Extracellular substance of bone tissue consisting of COLLAGEN fibers, ground substance, and inorganic crystalline minerals and 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.
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 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.
Bone loss due to osteoclastic activity.
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.
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 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.
The process of bone formation. Histogenesis of bone including ossification.
Renewal or repair of lost bone tissue. It excludes BONY CALLUS formed after BONE FRACTURES but not yet replaced by hard bone.
Process by which organic tissue becomes hardened by the physiologic deposit of calcium salts.
Bone-forming cells which secrete an EXTRACELLULAR MATRIX. HYDROXYAPATITE crystals are then deposited into the matrix to form bone.
The grafting of bone from a donor site to a recipient site.
Tumors or cancer located in bone tissue or specific BONES.
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.
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 soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
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.
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).
Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.
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.
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 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.
Diseases of 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.
The SKELETON of the HEAD including the FACIAL BONES and the bones enclosing the BRAIN.
A secreted endopeptidase homologous with INTERSTITIAL COLLAGENASE, but which possesses an additional fibronectin-like domain.
A family of zinc-dependent metalloendopeptidases that is involved in the degradation of EXTRACELLULAR MATRIX components.
Breaks in bones.
The longest and largest bone of the skeleton, it is situated between the hip and the knee.
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).
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.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.
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).
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.
X-RAY COMPUTERIZED TOMOGRAPHY with resolution in the micrometer range.
Benign unilocular lytic areas in the proximal end of a long bone with well defined and narrow endosteal margins. The cysts contain fluid and the cyst walls may contain some giant cells. Bone cysts usually occur in males between the ages 3-15 years.
Thin outer membrane that surrounds a bone. It contains CONNECTIVE TISSUE, CAPILLARIES, nerves, and a number of cell types.
The residual framework structure of the CELL NUCLEUS that maintains many of the overall architectural features of the cell nucleus including the nuclear lamina with NUCLEAR PORE complex structures, residual CELL NUCLEOLI and an extensive fibrogranular structure in the nuclear interior. (Advan. Enzyme Regul. 2002; 42:39-52)
A potent osteoinductive protein that plays a critical role in the differentiation of osteoprogenitor cells into OSTEOBLASTS.
The transference of BONE MARROW from one human or animal to another for a variety of purposes including HEMATOPOIETIC STEM CELL TRANSPLANTATION or MESENCHYMAL STEM CELL TRANSPLANTATION.
A circular structural unit of bone tissue. It consists of a central hole, the Haversian canal through which blood vessels run, surrounded by concentric rings, called lamellae.
Artificial substitutes for body parts and materials inserted into organisms during experimental studies.
One of a pair of irregularly shaped quadrilateral bones situated between the FRONTAL BONE and OCCIPITAL BONE, which together form the sides of the CRANIUM.
Tomography using x-ray transmission.
Non-collagenous, calcium-binding glycoprotein of developing bone. It links collagen to mineral in the bone matrix. In the synonym SPARC glycoprotein, the acronym stands for Secreted Protein, Acidic and Rich in Cysteine.
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.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
A member of the metalloproteinase family of enzymes that is principally responsible for cleaving FIBRILLAR COLLAGEN. It can degrade interstitial collagens, types I, II and III.
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 development of bony substance in normally soft structures.
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.
Compounds that inhibit the enzyme activity or activation of MATRIX METALLOPROTEINASES.
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.
Removal of minerals from bones during bone examination.
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.
A plant genus of the family EUPHORBIACEAE, order Euphorbiales, subclass Rosidae. The seed of Ricinus communis L. is the CASTOR BEAN which is the source of CASTOR OIL; RICIN; and other lectins.
Dissolution of bone that particularly involves the removal or loss of calcium.
An extracellular endopeptidase of vertebrate tissues similar to MATRIX METALLOPROTEINASE 1. It digests PROTEOGLYCAN; FIBRONECTIN; COLLAGEN types III, IV, V, and IX, and activates procollagenase. (Enzyme Nomenclature, 1992)
The physiological restoration of bone tissue and function after a fracture. It includes BONY CALLUS formation and normal replacement of bone tissue.
The largest and strongest bone of the FACE constituting the lower jaw. It supports the lower teeth.
A bone morphogenetic protein that is found at high concentrations in a purified osteoinductive protein fraction from BONE. Bone morphogenetic protein 3 is referred to as osteogenin, however it may play a role in variety of developmental processes.
The mineral component of bones and teeth; it has been used therapeutically as a prosthetic aid and in the prevention and treatment of osteoporosis.
Native, inorganic or fossilized organic substances having a definite chemical composition and formed by inorganic reactions. They may occur as individual crystals or may be disseminated in some other mineral or rock. (Grant & Hackh's Chemical Dictionary, 5th ed; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Bone in humans and primates extending from the SHOULDER JOINT to the ELBOW JOINT.
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.
A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.
Microscopy in which the object is examined directly by an electron beam scanning the specimen point-by-point. The image is constructed by detecting the products of specimen interactions that are projected above the plane of the sample, such as backscattered electrons. Although SCANNING TRANSMISSION ELECTRON MICROSCOPY also scans the specimen point by point with the electron beam, the image is constructed by detecting the electrons, or their interaction products that are transmitted through the sample plane, so that is a form of TRANSMISSION ELECTRON MICROSCOPY.
The shaft of long bones.
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Either of a pair of compound bones forming the lateral (left and right) surfaces and base of the skull which contains the organs of hearing. It is a large bone formed by the fusion of parts: the squamous (the flattened anterior-superior part), the tympanic (the curved anterior-inferior part), the mastoid (the irregular posterior portion), and the petrous (the part at the base of the skull).
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.
Synthetic or natural materials, other than DRUGS, that are used to replace or repair any body TISSUES or bodily function.
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.
A cysteine protease that is highly expressed in OSTEOCLASTS and plays an essential role in BONE RESORPTION as a potent EXTRACELLULAR MATRIX-degrading enzyme.
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.
Calcium salts of phosphoric acid. These compounds are frequently used as calcium supplements.
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.
A transmembrane protein belonging to the tumor necrosis factor superfamily that specifically binds RECEPTOR ACTIVATOR OF NUCLEAR FACTOR-KAPPA B and OSTEOPROTEGERIN. It plays an important role in regulating OSTEOCLAST differentiation and activation.
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.
Elements of limited time intervals, contributing to particular results or situations.
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.
A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.
The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth.
A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.
A secreted matrix metalloproteinase that plays a physiological role in the degradation of extracellular matrix found in skeletal tissues. It is synthesized as an inactive precursor that is activated by the proteolytic cleavage of its N-terminal propeptide.
The properties, processes, and behavior of biological systems under the action of mechanical forces.
A transmembrane domain-containing matrix metalloproteinase. It is synthesized as an inactive zymogen that is activated by the action of PROPROTEIN CONVERTASES such as FURIN. Matrix metalloproteinase 14 plays a direct role in the cleavage of proteins in the pericellular environment. In addition, it can function indirectly by enzymatically activating the proprotein form of MATRIX METALLOPROTEINASE 15.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
The smallest member of the MATRIX METALLOPROTEINASES. It plays a role in tumor progression.
Resorption or wasting of the tooth-supporting bone (ALVEOLAR PROCESS) in the MAXILLA or MANDIBLE.
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 hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.
Adhesives used to fix prosthetic devices to bones and to cement bone to bone in difficult fractures. Synthetic resins are commonly used as cements. A mixture of monocalcium phosphate, monohydrate, alpha-tricalcium phosphate, and calcium carbonate with a sodium phosphate solution is also a useful bone paste.
Excessive formation of dense trabecular bone leading to pathological fractures; OSTEITIS; SPLENOMEGALY with infarct; ANEMIA; and extramedullary hemopoiesis (HEMATOPOIESIS, EXTRAMEDULLARY).
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
Condition of having pores or open spaces. This often refers to bones, bone implants, or bone cements, but can refer to the porous state of any solid substance.
Restoration of integrity to traumatized tissue.
A group of thermoplastic or thermosetting polymers containing polyisocyanate. They are used as ELASTOMERS, as coatings, as fibers and as foams.
Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins.
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.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A sarcoma originating in bone-forming cells, affecting the ends of long bones. It is the most common and most malignant of sarcomas of the bones, and occurs chiefly among 10- to 25-year-old youths. (From Stedman, 25th ed)
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.
Established cell cultures that have the potential to propagate indefinitely.
A secreted member of the TNF receptor superfamily that negatively regulates osteoclastogenesis. It is a soluble decoy receptor of RANK LIGAND that inhibits both CELL DIFFERENTIATION and function of OSTEOCLASTS by inhibiting the interaction between RANK LIGAND and RECEPTOR ACTIVATOR OF NUCLEAR FACTOR-KAPPA B.
Pathologic deposition of calcium salts in tissues.
VERTEBRAE in the region of the lower BACK below the THORACIC VERTEBRAE and above the SACRAL VERTEBRAE.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.
The spinal or vertebral column.
Operative immobilization or ankylosis of two or more vertebrae by fusion of the vertebral bodies with a short bone graft or often with diskectomy or laminectomy. (From Blauvelt & Nelson, A Manual of Orthopaedic Terminology, 5th ed, p236; Dorland, 28th ed)
A bone morphogenetic protein that is widely expressed during EMBRYONIC DEVELOPMENT. It is both a potent osteogenic factor and a specific regulator of nephrogenesis.
Matrix metalloproteinases that are associated with the CELL MEMBRANE, either through transmembrane domains or GLYCOSYLPHOSPHATIDYLINOSITOL ANCHORS. Membrane-type matrix metalloproteinases may act within the pericellular environment to influence the process of CELL MIGRATION.

Noncollagenous bone matrix proteins, calcification, and thrombosis in carotid artery atherosclerosis. (1/363)

Advanced atherosclerosis is often associated with dystrophic calcification, which may contribute to plaque rupture and thrombosis. In this work, the localization and association of the noncollagenous bone matrix proteins osteonectin, osteopontin, and osteocalcin with calcification, lipoproteins, thrombus/hemorrhage (T/H), and matrix metalloproteinases (MMPs) in human carotid arteries from endarterectomy samples have been determined. According to the recent American Heart Association classification, 6 of the advanced lesions studied were type V (fibroatheroma) and 16 type VI (complicated). Osteonectin, osteocalcin, and osteopontin were identified by monoclonal antibodies IIIA(3)A(8), G12, and MPIIIB10(1) and antiserum LF-123. Apolipoprotein (apo) AI, B, and E; lipoprotein(a); fibrinogen; fibrin; fragment D/D-dimer; MMP-2 (gelatinase A); and MMP-3 (stromelysin-1) were identified with previously characterized antibodies. Calcium phosphate deposits (von Kossa's stain) were present in 82% of samples (3 type V and 15 type VI). Osteonectin was localized in endothelial cells, SMCs, and macrophages and was associated with calcium deposits in 33% of type V and 88% of type VI lesions. Osteopontin was distributed similarly to osteonectin and was associated with calcium deposits in 50% of type V and 94% of type VI lesions. Osteocalcin was localized in large calcified areas only (in 17% of type V and 38% of type VI lesions). ApoB colocalized with cholesterol crystals and calcium deposits. Lipoprotein(a) was localized in the intima, subintima, and plaque shoulder. Fibrin (T/H) colocalized with bone matrix proteins in 33% of type V and 69% of type VI lesions. MMP-3 was cytoplasmic in most cells and colocalized with calcium and fibrin deposits. MMP-2 was less often associated with calcification. The results of this study show that osteonectin, osteopontin, and osteocalcin colocalized with calcium deposits with apoB, fibrin, and MMP-3 in advanced, symptomatic carotid lesions. These data suggest that the occurrence of T/H might contribute to dystrophic arterial calcification in the progression and complications of atherosclerosis.  (+info)

Xenogenic demineralized bone matrix: osteoinduction and influence of associated skeletal defects in heterotopic bone formation in rats. (2/363)

Demineralized bone matrix (DBM) was ectopically implanted in 36 male Wistar rats. In 18 of the animals a bone defect in the femoral condyles was also created: the left was filled with DBM and the right was left empty as a control. The animals were killed after 2, 4 and 6 weeks and new bone was histologically evaluated, comparing ectopic bone formation with or without distant bone injury. Results showed: (1) osteoinductivity of xenogenic DBM, and (2) earlier mineralization of ectopically implanted DBM in the group with associated skeletal injury. Our results show that xenogenic bone matrix acts as an osteoinductive material and that skeletal injury improves osteogenesis at distant sites.  (+info)

Changes in the orientation of collagen fibers on the superficial layer of the mouse tibial bone after denervation: scanning electron microscopic observations. (3/363)

This study was undertaken to evaluate the relationship between the mechanical stress loaded onto the bone and the orientation of collagen fibers formed by osteoblasts. The femoral, obturator, and sciatic nerves in the left posterior legs of 7-week-old mice were exposed and electroscissored to reduce the mechanical stress loaded onto the leg. Four weeks after operation, the tibial bones in the control and denervated legs were removed and observed by scanning electron microscopy (SEM) after NaOCl treatment. In the control right tibia, collagen fibers on the superficial bone matrix tended to be arranged parallel to the longitudinal axis of the bone. However, the arrangement of collagen fibers in the left tibia, which were immobilized for 4 weeks by denervation, was disorganized and ran in random directions. The findings suggest that the direction of collagen fibers in the bone changes in response to the mechanical stress loaded onto the bone, probably due to changes in the activity of osteoblasts in the denervated leg.  (+info)

Bone morphogenetic proteins in human bone regeneration. (4/363)

Recently, the first clinical reports on bone regeneration by two recombinant human bone morphogenetic proteins (rhBMPs), BMP-2 and BMP-7 (also named osteogenic protein-1, OP-1) have been published (1-4). Although both BMPs were able to support bone regeneration, a significant variation in individual response was observed with both proteins. Animal studies and laboratory experiments reveal a number of conditions that influence the osteoinductivity of BMP, such as BMP concentration, carrier properties and influence of local and systemic growth factors and hormones. In this paper, these studies and the clinical reports are reviewed, and the conditions that modulate the BMP-dependent osteoinduction are discussed. The information may provide clues as to how the performance of recombinant human BMP as bone-graft substitute in humans can be improved.  (+info)

The cell biology of osteoclast function. (5/363)

Osteoclasts are multinucleated cells responsible for bone resorption. They have developed an efficient machinery for dissolving crystalline hydroxyapatite and degrading organic bone matrix rich in collagen fibers. When initiating bone resorption, osteoclasts become polarized, and three distinct membrane domains appear: a ruffled border, a sealing zone and a functional secretory domain. Simultaneously, the cytoskeleton undergoes extensive re-organisation. During this process, the actin cytoskeleton forms an attachment ring at the sealing zone, the membrane domain that anchors the resorbing cell to bone matrix. The ruffled border appears inside the sealing zone, and has several characteristics of late endosomal membrane. Extensive vesicle transport to the ruffled border delivers hydrochloric acid and proteases to an area between the ruffled border and the bone surface called the resorption lacuna. In this extracellular compartment, crystalline hydroxyapatite is dissolved by acid, and a mixture of proteases degrades the organic matrix. The degradation products of collagen and other matrix components are endocytosed, transported through the cell and exocytosed through a functional secretory domain. This transcytotic route allows osteoclasts to remove large amounts of matrix-degradation products without losing their tight attachment to underlying bone. It also facilitates further processing of the degradation products intracellularly during the passage through the cell.  (+info)

109Cd K x ray fluorescence measurements of tibial lead content in young adults exposed to lead in early childhood. (6/363)

OBJECTIVES: Tibia lead measurements were performed in a population of 19-29 year old people who had been highly exposed to lead in childhood to find whether lead had persisted in the bone matrix until adulthood. METHODS: (109)Cd K x ray fluorescence was used to measure the tibia lead concentrations of 262 exposed subjects and 268 age and sex matched controls. Questionnaire data allowed a years of residence index to be calculated for exposed subjects. A cumulative blood lead index was calculated from the time weighted integration of available data of blood lead. RESULTS: The mean (SEM) difference between exposed and control men was 4.51 (0.35) micrograms Pb/g bone mineral, and between exposed and control women was 3.94 (0. 61) micrograms Pb/g bone mineral. Grouped mean bone lead concentrations of exposed subjects were predicted best by age. When exposed and control subjects' data were combined, grouped mean bone lead concentrations were predicted best by cumulative blood lead index. The years of residence index was neither a good predictor of bone lead concentrations for exposed subjects nor for exposed and control subjects combined. Finally, exposed subjects had increased current blood lead concentrations that correlated significantly with bone lead values. CONCLUSION: Bone lead concentrations of exposed subjects were significantly increased compared with those of control subjects. Lead from exposure in early childhood had persisted in the bone matrix until adulthood. Exposed subjects had increased blood lead concentrations compared with controls. Some of this exposure could be related to ongoing exposure. However, some of the increase in blood lead concentration in adult exposed subjects seemed to be a result of endogenous exposure from increased bone lead stores. The endogenous exposure relation found for men was consistent with reported data, but the relation found for women was significantly lower. Further research is needed to find whether the observed differences are due to sex, or pregnancy and lactation.  (+info)

The roles of annexins and types II and X collagen in matrix vesicle-mediated mineralization of growth plate cartilage. (7/363)

Annexins II, V, and VI are major components of matrix vesicles (MV), i.e. particles that have the critical role of initiating the mineralization process in skeletal tissues. Furthermore, types II and X collagen are associated with MV, and these interactions mediated by annexin V stimulate Ca(2+) uptake and mineralization of MV. However, the exact roles of annexin II, V, and VI and the interaction between annexin V and types II and X collagen in MV function and initiation of mineralization are not well understood. In this study, we demonstrate that annexin II, V, or VI mediate Ca(2+) influx into phosphatidylserine (PS)-enriched liposomes, liposomes containing lipids extracted from authentic MV, and intact authentic MV. The annexin Ca(2+) channel blocker, K-201, not only inhibited Ca(2+) influx into fura-2-loaded PS-enriched liposomes mediated by annexin II, V, or VI, but also inhibited Ca(2+) uptake by authentic MV. Types II and X collagen only bound to liposomes in the presence of annexin V but not in the presence of annexin II or VI. Binding of these collagens to annexin V stimulated its Ca(2+) channel activities, leading to an increased Ca(2+) influx into the liposomes. These findings indicate that the formation of annexin II, V, and VI Ca(2+) channels in MV together with stimulation of annexin V channel activity by collagen (types II and X) binding can explain how MV are able to rapidly take up Ca(2+) and initiate the formation of the first crystal phase.  (+info)

Localization of alkaline phosphatase and osteopontin during matrix mineralization in the developing cartilage of coccygeal vertebrae. (8/363)

We observed the manner in which alkaline phosphatase (ALPase) and osteopontin were localized in the cartilage and intramembranous bone of coccygeal vertebrae during matrix mineralization, shedding considerable light on the manner in which they develop. In the cartilage matrix of coccygeal vertebrae, we observed the localization of ALPase activity in the boundary of the proliferative and the hypertrophic zones. Granular nodules of mineralization were consistently found in the boundary of both zones, and increased in size when close to the hypertrophic zone. While osteopontin was rarely present in the early stages of mineralization, its localization along the margins of mineralized matrices in the hypertrophic zone was prominent. In contrast to cartilage, mineralized nodules in the intramembranous bone in the mid-portion of the vertebra displayed osteopontin-immunoreactivity, indicating its early synthesis and subsequent accumulation to early-stage mineralized nodules. When blood vessels, accompanied by osteoblastic and osteoclastic cell populations, invaded the cartilage, osteopontin was localized in the lower region of the hypertrophic zone, despite its maintaining the localization of ALPase and early-stage mineralization. Thus, our investigation demonstrated ALPase activity consistent with early-stage mineralization in the cartilage matrix. However, the fact that osteopontin-localization could not be pinpointed might account for its multifunctionality as concerns both the regulation of mineralization and the attachment of migrating osteogenic and osteoclastic cells to the mineralized matrix.  (+info)

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.

Some common types of bone neoplasms include:

* Osteochondromas: These are benign tumors that grow on the surface of a bone.
* Giant cell tumors: These are benign tumors that can occur in any bone of the body.
* Chondromyxoid fibromas: These are rare, benign tumors that develop in the cartilage of a bone.
* Ewing's sarcoma: This is a malignant tumor that usually occurs in the long bones of the arms and legs.
* Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow.

Symptoms of bone neoplasms can include pain, swelling, or deformity of the affected bone, as well as weakness or fatigue. Treatment options depend on the type and location of the tumor, as well as the severity of the symptoms. Treatment may involve surgery, radiation therapy, chemotherapy, or a combination of these.

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.

* Osteogenesis imperfecta (OI): A genetic disorder that affects the formation of bone tissue, leading to fragile bones and an increased risk of fractures.
* Rickets: A vitamin D-deficient disease that causes softening of the bones in children.
* Osteomalacia: A condition similar to rickets, but affecting adults and caused by a deficiency of vitamin D or calcium.
* Hyperparathyroidism: A condition in which the parathyroid glands produce too much parathyroid hormone (PTH), leading to an imbalance in bone metabolism and an increase in bone resorption.
* Hypoparathyroidism: A condition in which the parathyroid glands produce too little PTH, leading to low levels of calcium and vitamin D and an increased risk of osteoporosis.

Bone diseases, metabolic are typically diagnosed through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests to evaluate bone metabolism. Treatment depends on the specific underlying cause of the disease and may include medications, dietary changes, or surgery.

There are several types of bone cysts, including:

1. Simple bone cysts: These are the most common type of bone cyst and typically occur in children and young adults. They are filled with air or fluid and do not contain any cancerous cells.
2. Angiomatous cysts: These are smaller than simple bone cysts and are usually found near the ends of long bones. They are also filled with blood vessels and do not contain any cancerous cells.
3. Unicameral (simple) bone cysts: These are similar to simple bone cysts but are larger and may be more complex in shape.
4. Multicameral bone cysts: These are larger than unicameral bone cysts and may contain multiple chambers filled with air or fluid.
5. Enchondromas: These are benign tumors that occur within the cartilage of a bone. They are usually found in the long bones of the arms and legs.
6. Chondromyxoid fibromas: These are rare, benign tumors that occur in the cartilage of a bone. They are typically found in the long bones of the arms and legs.
7. Osteochondromas: These are benign tumors that arise from the cartilage and bone of a joint. They are usually found near the ends of long bones.
8. Malignant bone cysts: These are rare and can be cancerous. They may occur in any bone of the body and can be aggressive, spreading quickly to other areas of the body.

The symptoms of bone cysts can vary depending on their size and location. They may cause pain, swelling, and limited mobility in the affected limb. In some cases, they may also lead to fractures or deformities.

Diagnosis of bone cysts usually involves imaging tests such as X-rays, CT scans, or MRI scans. A biopsy may also be performed to confirm the diagnosis and rule out other possible conditions.

Treatment for bone cysts depends on their size, location, and severity. Small, asymptomatic cysts may not require any treatment, while larger cysts may need to be drained or surgically removed. In some cases, medication such as bisphosphonates may be used to help reduce the risk of fractures.

In conclusion, bone cysts are abnormalities that can occur in any bone of the body. They can be benign or malignant and can cause a range of symptoms depending on their size and location. Diagnosis is usually made through imaging tests, and treatment may involve observation, draining, or surgical removal.

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.

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.

Osteolysis can be caused by several factors, including:

1. Infection: Bacterial or fungal infections can cause osteolysis by secreting enzymes that break down bone tissue.
2. Inflammation: Chronic inflammation can lead to the destruction of bone tissue, causing osteolysis.
3. Tumors: Malignant tumors like multiple myeloma or osteosarcoma can cause osteolysis by producing enzymes that destroy bone tissue.
4. Degenerative conditions: Conditions like osteoporosis, rheumatoid arthritis, and Paget's disease can lead to osteolysis due to the gradual breakdown of bone tissue.

Symptoms of osteolysis may include:

1. Bone pain or tenderness
2. Fractures or fracture risk
3. Limited mobility or stiffness in affected joints
4. Swelling or redness in the affected area
5. Difficulty healing from injuries or infections

Treatment for osteolysis depends on the underlying cause and may include:

1. Antibiotics to treat infections
2. Pain management with medication or physical therapy
3. Surgery to repair or replace damaged bone tissue
4. Orthotics or assistive devices to support affected joints
5. Medications to slow down or stop bone loss, such as bisphosphonates or denosumab

In conclusion, osteolysis is a condition where there is a gradual loss or destruction of bone tissue, leading to a decrease in bone density and structural integrity. It can be caused by various factors, including infection, inflammation, tumors, and degenerative conditions. Treatment depends on the underlying cause and may include antibiotics, pain management, surgery, orthotics, and medications to slow down or stop bone loss.

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.

The alveolar bone is a specialized type of bone that forms the socket in which the tooth roots are embedded. It provides support and stability to the teeth and helps maintain the proper position of the teeth in their sockets. When the alveolar bone is lost, the teeth may become loose or even fall out completely.

Alveolar bone loss can be detected through various diagnostic methods such as dental X-rays, CT scans, or MRI scans. Treatment options for alveolar bone loss depend on the underlying cause and may include antibiotics, bone grafting, or tooth extraction.

In the context of dentistry, alveolar bone loss is a common complication of periodontal disease, which is a chronic inflammatory condition that affects the supporting structures of the teeth, including the gums and bone. The bacteria that cause periodontal disease can lead to the destruction of the alveolar bone, resulting in tooth loss.

In addition to periodontal disease, other factors that can contribute to alveolar bone loss include:

* Trauma or injury to the teeth or jaw
* Poorly fitting dentures or other prosthetic devices
* Infections or abscesses in the mouth
* Certain systemic diseases such as osteoporosis or cancer

Overall, alveolar bone loss is a significant issue in dentistry and can have a major impact on the health and function of the teeth and jaw. It is essential to seek professional dental care if symptoms of alveolar bone loss are present to prevent further damage and restore oral health.

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.

The word "osteopetrosis" comes from the Greek words "osteon," meaning bone, and "petros," meaning rock or stone. This name reflects the dense and hard nature of the bones affected by the disorder.

Osteopetrosis can be caused by mutations in several genes that are involved in bone development and growth. The condition is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the disorder. However, some cases may be caused by spontaneous mutations or other factors.

Symptoms of osteopetrosis can vary depending on the severity of the disorder and the specific affected bones. Common symptoms include bone pain, limited mobility, and an increased risk of fractures. Other symptoms may include fatigue, fever, and difficulty swallowing or breathing.

Treatment for osteopetrosis usually involves a combination of medications and surgery. Medications such as bisphosphonates and denintuzumab mafodotin can help reduce bone pain and the risk of fractures, while surgery may be necessary to correct deformities or repair broken bones. In some cases, bone marrow transplantation may be recommended to replace damaged bone marrow with healthy cells.

Overall, osteopetrosis is a rare and debilitating disorder that can have a significant impact on quality of life. Early diagnosis and appropriate treatment are important for managing symptoms and preventing complications.

There are several types of osteosarcomas, including:

1. High-grade osteosarcoma: This is the most common type of osteosarcoma and tends to grow quickly.
2. Low-grade osteosarcoma: This type of osteosarcoma grows more slowly than high-grade osteosarcoma.
3. Chondrosarcoma: This is a type of osteosarcoma that arises in the cartilage cells of the bone.
4. Ewing's family of tumors: These are rare types of osteosarcoma that can occur in any bone of the body.

The exact cause of osteosarcoma is not known, but certain risk factors may increase the likelihood of developing the disease. These include:

1. Previous radiation exposure
2. Paget's disease of bone
3. Li-Fraumeni syndrome (a genetic disorder that increases the risk of certain types of cancer)
4. Familial retinoblastoma (a rare inherited condition)
5. Exposure to certain chemicals, such as herbicides and industrial chemicals.

Symptoms of osteosarcoma may include:

1. Pain in the affected bone, which may be worse at night or with activity
2. Swelling and redness around the affected area
3. Limited mobility or stiffness in the affected limb
4. A visible lump or mass on the affected bone
5. Fractures or breaks in the affected bone

If osteosarcoma is suspected, a doctor may perform several tests to confirm the diagnosis and determine the extent of the disease. These may include:

1. Imaging studies, such as X-rays, CT scans, or MRI scans
2. Biopsy, in which a sample of tissue is removed from the affected bone and examined under a microscope for cancer cells
3. Blood tests to check for elevated levels of certain enzymes that are produced by osteosarcoma cells
4. Bone scans to look for areas of increased activity or metabolism in the bones.

There are several different types of calcinosis, each with its own unique causes and symptoms. Some common forms of calcinosis include:

1. Dystrophic calcinosis: This type of calcinosis occurs in people with muscular dystrophy, a group of genetic disorders that affect muscle strength and function. Dystrophic calcinosis can cause calcium deposits to form in the muscles, leading to muscle weakness and wasting.
2. Metastatic calcinosis: This type of calcinosis occurs when cancer cells spread to other parts of the body and cause calcium deposits to form. Metastatic calcinosis can occur in people with a variety of different types of cancer, including breast, lung, and prostate cancer.
3. Idiopathic calcinosis: This type of calcinosis occurs for no apparent reason, and the exact cause is not known. Idiopathic calcinosis can affect people of all ages and can cause calcium deposits to form in a variety of different tissues.
4. Secondary calcinosis: This type of calcidosis occurs as a result of an underlying medical condition or injury. For example, secondary calcinosis can occur in people with kidney disease, hyperparathyroidism (a condition in which the parathyroid glands produce too much parathyroid hormone), or traumatic injuries.

Treatment for calcinosis depends on the underlying cause and the severity of the condition. In some cases, treatment may involve managing the underlying disease or condition that is causing the calcium deposits to form. Other treatments may include medications to reduce inflammation and pain, physical therapy to improve mobility and strength, and surgery to remove the calcium deposits.

No data available that match "bone matrix"


This article presents a histological analysis of demineralised bone matrix and its effectiveness in enhancing posterior fusion ... Histological Remodelling of Demineralised Bone Matrix Allograft in Posterolateral Fusion of the Spine. An Ex Vivo Study. ... Histological Remodelling of Demineralised Bone Matrix Allograft in Posterolateral Fusion of the Spine ... indicating relationship between DBM and newly formed bone. ...
Tuberculosis in patients who had recently undergone spinal surgery that used a single lot of bone repair product. ... CDC is working to respond to tuberculosis (TB) disease cases associated with viable bone matrix material. The cases appear to ... For more information on the product recall: Aziyo Biologics Announces Voluntary Recall of Viable Bone Matrix Products , Aziyo ... Tuberculosis (TB) Disease Associated with Suspected Contaminated Viable Bone Matrix Material Used in Surgical and Dental ...
This group aims to elucidate the mechanisms by which primary gene defects cause skeletal fragility and other matrix disorders ... Matrix biology is central to the NICHD mission because it is intrinsic to the formation and reshaping of tissues before and ... Bone and Matrix Biology in Development and Disease Matrix biology is central to the NICHD mission because it is intrinsic to ... Joan Marini Lab: Section on Heritable Disorders of Bone and Extracellular Matrix ...
It has been assumed that osteoblasts produce the fibronectin required for bone matrix formation. Using transgenic mice, we ... but the initial and continuous presence of fibronectin was found to be crucial for collagen matrix integrity in vitro. ... The bone matrix is composed mostly of collagen, ... The bone matrix is composed mostly of collagen, but the initial ... Circulating fibronectin affects bone matrix, whereas osteoblast fibronectin modulates osteoblast function Anke Bentmann 1 , ...
Allogeneic blood and bone marrow cells for the treatment of severe epidermolysis bullosa: repair of the extracellular matrix ... Allogeneic blood and bone marrow cells for the treatment of severe epidermolysis bullosa: repair of the extracellular matrix ... Bone marrow stem cell therapy for recessive dystrophic epidermolysis bullosa. Kiuru M, Itoh M, Cairo MS, Christiano AM. Kiuru M ... Bone marrow transplantation for recessive dystrophic epidermolysis bullosa. Wagner JE, Ishida-Yamamoto A, McGrath JA, Hordinsky ...
Bone matrix. Bone as a whole has a low cell content and is made primarily of noncellular matrices. There are 2 forms of ... Cortical bone. Cortical bone is the dense, extremely strong bone that is found at the periphery of bones. [3, 1] It makes up 80 ... Osteoid is immature matrix excreted by osteoblasts. It is then converted to mature mineralized matrix over time. Bone matrix ... Woven bone. Woven bone is disorganized bone (see the image below). [3] It is the primary bone that is formed by intramembranous ...
Bone matrix. Bone as a whole has a low cell content and is made primarily of noncellular matrices. There are 2 forms of ... Cortical bone. Cortical bone is the dense, extremely strong bone that is found at the periphery of bones. [3, 1] It makes up 80 ... Osteoid is immature matrix excreted by osteoblasts. It is then converted to mature mineralized matrix over time. Bone matrix ... Woven bone. Woven bone is disorganized bone (see the image below). [3] It is the primary bone that is formed by intramembranous ...
Endochondral bone formation in gelatin methacrylamide hydrogel with embedded cartilage-derived matrix particles.. Visser, Jetze ... This work offers a new avenue for the engineering of relevant-size bone grafts, by the formation of endochondral bone within a ... In a subcutaneous rat model, this template was subsequently remodeled into mineralized bone tissue, including bone-marrow ... The natural process of endochondral bone formation in the growing skeletal system is increasingly inspiring the field of bone ...
... while comparing these results by means of a histomorphometric analysis of bone matrix and fibrous deposition on bone repair. ... prevents the collagen III degradation and impairs the bone matrix development in artificial defect of rabbit calvaria, ... the histomorphometric results of the L-PRP groups demonstrated intense fibrotic deposition along with hindered bone matrix ... Palavras-chave : bone regeneration; metalloproteinases; collagen III; platelet-rich plasma.. · texto em Inglês · pdf em Inglês ...
... researchers have found another genetic defect involved in the bone-weakening disorder. ... Second Gene Discovered for Form of Brittle Bone Disease. Normal bone is a dense, strong matrix. National Osteoporosis ... Of the five, three had a lethal form of OI; the other two had a nonfatal form with severely abnormal bone development. Dr. ... resulting in defective bone formation. Patients who have a loss of function of either CRTAP or P3H1 will develop severe OI, but ...
Gentili C, Cancedda R. Cartilage and bone extracellular matrix. Curr Pharm Des. 2009;15(12):1334-48. doi: 10.2174/ ... caused by detachment of cartilage and a piece of the underlying bone from the end of the bone at a joint. People with this ... Cartilage is a tough but flexible tissue that covers the ends of the bones at joints and is also part of the developing ... Osteoarthritis is characterized by the breakdown of joint cartilage and the underlying bone. It causes pain and stiffness and ...
A bone matrix modifier of (. NH. 4. ). 3. PO. 4. and calcium nitrate [. Ca. (. NO. 3. ). 2. ] was used to stabilize lead during ... bone: F. (. 3,19. ). =. 0.16. , p. =. 0.69. ]. Specifically, F3 bone Pb means and standard errors (SEs) were 0.00. μ. g. /. dL ... Bone remodeling during pregnancy and post-partum assessed by metal lead levels and isotopic concentrations. Bone 89:40-51, PMID ... Bone was isolated from 120-d-old F3 offspring and digested with HNO. 3. and brought to a constant volume for determination of ...
Osteogenesis, angiogenesis and matrix remodeling during bone regeneration.. *Augmentation of craniofacial bone regeneration. ... Engineering of composite multi-tissue constructs, such as vascularized and innervated bone and skeletal muscle. ... Destruction and regeneration of the periodontium and inflammatory bone erosion associated with periodontal disease. ... Distinct molecular and cellular mechanisms of intramembranous and endochondral bone regeneration.. * ...
This program supports research on bone biology, clinical research on osteoporosis, metabolic bone disorders and bone quality. ... Bone matrix composition, structure, and function.. *Pre-clinical development of novel therapeutics for osteoporosis. ... Bone quality and skeletal imaging:. *In vivo methods for macro and micro scale imaging of bone. ... Bone biology & skeletal homeostasis studies include:. *Osteoclasts, osteoblasts, and osteocytes in bone remodeling and ...
... which was incorporated inside the matrix. While incorporated in bone matrix, alendronate is not pharmacologically active. Thus ... Osteoporosis occurs as a result of inhibited bone formation and increased bone resorption resulting in net bone loss. ... the bone-resorbing cells. Alendronate reduces bone resorption with no direct effect on bone formation, although the latter ... even where preexisting bone was woven and disorganized. Overall, bone histology data support the conclusion that bone formed ...
Age-related changes in the cellular and matrix components of bone and cartilage ... Bone and Cartilage Program. This program aims to understand the mechanisms by which bones and cartilage change with age. Topics ... Age-related changes in the cellular and matrix components of muscle and tendon ...
... assemble nanostructured fibrous scaffolds reminiscent of extracellular matrix that can be used to mimic properties of bone; and ...
Silencing inflammatory mediators, matrix metalloproteinases, and osteoclastic factors that cause bone erosion in periodontal ... These areas include tooth and bone disorders, oral cancer, chronic inflammatory conditions, viral infections, autoimmune ...
Matrix vesicles in bone tumors. Ultrastructural analysis and their significance in neoplastic bone formation.. Yoshida H; ... Expression of bone morphogenetic proteins in giant cell tumor of bone.. Kudo N; Ogose A; Ariizumi T; Kawashima H; Hotta T; ... Immunohistochemical study of bone GLA protein in primary bone tumors.. Iwasaki R; Yamamuro T; Kotoura Y; Okumura H; Kasai R; ... Malignant bone tumors of the lower extremity.. Buxbaum FD. J Foot Surg; 1976; 15(3):85-92. PubMed ID: 1071753. [TBL] ...
Coherent scattering and matrix correction in bone-lead measurements. Physics in Medicine and Biology 45(7):1953-1963. PMID: ... Maternal bone lead contribution to blood lead during and after pregnancy. Environ Res 82(1):81-90. doi:10.1006/enrs.1999.4007 ... A combined K and L XRF method for in vivo bone lead measurement. In: Proceedings of the 1999 IRRMA (Industrial Radiation and ... An integrated model of blood lead and bone lead during and after pregnancy in latina immigrants. Society of Toxicology 49:49. ...
Coherent scattering and matrix correction in bone-lead measurements. Physics in Medicine and Biology 45(7):1953-1963. PMID: ... A combined K and L XRF method for in vivo bone lead measurement. In: Proceedings of the 1999 IRRMA (Industrial Radiation and ... Contamination of in vivo bone-lead measurements. Physics in Medicine and Biology 45(1):229-240. PMID:10661594 ... The relationship between blood lead, bone lead and child intelligence. Child Neuropsychology (Neuropsychology, Development and ...
Joan Marini, MD, PhD, Senior Investigator, Section on Heritable Disorders of Bone and Extracellular Matrix, NICHD ... Cracking the "Tough Nut": Somatic Mutations in the Candle Wax Bone Disease Melorheostosis ...
Joan Marini, MD, PhD, Senior Investigator, Section on Heritable Disorders of Bone and Extracellular Matrix, NICHD ... Cracking the "Tough Nut": Somatic Mutations in the Candle Wax Bone Disease Melorheostosis ...
The bone matrix elsewhere also becomes more radiolucent. Characteristic deformities result from the bones bending at the ... Symptoms... read more , inadequate dietary calcium, and disorders or drugs that impair the mineralization of bone matrix. ... Later, the bone matrix becomes calcified and opacified at the subperiosteal level. ... Bone changes, seen on x-rays, precede clinical signs. In rickets, changes are most evident at the lower ends of the radius and ...
  • The extracellular matrix (ECM) is a complex of self assembled macromolecules. (nih.gov)
  • We are expanding our research to extracellular matrix (ECM) development and pathology in other tissues and organs. (nih.gov)
  • The demonstration that fibrillin-1 mutations perturb transforming growth factor (TGF)-β bioavailability/signaling in Marfan syndrome (MFS) changed the view of the extracellular matrix as a passive structural support to a dynamic modulator of cell behavior. (rupress.org)
  • The dominant OI model showed a more detrimental effect in the extracellular matrix organization . (bvsalud.org)
  • In this study, we developed a hybrid biomaterial incorporating decellularized cartilage extracellular matrix (CD-ECM) as a template and silk fibroin (SF) as a carrier to assess the bone regeneration capacity of bone marrow-derived mesenchymal stem cells (hBMSC's) via the endochondral ossification (ECO) route. (kl.ac.at)
  • Gentili C, Cancedda R. Cartilage and bone extracellular matrix. (medlineplus.gov)
  • Its expression is crucial for bone remodeling since it functions in recruiting osteoclasts for bone resorption and facilitates their adhesion to the bone matrix. (temple.edu)
  • Cytokines this kind of as IL 6, IL 8 and IL eleven secreted by breast cancer cells also promote osteoclast di?erentiation and bone resorption. (atpase-signal.com)
  • Its porous structure, like normal bone, is osteoconductive but resistant to resorption, although osteoclasts are identified in lacunae on the surfaces. (healthbenefitstimes.com)
  • In osteoporosis, disproportionate bone resorption leads to low bone mineral density and consequently weak and fracture-prone bones. (sciencemission.com)
  • Most current osteoporosis therapies include the use of bisphosphonates, which block the activity of bone resorbing cells, and thus prevent excessive bone resorption. (sciencemission.com)
  • This has major advantages as excessive bone resorption can be prevented in a targeted manner but normal bone turn-over will still continue. (sciencemission.com)
  • However, the neoplastic element of the tumour consists of propagative osteoblast-like stromal cells that may play a role in bone resorption. (benthamopen.com)
  • IL eleven, generally developed by bone marrow stromal cells and osteoblasts, is definitely an critical regulator of hematopoiesis plus a potent promoter of osteoclast formation. (atpase-signal.com)
  • Collagen can be used in combination with blood, PRF, PRP and bone marrow as a growth factor carrier. (mbi-bio.com)
  • The hollow centre is called the medullary cavity, it is filled with bone marrow. (earthlife.net)
  • Bone marrow comes in two sorts, either red or yellow. (earthlife.net)
  • Yellow bone marrow is mostly fat. (earthlife.net)
  • Red bone marrow is a partly fat but it is interlaced with a network of blood vessels, connective tissue, and blood-forming cells. (earthlife.net)
  • It is in the Red Bone Marrow that the formation of Blood Cells occurs. (earthlife.net)
  • Aim: Matrix metalloproteinases (MMPs), together with their tissue inhibitors (TIMPs), are responsible for the controlled degradation of collagen and other matrix substrates in bone and other tissues. (edu.au)
  • Cell differentiation and matrix organization are differentially affected during bone formation in osteogenesis imperfecta zebrafish models with different genetic defects impacting collagen type I structure. (bvsalud.org)
  • The regeneration of the bony caudal fin of Chi/+ and p3h1-/- was employed to investigate the impact of abnormal collagen synthesis on bone cell differentiation . (bvsalud.org)
  • Interestingly, the chemical chaperone 4-phenylbutyrate (4-PBA), known to reduce cellular stress and increase collagen secretion , improved bone formation only in p3h1-/- by favoring caudal fin growth without affecting bone cell markers expression. (bvsalud.org)
  • Taken together, our in vivo data proved the negative impact of structurally abnormal collagen type I on bone formation but revealed a gene mutation -specific effect on bone cell differentiation and matrix organization in OI. (bvsalud.org)
  • A deficiency can therefore lead to reduced collagen production, increasing the risk of joint and bone problems. (euro-nutrador.eu)
  • Collagen is an important component of connective tissue, which is responsible for the health of joints, bones and soft tissues, among other things. (euro-nutrador.eu)
  • These compounds have been shown to support joint and bone health by reducing inflammation and stimulating collagen production. (euro-nutrador.eu)
  • The small amount of collagen improves the handling capacities and the bone substitute material encourages effective and reliable bone formation. (mbi-bio.com)
  • Introduction and Objective: Because L-PRP constitutes an important source of growth factor that is associated with osteogenesis and fibrogenesis, the aim of this study was to evaluate the effect of L-PRP on the presence of collagen III and MMP-2 and MMP-9, while comparing these results by means of a histomorphometric analysis of bone matrix and fibrous deposition on bone repair. (bvsalud.org)
  • About 85% of all cases are caused by dominant mutations in the two genes for type I collagen, an important building block for bone. (nih.gov)
  • CRTAP is one of the proteins that modify newly made collagen into its final form before it is secreted from cells to become part of the structure of bone. (nih.gov)
  • Osteoblasts are the most common, they form the bone matrix around themselves by laying down collagen fibres and depositing the crystals of mineral material. (earthlife.net)
  • Extracellular substance of bone tissue consisting of COLLAGEN fibers, ground substance, and inorganic crystalline minerals and salts. (nih.gov)
  • Cartilage ECM is composed mainly of two components defining its mechano-physical properties: the collagenous network, responsible for the tensile strength of the cartilage matrix, and the proteoglycans (mainly aggrecan), responsible for the osmotic swelling and the elastic properties of the cartilage tissue. (nih.gov)
  • Results: Matrix metalloproteinases and their tissue inhibitors (TIMPs) expression levels were marked at 3 months and decreased thereafter becoming similar to undistracted controls by 12 months. (edu.au)
  • Firstly, it is osteoinductive, meaning it can stimulate the body's own cells to form new bone tissue. (amhyco.com)
  • It also has variable efficacy depending on the source of the bone tissue and the processing method used. (amhyco.com)
  • Allograft DBM is derived from human bone tissue obtained from cadavers, while xenograft DBM is obtained from animal bones, such as bovine or porcine bones. (amhyco.com)
  • The bone tissue is first cleaned to remove any residual soft tissue, such as blood and fat. (amhyco.com)
  • The matrix is also important for the formation and maintenance of tissues such as bone, cartilage and connective tissue. (euro-nutrador.eu)
  • Bone tissue engineering represents a promising alternative. (nature.com)
  • The field of bone tissue engineering relies on the development of biomaterials able to give the advantages of autografts without the related donor site morbidity. (nature.com)
  • Bone arises or is created within a matrix of connective tissue (cartilage) as a result of the action of specific bone cells called osteoblasts. (earthlife.net)
  • Tissue engineering strategies promote bone regeneration for large bone defects by stimulating the osteogenesis route via intramembranous ossification in engineered grafts, which upon implantation are frequently constrained by insufficient integration and functional anastomosis of vasculature from the host tissue. (kl.ac.at)
  • Our data indicate a new method to prime hBMSC'S into the late hypertrophic stage in vitro in mechanically stable constructs for ECO-mediated bone tissue regeneration. (kl.ac.at)
  • Engineering of composite multi-tissue constructs, such as vascularized and innervated bone and skeletal muscle. (nih.gov)
  • Osteopenia and osteoporosis are deterioration of bone tissue, leading to common in chronic HCV patients. (who.int)
  • Turnover and degradation of normal and pathological matrices are dependent on the responses of the local cell to auto and paracrine anabolic and catabolic pathway. (nih.gov)
  • This remarkable method of bone degradation and formation is synchronized by direct cell get in touch with and also a variety of secreted aspects. (atpase-signal.com)
  • The position of PTHrP in bone metabolic process isn't thoroughly understood, but it is known to bring about upregulation of RANKL and downregulation of OPG, hence enhan cing osteoclast perform leading to bone degradation. (atpase-signal.com)
  • Destruction and regeneration of the periodontium and inflammatory bone erosion associated with periodontal disease. (nih.gov)
  • Distinct molecular and cellular mechanisms of intramembranous and endochondral bone regeneration. (nih.gov)
  • Osteogenesis, angiogenesis and matrix remodeling during bone regeneration. (nih.gov)
  • Augmentation of craniofacial bone regeneration. (nih.gov)
  • Skeletal development is a tightly regulated homeostatic process that requires proper functioning of osteoblasts, the bone forming cells, and osteoclasts, the bone resorbing cells. (temple.edu)
  • The presence of tumor cells during the bone microenvironment perturbs the balance between osteoblasts and osteoclasts, resulting in extra bone reduction or formation. (atpase-signal.com)
  • Osteoclasts as well as the vicious cycle model of bone loss The entry of breast cancer cells into the bone micro atmosphere synergistically increases the complexity of cell cell interactions. (atpase-signal.com)
  • The minimum vital compo nents are osteoblasts, osteoclasts, tumor cells BGB324 along with the mineralized bone matrix. (atpase-signal.com)
  • Osteoclasts break down the matrix during normal bone renewal and growth, they are also important in the healing of fractures. (earthlife.net)
  • Osteoclasts, osteoblasts, and osteocytes in bone remodeling and mechanotransduction. (nih.gov)
  • Hot on the heels of the discovery of a gene involved in a previously unexplained form of osteogenesis imperfecta (OI), researchers have found another genetic defect involved in the bone-weakening disorder. (nih.gov)
  • doi: 10.1083/jcb.201003089) advance this concept by demonstrating how fibrillin-1 and -2 regulate TGF-β and bone morphogenetic protein (BMP) action during osteoblast maturation. (rupress.org)
  • This group aims to elucidate the mechanisms by which primary gene defects cause skeletal fragility and other matrix disorders and to apply this knowledge to the treatment of affected children. (nih.gov)
  • The current primary focus of the group is on translational studies of skeletal dysplasias and related bone disorders. (nih.gov)
  • skeletal health and bone formation. (pickcategory.com)
  • According to the latest research report published by Dhirtek Business Research, the global demineralized bone matrix market report provides detailed information on the factors driving the growth of the demineralized bone matrix market. (articlepedia.xyz)
  • It is processed to remove inorganic minerals and retain the organic matrix, which is rich in growth factors and other signaling molecules that promote bone healing. (amhyco.com)
  • Demineralized bone matrix is rich in various growth factors and signaling molecules that promote bone healing. (amhyco.com)
  • These include bone morphogenetic proteins (BMPs), transforming growth factor-beta (TGF-β), fibroblast growth factor (FGF), insulin-like growth factor (IGF), and platelet-derived growth factor (PDGF). (amhyco.com)
  • DBM is a biocompatible and osteoconductive material that contains various growth factors, such as bone morphogenetic proteins (BMPs), transforming growth factor-beta (TGF-β), and insulin-like growth factor (IGF). (amhyco.com)
  • It is biocompatible, osteoconductive, and contains various growth factors that promote new bone formation. (amhyco.com)
  • BKM120 While in the system, development components stored while in the matrix, this kind of as transforming development aspect B, vascular endothelial development aspect, insulin like growth factors, bone morphogenic proteins and ?broblast derived elements, too as calcium, are launched into the bone microenvironment. (atpase-signal.com)
  • With multi-stage biodegradation, it provides space for bone cell migration and new bone growth to cooperate with new bone growth rate. (mbi-bio.com)
  • Our data suggest that this biomaterial could represent a promising tool for the reconstruction of large bone defects, without using exogenous living cells or growth factors. (nature.com)
  • Researchers have suggested that a disorganized cartilage network in growing bones impairs their growth, leading to short stature. (medlineplus.gov)
  • Signaling mechanisms mediating effects of hormones, growth factors, and cytokines in bone cells. (nih.gov)
  • Homeostasis of cartilage and bone is maintained by complex mechanisms controlling turnover and remodeling of ECM. (nih.gov)
  • Matrix biology is central to the NICHD mission because it is intrinsic to the formation and reshaping of tissues before and after birth. (nih.gov)
  • It helps maintain the elasticity and strength of tissues, improving joint and bone health. (euro-nutrador.eu)
  • The bone grafting is the classical way to treat large bone defects. (nature.com)
  • Repairing large bone defects frequently requires transplantation strategies to restore the anatomical and functional status of the injury sites unable to heal spontaneously. (nature.com)
  • Material and methods: Four bone defects of 8 × 2 mm were created on the calvaria of 21 rabbits. (bvsalud.org)
  • Right here we go over many of the proposed mechanisms that contribute to metastatic breast cancer induced bone loss. (atpase-signal.com)
  • When it does, the body's automatic bone healing mechanisms swing into action. (earthlife.net)
  • This program aims to understand the mechanisms by which bones and cartilage change with age. (nih.gov)
  • Osteopontin (Opn) is an example of a major non-collagenous protein present in bone. (temple.edu)
  • Using genetic analysis in a small laboratory fish model, the Japanese medaka (Oryzias latipes), the research team identified a small protein, the chemokine CXCL9, that, under osteoporotic conditions, diffuses towards reservoirs that hold bone resorbing cell precursors. (sciencemission.com)
  • The infants and children described in Marini's studies have two defective copies of either CRTAP or P3H1 so that almost no protein is produced, resulting in defective bone formation. (nih.gov)
  • Clinical studies related to bone strength and density. (nih.gov)
  • Osteoporosis is the most common age-related bone disease which affects hundreds of millions of individuals worldwide. (sciencemission.com)
  • Osteoporosis is caused by excessive activity of bone resorbing cells, while activity of bone-forming cells is reduced. (sciencemission.com)
  • This offers potential to avoid increased fracture risks in osteoporosis patients and to maintain healthy bone for improved quality of life. (sciencemission.com)
  • Autologous bone grafts have been considered the gold standard, due to the higher osteogenic potential and the absence of immune response. (nature.com)
  • The objectives of this study were to determine the expression and activity of the gelatinases, matrix metalloproteinase (MMP)- 2 and -9, in GCT stromal cells, and to determine if these cells have bone-resorbing capabilities. (benthamopen.com)
  • 23. Distribution and activity levels of matrix metalloproteinase 2 and 9 in canine and feline osteosarcoma. (nih.gov)
  • The results indicate that bone augmentation and angiogenesis could spontaneously occur into the biomaterial, probably by the recruitment of host cells, and that the composition of the scaffolds is crucial. (nature.com)
  • The new strategy allows a fine-tuned modulation of osteoclast numbers that are recruited to bone matrix rather than a widespread blockage of osteoclast activity as in traditional therapies. (sciencemission.com)
  • involved in bone health and calcium metabolism. (pickcategory.com)
  • Particular anorganic bovine bone substitute with a calcium‐deficient carbonate hydroxyapatite having a crystal size of approximately 10 nm. (healthbenefitstimes.com)
  • As well as the main minerals of calcium and phosphorous, bones also contain sodium, magnesium, carbonate and citrate. (earthlife.net)
  • Crucial for the proper maintenance of the skeleton is the bone matrix, which encompasses both organic and inorganic components. (temple.edu)
  • The bone is first cleaned and disinfected, and then the inorganic minerals are removed through various methods, such as acid treatment, ethylenediaminetetraacetic acid (EDTA) treatment, or high-pressure water jetting. (amhyco.com)
  • Bone matrix consists of two parts, an inorganic portion (around 65% dry weight) and an organic portion (around 35% dry weight). (earthlife.net)
  • This condition is characterized by areas of bone damage (lesions) caused by the detachment of cartilage and some of the underlying bone from the end of the bone at a joint. (medlineplus.gov)
  • 32. Comparative Assessment of the Accuracy of Cytological and Histologic Biopsies in the Diagnosis of Canine Bone Lesions. (nih.gov)
  • Alendronate sodium tablets are indicated for the treatment of Paget's disease of bone in men and women. (nih.gov)
  • Treatment is indicated in patients with Paget's disease of bone who have alkaline phosphatase at least two times the upper limit of normal, or those who are symptomatic, or those at risk for future complications from their disease. (nih.gov)
  • for bone & tooth formation. (pickcategory.com)
  • It also has a porous structure that allows for the infiltration of cells and blood vessels, facilitating the process of new bone formation. (amhyco.com)
  • When new bone formation is unable to catch up with bone loss, bone eventually weakens, and becomes more prone to fractures. (sciencemission.com)
  • hBMSC's were primed two weeks for chondrogenesis, followed by six weeks for hypertrophy onto hybrid CD-ECM/SF or SF alone scaffolds and evaluated for the mineralized matrix formation in vitro. (kl.ac.at)
  • 1- Patients with liver disease due to multiple decrease bone formation [20]. (who.int)
  • In healthy individuals, a balanced activity of these two cell types allows constant bone turnover to maintain healthy and strong bones. (sciencemission.com)
  • In enhanced bone fragility and a most studies suggesting that HCV by consequent increase in fracture risk itself provokes osteopenia [9-12]. (who.int)
  • It is estimated that one in three women and one in five men aged over 50 suffer from osteoporotic bone fractures. (sciencemission.com)
  • In postmenopausal women, alendronate sodium tablets increase bone mass and reduce the incidence of fractures, including those of the hip and spine (vertebral compression fractures). (nih.gov)
  • 31. Use of routine histopathology and factor VIII-related antigen/von Willebrand factor immunohistochemistry to differentiate primary hemangiosarcoma of bone from telangiectatic osteosarcoma in 54 dogs. (nih.gov)
  • 34. Osteocalcin expression in primary bone tumors--in situ hybridization and immunohistochemical study. (nih.gov)
  • Matrix metalloproteinases and TIMP expression were comparable to undistracted controls by 12 months, suggesting that equilibrium had been achieved and that bony relapse is unlikely. (edu.au)
  • Although its role is unclear, aggrecan affects bone development. (medlineplus.gov)
  • Inhibition of etiologies or with other liver conditions (HBV, osteoblast (bone forming cell) may be mediated primary biliary cirrhosis, autoimmune or by retained substances of cholestasis as metabolic cause like Diabetes Miletus, hemo- unconjugated bilirubin, retained bile acids, toxic chromatosis, Willson`s disease). (who.int)
  • A operating model to describe the bone remodeling compartment while in the presence of metastatic cancer cells is called the vicious cycle of bone metastasis. (atpase-signal.com)
  • Giant cell tumor of bone (GCT) is a destructive and potentially metastatic bone tumour in which the characteristic giant cells have classically been considered the culprits in bone destruction. (benthamopen.com)
  • 35. Evaluation of osteonectin as a diagnostic marker of osteogenic bone tumors. (nih.gov)
  • All bones have blood vessels and nerves, supplying them nutrients and information. (earthlife.net)
  • Results: In contrast to the results of the L-PRP-free groups, the histomorphometric results of the L-PRP groups demonstrated intense fibrotic deposition along with hindered bone matrix deposition. (bvsalud.org)
  • QuikPlus Bone Matrix contains atom-sized ionic minerals in ideal forms and ratios, to support healthy bones and teeth. (pickcategory.com)
  • It is associated with whatever its cause, affects bone mineral multisystemic manifestations. (who.int)
  • In particular, the biomaterial more closely mimicking the native bone drives the process of bone augmentation more efficiently. (nature.com)
  • Multi-scale modeling of the human bone. (nih.gov)
  • The surface area is very large, and the modulus of elasticity is similar to that of normal bone. (healthbenefitstimes.com)
  • Normal bone is a dense, strong matrix. (nih.gov)
  • The conversion of cartilage into bone requires several processes that directly involve the different ECM components. (nih.gov)
  • These factors can stimulate BKM120 the tumor cells to proliferate and produce far more development factors and more PTHrP, even more perpetuating the vicious cycle of bone buy PHA-665752 metastasis. (atpase-signal.com)
  • 22. KPNA2 expression is a potential marker for differential diagnosis between osteosarcomas and other malignant bone tumor mimics. (nih.gov)
  • In bone, as well as in cartilage, the ECM resident cells produce local factors, inflammatory mediators, and matrix-degrading enzymes. (nih.gov)
  • We studied the ability of the Vnr cells to adhere to different extracellular matrices including osteopontin. (temple.edu)
  • The research team showed that these inhibitors are highly effective in blocking bone resorbing cells' recruitment and protecting bone from osteoporotic insult. (sciencemission.com)
  • These cells may therefore play a role in bone destruction in GCT. (benthamopen.com)
  • the other two had a nonfatal form with severely abnormal bone development. (nih.gov)
  • It thus contributes significantly to the health of our joints and bones. (euro-nutrador.eu)
  • Matrix Support contains special ingredients that support the health and thus indirectly promote the health of joints and bones. (euro-nutrador.eu)
  • Joints occur where different bones meet. (earthlife.net)
  • In some joints, the bones are very strongly linked together. (earthlife.net)
  • There is no movement in these joints and the resulting pair, or group of bones, act as a single bone. (earthlife.net)
  • The joints between the various vertebrae in our back bones are called Cartiliginous joints. (earthlife.net)
  • This feature enables the cartilage to resist compression, protecting bones and joints. (medlineplus.gov)