Bone Matrix
Bone and Bones
Bone Demineralization Technique
Bone Remodeling
Extracellular Matrix
Bone Density
Bone Development
Bone Regeneration
Calcification, Physiologic
Osteoblasts
Bone Substitutes
Osteocytes
Bone Marrow
Osteocalcin
Extracellular Matrix Proteins
Bone Marrow Cells
Integrin-Binding Sialoprotein
Osteoclasts
Osteopontin
Sialoglycoproteins
Matrix Metalloproteinase 2
Matrix Metalloproteinases
Collagen
Bone Morphogenetic Proteins
Alkaline Phosphatase
Osseointegration
Tibia
Bone Cysts
Periosteum
Nuclear Matrix
Bone Morphogenetic Protein 2
Bone Marrow Transplantation
Haversian System
Implants, Experimental
Parietal Bone
Osteonectin
Cartilage
Cell Differentiation
Matrix Metalloproteinase 1
Cells, Cultured
Collagen Type I
Matrix Metalloproteinase Inhibitors
Diphosphonates
Osteoporosis
Ricinus
Matrix Metalloproteinase 3
Fracture Healing
Mandible
Bone Morphogenetic Protein 3
Durapatite
Minerals
Tissue Scaffolds
Transforming Growth Factor beta
Microscopy, Electron, Scanning
Tissue Engineering
Immunohistochemistry
Temporal Bone
Alendronate
Biocompatible Materials
Core Binding Factor Alpha 1 Subunit
Cathepsin K
Osteogenesis Imperfecta
Calcium Phosphates
Stress, Mechanical
RANK Ligand
Mesenchymal Stromal Cells
RNA, Messenger
Etidronic Acid
Alveolar Process
Parathyroid Hormone
Matrix Metalloproteinase 13
Biomechanical Phenomena
Matrix Metalloproteinase 14
Cattle
Matrix Metalloproteinase 7
Alveolar Bone Loss
Disease Models, Animal
Hydroxyproline
Bone Cements
Osteopetrosis
Models, Animal
Porosity
Polyurethanes
Fibronectins
Bone Density Conservation Agents
Mice, Knockout
Osteosarcoma
Molecular Sequence Data
Osteoprotegerin
Lumbar Vertebrae
Glycoproteins
Phosphorus
Spinal Fusion
Bone Morphogenetic Protein 7
Matrix Metalloproteinases, Membrane-Associated
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"
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Vitamin D Deficiency and Dependency - Nutritional Disorders - MSD Manual Professional Edition
Extracellular matrix6
- 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)
Resorption7
- 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)
Marrow7
- 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)
Collagen14
- 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)
Tissue14
- 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)
Degradation3
- 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)
Regeneration4
- 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)
Osteoclasts6
- 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)
20231
- Matrix Biol;121: 105-126, 2023 08. (bvsalud.org)
Osteogenesis1
- 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)
Morphogenetic protein1
- 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)
Skeletal3
- 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)
Growth11
- 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)
Homeostasis1
- Homeostasis of cartilage and bone is maintained by complex mechanisms controlling turnover and remodeling of ECM. (nih.gov)
Tissues2
- 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)
Defects3
- 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)
Mechanisms3
- 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)
Protein3
- 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)
Density1
- Clinical studies related to bone strength and density. (nih.gov)
Osteoporosis3
- 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)
Grafts1
- Autologous bone grafts have been considered the gold standard, due to the higher osteogenic potential and the absence of immune response. (nature.com)
Metalloproteinase2
- 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)
Silica1
- Will the Silica in Bone Matrix Build up in my Gut? (listentoyourgut.com)
Angiogenesis1
- 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)
Osteoclast1
- 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)
Calcium3
- 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)
Inorganic3
- 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)
Lesions2
- 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)
Paget's2
- 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)
Formation5
- 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)
Turnover1
- In healthy individuals, a balanced activity of these two cell types allows constant bone turnover to maintain healthy and strong bones. (sciencemission.com)
Fragility1
- In enhanced bone fragility and a most studies suggesting that HCV by consequent increase in fracture risk itself provokes osteopenia [9-12]. (who.int)
Fractures2
- 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)
Immunohistochemistry1
- 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)
Situ1
- 34. Osteocalcin expression in primary bone tumors--in situ hybridization and immunohistochemical study. (nih.gov)
Metalloproteinases1
- 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)
Aggrecan1
- Although its role is unclear, aggrecan affects bone development. (medlineplus.gov)
Osteoblast1
- 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)
Metastatic2
- 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)
Osteogenic1
- 35. Evaluation of osteonectin as a diagnostic marker of osteogenic bone tumors. (nih.gov)
Blood vessels1
- All bones have blood vessels and nerves, supplying them nutrients and information. (earthlife.net)
Deposition1
- 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)
Minerals1
- QuikPlus Bone Matrix contains atom-sized ionic minerals in ideal forms and ratios, to support healthy bones and teeth. (pickcategory.com)
Affects bone1
- It is associated with whatever its cause, affects bone mineral multisystemic manifestations. (who.int)
Augmentation1
- In particular, the biomaterial more closely mimicking the native bone drives the process of bone augmentation more efficiently. (nature.com)
Human bone1
- Multi-scale modeling of the human bone. (nih.gov)
Normal bone2
- 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)
Components1
- The conversion of cartilage into bone requires several processes that directly involve the different ECM components. (nih.gov)
Tumor2
- 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)
Cells4
- 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)
Severely1
- the other two had a nonfatal form with severely abnormal bone development. (nih.gov)
Joints7
- 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)