …

https://pubmed.ncbi.nlm.nih.gov/28846932/

Osteogenesis imperfecta. *Parkinsons Disease. *Post herpetic neuralgia. *Post-surgical back pain with a condition called ...

https://norml.org/laws/medical-laws/connecticut-medical-marijuana-law/?utm_source=ct-uncasville-dis&utm_medium=faqtext&utm_campaign=bud.com&utm_content=sources

Mutation analysis of COL1A1 and COL1A2 in patients diagnosed with osteogenesis imperfecta type I-IV. Human Mutation. 2006 Jul; ... Mutation analysis of COL1A1 and COL1A2 in patients diagnosed with osteogenesis imperfecta type I-IV. In: Human Mutation. 2006 ... Osteogenesis Imperfecta (OI) is a heterogeneous group of inherited disorders characterized by increased bone fragility, with ... N2 - Osteogenesis Imperfecta (OI) is a heterogeneous group of inherited disorders characterized by increased bone fragility, ...

https://research.aber.ac.uk/en/publications/mutation-analysis-of-col1a1-and-col1a2-in-patients-diagnosed-with

He is later referred to a geneticist who makes the diagnosis of osteogenesis imperfecta. Case 2 A 16-year-old male presents to ... 9. Tosi L. Osteogenesis imperfecta. Curr Opin Pediatr 1997;9:94-99. Answers to questions 1. These can be difficult to ... Osteogenesis imperfecta (OI) is a group of disorders often defined by recurrent fractures with minimal trauma, low bone mass ... 1. How is osteogenesis imperfecta differentiated from child abuse? 2. How are future fractures prevented in children with OI? 3 ...

http://www.hawaii.edu/medicine/pediatrics/pedtext/s04c05.html

The vascular contribution to osteogenesis. I. Studies by the injection method. J Bone Joint Surg Br. 1960 Feb. 42-B:97-109. [ ...

http://emedicine.medscape.com/article/1248682-overview

... and inducing endogenous osteogenesis. Aim: This study was intended to discover the effect of hUCMSCs on an implant ... and inducing endogenous osteogenesis. Aim: This study was intended to discover the effect of hUCMSCs on an implant ... and inducing endogenous osteogenesis. Aim: This study was intended to discover the effect of hUCMSCs on an implant ... and inducing endogenous osteogenesis. Aim: This study was intended to discover the effect of hUCMSCs on an implant ...

https://scholar.unair.ac.id/en/publications/human-umbilical-cord-mesenchymal-stem-cells-induction-in-peri-imp

Valuation of Lost Productivity for Individuals Diagnosed with Osteogenesis Imperfecta: Follow-up Findingsfrom the Rudy Cohort ... Valuation of Lost Productivity for Individuals Diagnosed with Osteogenesis Imperfecta: Follow-up Findingsfrom the Rudy Cohort ...

https://www.ndorms.ox.ac.uk/publications/1281414

... deformity correction in the setting of LLD using the technique of a distal tibial corticotomy and distraction osteogenesis is ... ankle deformity correction utilizing Ilizarov circular external fixation with concurrent distal tibial distraction osteogenesis ... Distraction osteogenesis in the treatment of long bone defects of the lower limbs. Bone Joint J. 2013;95-B(12):1673-80. ... Chappell, T.M., Ebert, C.C., McCann, K.M. et al. Distal tibial distraction osteogenesis-an alternative approach to addressing ...

https://josr-online.biomedcentral.com/articles/10.1186/s13018-019-1264-0

Age-groups; Age-factors; Racial-factors; Men; Risk-analysis; Risk-factors; Health-surveys; Osteogenesis; Bone-disorders; ...

http://www2a.cdc.gov/nioshtic-2/BuildQyr.asp?s1=surveillance%2A&f1=KW&Startyear=&terms=3&Adv=1&ct=&B1=Search&Limit=500&Sort=DP+DESC&whichdate=DP&D1=10&EndYear=&PageNo=226&RecNo=2253&View=f&

Introduction to Osteogenesis Imperfecta: A Guide for Medical Professionals, Individuals and Families Affected by OI. Available ... Physical and Occupational Therapists Guide to Treating Osteogenesis Imperfecta. Available through Online Store or as a PDF ... The Osteogenesis Imperfecta Foundation. Available through Online Store or as a PDF ...

https://oif.org/informationcenter/oif-publications/

There are at least 19 recognized forms of osteogenesis imperfecta, designated type I through type XIX. (medlineplus.gov)
Increasingly, genetic causes are used to define rarer forms of osteogenesis imperfecta. (medlineplus.gov)
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. (medlineplus.gov)
The most severe forms of osteogenesis imperfecta, particularly type II, can include an abnormally small, fragile rib cage and underdeveloped lungs. (medlineplus.gov)
Mutations in other genes cause rare forms of osteogenesis imperfecta. (medlineplus.gov)
The several forms of osteogenesis imperfecta ( OI ) have been classified. (ritlen.ru)

Type I (also known as classic non-deforming osteogenesis imperfecta with blue sclerae) is the mildest form of osteogenesis imperfecta. (medlineplus.gov)
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. (medlineplus.gov)

The term "osteogenesis imperfecta" means imperfect bone formation. (medlineplus.gov)
Other types of osteogenesis imperfecta are more severe, causing frequent bone fractures that are present at birth and result from little or no trauma. (medlineplus.gov)
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. (medlineplus.gov)
Other genes involved in osteogenesis imperfecta provide instructions for making proteins that control the development and function of bone-forming cells. (medlineplus.gov)
Osteogenesis imperfecta is a phenotypically and molecularly heterogeneous group of inherited connective tissue disorders that share similar skeletal abnormalities causing bone fragility and deformity. (qxmd.com)
This article includes discussion of osteogenesis imperfecta type II: cerebral dysgenesis and brittle bone disease. (ritlen.ru)
Definition: An osteogenesis imperfecta that is characterized by bone fragility and. (ritlen.ru)
Introduction: Osteogenesis imperfecta is a rare genetic condition, which the main clinical manifestation is bone fragility with different degrees of severity. (bvsalud.org)
Osteogenesis imperfecta is a heterogeneous group of inherited disorders chiefly affecting type I collagen, resulting in bone fragility responsible for a host of recurrent fractures. (omeka.net)
The role of growth hormone and bone marrow transplantation in the treatment of osteogenesis imperfecta is still unresolved. (omeka.net)
Osteogenesis Imperfecta (OI) is a heterogeneous group of inherited disorders characterized by increased bone fragility, with clinical severity ranging from mild to lethal. (aber.ac.uk)
Osteogenesis imperfecta (OI) is a group of disorders often defined by recurrent fractures with minimal trauma, low bone mass and skeletal fragility. (hawaii.edu)
Human umbilical cord mesenchymal stem cells (hUCMSCs) produce a high osteogenic effect and are capable of modulating the immune system by suppressing inflammatory response, modulating bone resorption, and inducing endogenous osteogenesis. (unair.ac.id)
The brittle bone syndrome : osteogenesis imperfecta / Roger Smith, Martin J. O. Francis, Gregory R. Houghton. (who.int)

Hydrogen Sulfide Promotes Osteogenesis by Modulating Macrophage Polarization. (bvsalud.org)

Our diagnosis based on the ultrasound images was osteogenesis imperfecta, type II. (ritlen.ru)
The diagnosis of osteogenesis imperfecta type III was performed based on clinical and radiographic findings along with the patient's previous medical history. (bvsalud.org)
He is later referred to a geneticist who makes the diagnosis of osteogenesis imperfecta. (hawaii.edu)

Osteogenesis imperfecta type I is caused by mutations in the COL1A1 gene or, less commonly, the COL1A2 gene. (medlineplus.gov)
The mutations that cause osteogenesis imperfecta types II, III, and IV occur in either the COL1A1 or COL1A2 gene. (medlineplus.gov)
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. (medlineplus.gov)

Osteogenesis imperfecta (OI) is a group of genetic disorders that mainly affect the bones. (medlineplus.gov)

Campbell, B.G., Wootton, J.A.M., MacLeod, J.N., Minor, R.R. : Sequence of normal canine COL1A1 cDNA and identification of a heterozygous alpha 1(I) collagen Gly208Ala mutation in a severe case of canine osteogenesis imperfecta Archives of Biochemistry & Biophysics 384:37-46, 2000. (genomia.cz)

Type II (also known as perinatally lethal osteogenesis imperfecta) is the most severe. (medlineplus.gov)
OI type II is the most severe type of osteogenesis imperfecta. (ritlen.ru)
Type II osteogenesis imperfecta is lethal in the perinatal period, owing to severe fractures and deformity. (ritlen.ru)

We report a new case of osteogenesis imperfecta ( OI ) type II which is a perinatal lethal form. (ritlen.ru)

Osteogenesis imperfecta type 3 (OI) is a connective tissue disease characterized by thinning of the bones, leading to multiple fractures of the long bones and ribs. (genomia.cz)
Osteogenesis imperfecta (OI) is a disease that causes your bones to break (fracture) easily. (nih.gov)

The common inherited connective tissue disorders discussed herein include osteogenesis imperfecta, Marfan syndrome, and Ehlers-Danlos syndromes. (hawaii.edu)

Defects in proteins with very different functions, ranging from structural to enzymatic and from intracellular transport to chaperones, have been described in patients with osteogenesis imperfecta. (qxmd.com)
Patients with type III or type IV osteogenesis imperfecta. (ritlen.ru)
All patients with osteogenesis imperfecta who will undergo telescoping femoral nail application in Assiut University Hospital - Department of Orthopaedic and Trauma Surgery between April 2022 and March 2023. (who.int)

Select one of the following links to view ClinicalTrials.gov search results for studies on osteogenesis imperfecta. (nih.gov)

NICHD conducts and supports a variety of clinical research related to osteogenesis imperfecta. (nih.gov)

The successful treatment of hindfoot and ankle deformity correction in the setting of LLD using the technique of a distal tibial corticotomy and distraction osteogenesis is reported and illustrates an additional treatment technique with comparable measured outcomes to those previously described. (biomedcentral.com)

This study was conducted in order to familiarize health professionals with possible systemic manifestations of osteogenesis imperfecta associated with dentinogenesis imperfecta, as well as the oral aspects of this condition, since the severity of the disease is quite variable. (bvsalud.org)

This research was also supported by the National Institute of Dental and Craniofacial Research, the National Institute of Environmental Health Sciences, the National Institute of Child Health and Human Development, the Baylor College of Medicine Mental Retardation Developmental Disabilities Research Center, the Shriners of North America, the Osteogenesis Imperfecta Foundation and the Bone Diseases Program of Texas. (nih.gov)

Recessive osteogenesis imperfecta is caused by deficiency of any of the three components of the collagen prolyl 3-hydroxylation complex. (nih.gov)
Other causes of recessive osteogenesis imperfecta include deficiency of the collagen chaperones FKBP10 or Serpin H1. (nih.gov)
Murine models are crucial to uncovering the common pathways in dominant and recessive osteogenesis imperfecta bone dysplasia. (nih.gov)
Recessive osteogenesis imperfecta is collagen-related / Joan C. Marini. (nih.gov)
CRTAP is required for prolyl 3-hydroxylation and mutations cause recessive osteogenesis imperfecta. (nih.gov)

RESEARCH OBJECTIVES Background Osteogenesis imperfecta (OI) is a genetic disease of bone, caused by mutations in a gene for type I collagen, the principal structural protein of bone. (nih.gov)
Background Osteogenesis imperfecta (OI) is a heritable bone dysplasia caused by defects in collagen processing and synthesis. (nih.gov)

Smith R, Francis MJ, Houghton GR. The Brittle Bone Syndrome: Osteogenesis Imperfecta . (medscape.com)
Also known as "brittle bone disease," osteogenesis imperfecta (OI) is a genetic disorder that causes weak bones that break easily in addition to other symptoms. (nih.gov)

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. (medlineplus.gov)

A new paradigm has emerged for osteogenesis imperfecta as a collagen-related disorder. (nih.gov)

PURPOSE This initiative is intended to stimulate and support new research projects that have the potential to increase our understanding of skeletal pathology in osteogenesis imperfecta (OI), and to lead to improved therapeutic approaches to the disease. (nih.gov)

Steinberg B, Fattahi T. Distraction osteogenesis in management of pediatric airway: evidence to support its use. (medscape.com)

Osteogenesis imperfecta can be caused by mutations in one of several genes. (medlineplus.gov)
Osteogenesis imperfecta type I is caused by mutations in the COL1A1 gene or, less commonly, the COL1A2 gene. (medlineplus.gov)
The mutations that cause osteogenesis imperfecta types II, III, and IV occur in either the COL1A1 or COL1A2 gene. (medlineplus.gov)

In 1835, Lobstein coined the term osteogenesis imperfecta and was one of the first to correctly understand the etiology of the condition. (medscape.com)

Management of severe maxillary deficiency in childhood and adolescence through distraction osteogenesis with an external, adjustable, rigid distraction device. (medscape.com)

What are the treatments for osteogenesis imperfecta (OI)? (nih.gov)

Cardiovascular abnormalities and its correlation with genotypes of children with osteogenesis imperfecta. (nih.gov)
Clinical management of osteogenesis imperfecta is multidisciplinary, encompassing substantial progress in physical rehabilitation and surgical procedures, management of hearing, dental and pulmonary abnormalities, as well as drugs, such as bisphosphonates and recombinant human growth hormone. (nih.gov)

What Are the Symptoms of Osteogenesis Imperfecta (OI)? (nih.gov)
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. (medlineplus.gov)

The workup primarily relies on radiographic information to define the anatomic deformity and to assess whether distraction osteogenesis is a viable alternative to conventional surgery. (medscape.com)

Modern approach to children with osteogenesis imperfecta. (medscape.com)
Feeding and mandibular distraction osteogenesis in children with Pierre Robin sequence: A case series of functional outcomes. (medscape.com)

A roadmap to surgery in osteogenesis imperfecta: results of an international collaboration of patient organizations and interdisciplinary care teams. (medscape.com)

Type I (also known as classic non-deforming osteogenesis imperfecta with blue sclerae) is the mildest form of osteogenesis imperfecta. (medlineplus.gov)

Yamauchi K, Takahashi T, Nogami S, Kataoka Y, Miyamoto I, Funaki K. Horizontal alveolar distraction osteogenesis for dental implant: long-term results. (medscape.com)

This Request for Applications (RFA), New Research Strategies in Osteogenesis Imperfecta, is related to the priority areas of fetal, infant and child deaths, and developmental disabilities. (nih.gov)

Curative Cell and Gene Therapy for Osteogenesis Imperfecta. (nih.gov)
Factors that contribute to the mechanism of dominant osteogenesis imperfecta include intracellular stress, disruption of interactions between collagen and noncollagenous proteins, compromised matrix structure, abnormal cell-cell and cell-matrix interactions and tissue mineralization. (nih.gov)

Osteogenesis imperfecta affects approximately 1 in 10,000 to 20,000 people worldwide. (medlineplus.gov)

How Do Health Care Providers Diagnose Osteogenesis Imperfecta (OI)? (nih.gov)
This study was conducted in order to familiarize health professionals with possible systemic manifestations of osteogenesis imperfecta associated with dentinogenesis imperfecta, as well as the oral aspects of this condition, since the severity of the disease is quite variable. (bvsalud.org)

Anatomy37

Organisms2

Diseases35

Chemicals and Drugs38

Analytical, Diagnostic and Therapeutic Techniques and Equipment27

Phenomena and Processes37

Disciplines and Occupations1

Technology, Industry, Agriculture6

Information Science3

Named Groups1

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

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

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

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

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

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

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

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

Osteogenesis Imperfecta

Osteogenesis

Osteogenesis, Distraction

Osteoblasts

Bone Regeneration

Procollagen

Calcification, Physiologic

Bone and Bones

Mandible

Core Binding Factor Alpha 1 Subunit

Skull

External Fixators

Mesenchymal Stromal Cells

Alkaline Phosphatase

Bone Matrix

Bone Morphogenetic Protein 2

Bony Callus

Tibia

Collagen

Collagen Type I

X-Ray Microtomography

Ilizarov Technique

Periosteum

Dentinogenesis Imperfecta

Mandibular Osteotomy

Bone Development

Cell Differentiation

Fracture Healing

Osteocalcin

Adipogenesis

Ossification, Heterotopic

Integrin-Binding Sialoprotein

Osseointegration

Osteocytes

Femur

Chondrogenesis

Micrognathism

Glycine

Mandibular Fractures

Bone Morphogenetic Proteins

Osteotomy

Cells, Cultured

Jaw Fixation Techniques

Bone Diseases

Cranial Sutures

Mutation

Bone Substitutes

Bone Lengthening

Alveolar Process

Cartilage

Bone Marrow Cells

Fractures, Bone

Stromal Cells

Genes, Lethal

Tissue Scaffolds

Bone Remodeling

Bone Density

Bone Transplantation

Durapatite

Diphosphonates

Fractures, Spontaneous

Tissue Engineering

Implants, Experimental

Scleral Diseases

Elaeagnaceae

Bone Demineralization Technique

Ulna

Arthrogryposis

Leg Length Inequality

Alveolar Ridge Augmentation

Fibroblasts

Cyclophilins

Tropocollagen

Osteopontin

Pedigree

Skin

Chondrodysplasia Punctata

Ehlers-Danlos Syndrome

Base Sequence

Procollagen N-Endopeptidase