Bone Morphogenetic Proteins
Bone Morphogenetic Protein 2
Bone Morphogenetic Protein 4
Bone Morphogenetic Protein 7
Bone Morphogenetic Protein Receptors, Type I
Bone Morphogenetic Protein Receptors
Bone Morphogenetic Protein 6
Bone Morphogenetic Protein Receptors, Type II
Bone and Bones
Bone Morphogenetic Protein 5
Bone Morphogenetic Protein 3
Bone Morphogenetic Protein 15
Bone Morphogenetic Protein 1
Transforming Growth Factor beta
Growth Differentiation Factor 2
Receptors, Growth Factor
Growth Differentiation Factors
Growth Differentiation Factor 5
Gene Expression Regulation, Developmental
Growth Differentiation Factor 9
Activin Receptors, Type I
Growth Differentiation Factor 6
Intercellular Signaling Peptides and Proteins
Activin Receptors, Type II
Bone Marrow Cells
Inhibitor of Differentiation Protein 1
Smad Proteins, Receptor-Regulated
In Situ Hybridization
MSX1 Transcription Factor
Core Binding Factor Alpha 1 Subunit
Reverse Transcriptase Polymerase Chain Reaction
Gene Expression Regulation
Mesenchymal Stromal Cells
Receptors, Transforming Growth Factor beta
Molecular Sequence Data
Bone Marrow Transplantation
Fibroblast Growth Factors
Embryonic Stem Cells
Amino Acid Sequence
Limb Deformities, Congenital
Antimicrobial Cationic Peptides
Receptors, Cell Surface
Extracellular Matrix Proteins
Transforming Growth Factor beta1
Bone Demineralization Technique
Inhibitor of Differentiation Proteins
Growth Differentiation Factor 10
Disease Models, Animal
SOX9 Transcription Factor
Collagen Type I
Myocytes, Smooth Muscle
Promoter Regions, Genetic
Protein Structure, Tertiary
Fibroblast Growth Factor 8
Culture Media, Conditioned
Transforming Growth Factor beta3
Gene Expression Profiling
Transforming Growth Factor beta2
A Drosophila doublesex-related gene, terra, is involved in somitogenesis in vertebrates. (1/1473)The Drosophila doublesex (dsx) gene encodes a transcription factor that mediates sex determination. We describe the characterization of a novel zebrafish zinc-finger gene, terra, which contains a DNA binding domain similar to that of the Drosophila dsx gene. However, unlike dsx, terra is transiently expressed in the presomitic mesoderm and newly formed somites. Expression of terra in presomitic mesoderm is restricted to cells that lack expression of MyoD. In vivo, terra expression is reduced by hedgehog but enhanced by BMP signals. Overexpression of terra induces rapid apoptosis both in vitro and in vivo, suggesting that a tight regulation of terra expression is required during embryogenesis. Terra has both human and mouse homologs and is specifically expressed in mouse somites. Taken together, our findings suggest that terra is a highly conserved protein that plays specific roles in early somitogenesis of vertebrates. (+info)
Requirement of a novel gene, Xin, in cardiac morphogenesis. (2/1473)A novel gene, Xin, from chick (cXin) and mouse (mXin) embryonic hearts, may be required for cardiac morphogenesis and looping. Both cloned cDNAs have a single open reading frame, encoding proteins with 2,562 and 1,677 amino acids for cXin and mXin, respectively. The derived amino acid sequences share 46% similarity. The overall domain structures of the predicted cXin and mXin proteins, including proline-rich regions, 16 amino acid repeats, DNA-binding domains, SH3-binding motifs and nuclear localization signals, are highly conserved. Northern blot analyses detect a single message of 8.9 and 5.8 kilo base (kb) from both cardiac and skeletal muscle of chick and mouse, respectively. In situ hybridization reveals that the cXin gene is specifically expressed in cardiac progenitor cells of chick embryos as early as stage 8, prior to heart tube formation. cXin continues to be expressed in the myocardium of developing hearts. By stage 15, cXin expression is also detected in the myotomes of developing somites. Immunofluorescence microscopy reveals that the mXin protein is colocalized with N-cadherin and connexin-43 in the intercalated discs of adult mouse hearts. Incubation of stage 6 chick embryos with cXin antisense oligonucleotides results in abnormal cardiac morphogenesis and an alteration of cardiac looping. The myocardium of the affected hearts becomes thickened and tends to form multiple invaginations into the heart cavity. This abnormal cellular process may account in part for the abnormal looping. cXin expression can be induced by bone morphogenetic protein (BMP) in explants of anterior medial mesoendoderm from stage 6 chick embryos, a tissue that is normally non-cardiogenic. This induction occurs following the BMP-mediated induction of two cardiac-restricted transcription factors, Nkx2.5 and MEF2C. Furthermore, either MEF2C or Nkx2.5 can transactivate a luciferase reporter driven by the mXin promoter in mouse fibroblasts. These results suggest that Xin may participate in a BMP-Nkx2.5-MEF2C pathway to control cardiac morphogenesis and looping. (+info)
Cloning and functional characterization of the 5'-flanking region of the human bone morphogenetic protein-2 gene. (3/1473)Bone morphogenetic protein-2 (BMP-2) is involved in bone formation, organogenesis or pattern formation during development. The expression of BMP-2 is regulated accurately and coordinately with that of other transforming growth factor-beta (TGF-beta) superfamily members. To elucidate the mechanism underlying the regulation of BMP-2 expression, a 6.7 kb SpeI-SalI fragment, from the P1 phage library, encompassing the 5'-flanking region of the human BMP-2 gene, was isolated and sequenced. Transcription start sites were mapped by the 5'-rapid amplification of cDNA ends (RACE) method. It has been found that the human BMP-2 gene contains, largely, two promoter regions surrounded by GC-rich sequences with several Sp1 consensus motifs. The proximal promoter possesses a single start site, whereas several start sites are clustered in the distal promoter region. Neither TATA nor CAAT consensus sequences are found in the proximity of the start sites for either promoter. Interestingly, in no case is the transcription-initiation site common between the human and mouse BMP-2 genes, although the sequence of the BMP-2 gene is well conserved in the promoter region between two species. Transient transfection experiments with the reporter fused with various lengths of the BMP-2 promoter sequence demonstrated that there exist enhancer elements in an 1.1 kb GC-rich fragment covering both promoter regions. It is noteworthy that the enhancer elements are 5'-flanked by a 790 bp strong repressor element that is characterized by numerous AT stretches. This intriguing organization may be amenable to the tight control of the expression of BMP-2 that is essential for development or bone morphogenesis. (+info)
Lack of regulation in the heart forming region of avian embryos. (4/1473)The ability to regenerate a heart after ablation of cardiogenic mesoderm has been demonstrated in early stage fish and amphibian embryos but this type of regulation of the heart field has not been seen in avians or mammals. The regulative potential of the cardiogenic mesoderm was examined in avian embryos and related to the spatial expression of genes implicated in early cardiogenesis. With the identification of early cardiac regulators such as bmp-2 and nkx-2.5, it is now possible to reconcile classical embryological studies with molecular mechanisms of cardiac lineage determination in vivo. The most anterior lateral embryonic cells were identified as the region that becomes the heart and removal of all or any subset of these cells resulted in the loss of corresponding cardiac structures. In addition, removal of the lateral heart forming mesoderm while leaving the lateral endoderm intact also results in loss of cardiac structures. Thus the medial anterior mesoderm cannot be recruited into the heart lineage in vivo even in the presence of potentially cardiac inducing endoderm. In situ analysis demonstrated that genes involved in early events of cardiogenesis such as bone morphogenetic protein 2 (bmp-2) and nkx-2.5 are expressed coincidentally with the mapped far lateral heart forming region. The activin type IIa receptor (actR-IIa) is a potential mediator of BMP signaling since it is expressed throughout the anterior mesoderm with the highest level of expression occurring in the lateral prospective heart cells. The posterior boundary of actR-IIa is consistent with the posterior boundary of nkx-2.5 expression, supporting a model whereby ActR-IIa is involved in restricting the heart forming region to an anterior subset of lateral cells exposed to BMP-2. Analysis of the cardiogenic potential of the lateral plate mesoderm posterior to nkx-2.5 and actR-IIa expression demonstrated that these cells are not cardiogenic in vitro and that removal of these cells from the embryo does not result in loss of heart tissue in vivo. Thus, the region of the avian embryo that will become the heart is defined medially, laterally, and posteriorly by nkx-2.5 gene expression. Removal of all or part of the nkx-2.5 expressing region results in the loss of corresponding heart structures, demonstrating the inability of the chick embryo to regenerate cardiac tissue in vivo at stages after nkx-2.5 expression is initiated. (+info)
A binding site for homeodomain and Pax proteins is necessary for L1 cell adhesion molecule gene expression by Pax-6 and bone morphogenetic proteins. (5/1473)The cell adhesion molecule L1 regulates axonal guidance and fasciculation during development. We previously identified the regulatory region of the L1 gene and showed that it was sufficient for establishing the neural pattern of L1 expression in transgenic mice. In the present study, we characterize a DNA element within this region called the HPD that contains binding motifs for both homeodomain and Pax proteins and responds to signals from bone morphogenetic proteins (BMPs). An ATTA sequence within the core of the HPD was required for binding to the homeodomain protein Barx2 while a separate paired domain recognition motif was necessary for binding to Pax-6. In cellular transfection experiments, L1-luciferase reporter constructs containing the HPD were activated an average of 4-fold by Pax-6 in N2A cells and 5-fold by BMP-2 and BMP-4 in Ng108 cells. Both of these responses were eliminated on deletion of the HPD from L1 constructs. In transgenic mice, deletion of the HPD from an L1-lacZ reporter resulted in a loss of beta-galactosidase expression in the telencephalon and mesencephalon. Collectively, our experiments indicate that the HPD regulates L1 expression in neural tissues via homeodomain and Pax proteins and is likely to be a target of BMP signaling during development. (+info)
Type IIA procollagen containing the cysteine-rich amino propeptide is deposited in the extracellular matrix of prechondrogenic tissue and binds to TGF-beta1 and BMP-2. (6/1473)Type II procollagen is expressed as two splice forms. One form, type IIB, is synthesized by chondrocytes and is the major extracellular matrix component of cartilage. The other form, type IIA, contains an additional 69 amino acid cysteine-rich domain in the NH2-propeptide and is synthesized by chondrogenic mesenchyme and perichondrium. We have hypothesized that the additional protein domain of type IIA procollagen plays a role in chondrogenesis. The present study was designed to determine the localization of the type IIA NH2-propeptide and its function during chondrogenesis. Immunofluorescence histochemistry using antibodies to three domains of the type IIA procollagen molecule was used to localize the NH2-propeptide, fibrillar domain, and COOH-propeptides of the type IIA procollagen molecule during chondrogenesis in a developing human long bone (stage XXI). Before chondrogenesis, type IIA procollagen was synthesized by chondroprogenitor cells and deposited in the extracellular matrix. Immunoelectron microscopy revealed type IIA procollagen fibrils labeled with antibodies to NH2-propeptide at approximately 70 nm interval suggesting that the NH2-propeptide remains attached to the collagen molecule in the extracellular matrix. As differentiation proceeds, the cells switch synthesis from type IIA to IIB procollagen, and the newly synthesized type IIB collagen displaces the type IIA procollagen into the interterritorial matrix. To initiate studies on the function of type IIA procollagen, binding was tested between recombinant NH2-propeptide and various growth factors known to be involved in chondrogenesis. A solid phase binding assay showed no reaction with bFGF or IGF-1, however, binding was observed with TGF-beta1 and BMP-2, both known to induce endochondral bone formation. BMP-2, but not IGF-1, coimmunoprecipitated with type IIA NH2-propeptide. Recombinant type IIA NH2-propeptide and type IIA procollagen from media coimmunoprecipitated with BMP-2 while recombinant type IIB NH2-propeptide and all other forms of type II procollagens and mature collagen did not react with BMP-2. Taken together, these results suggest that the NH2-propeptide of type IIA procollagen could function in the extracellular matrix distribution of bone morphogenetic proteins in chondrogenic tissue. (+info)
Prospective identification, isolation by flow cytometry, and in vivo self-renewal of multipotent mammalian neural crest stem cells. (7/1473)Multipotent and self-renewing neural stem cells have been isolated in culture, but equivalent cells have not yet been prospectively identified in neural tissue. Using cell surface markers and flow cytometry, we have isolated neural crest stem cells (NCSCs) from mammalian fetal peripheral nerve. These cells are phenotypically and functionally indistinguishable from NCSCs previously isolated by culturing embryonic neural tube explants. Moreover, in vivo BrdU labeling indicates that these stem cells self-renew in vivo. NCSCs freshly isolated from nerve tissue can be directly transplanted in vivo, where they generate both neurons and glia. These data indicate that neural stem cells persist in peripheral nerve into late gestation by undergoing self-renewal. Such persistence may explain the origins of some PNS tumors in humans. (+info)
Bone morphogenetic protein 2 inhibits platelet-derived growth factor-induced c-fos gene transcription and DNA synthesis in mesangial cells. Involvement of mitogen-activated protein kinase. (8/1473)Bone morphogenetic proteins (BMPs) play an important role in nephrogenesis. The biologic effect and mechanism of action of these proteins in the adult kidney has not yet been studied. We investigated the effect of BMP2, a member of these growth and differentiation factors, on mitogenic signal transduction pathways induced by platelet-derived growth factor (PDGF) in glomerular mesangial cells. PDGF is a growth and survival factor for these cells in vitro and in vivo. Incubation of mesangial cells with increasing concentrations of BMP2 inhibited PDGF-induced DNA synthesis in a dose-dependent manner with maximum inhibition at 250 ng/ml. Immune complex tyrosine kinase assay of PDGF receptor beta immunoprecipitates from lysates of mesangial cells treated with PDGF showed no inhibitory effect of BMP2 on PDGF receptor tyrosine phosphorylation. This indicates that the inhibition of DNA synthesis is likely due to postreceptor events. However, BMP2 significantly inhibited PDGF-stimulated mitogen-activated protein kinase (MAPK) activity that phosphorylates the Elk-1 transcription factor, a component of the ternary complex factor. Using a fusion protein-based reporter assay, we also show that BMP2 blocks PDGF-induced Elk-1-mediated transcription. Furthermore, we demonstrate that BMP2 inhibits PDGF-induced transcription of c-fos gene, a natural target of Elk-1 that normally forms a ternary complex that activates the serum response element of the c-fos gene. These data provide the first evidence that in mesangial cells, BMP2 signaling cross-talks with MAPK-based transcriptional events to inhibit PDGF-induced DNA synthesis. One target for this inhibition is the early response gene c-fos. (+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.
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.
Example Sentence: The patient was diagnosed with pulmonary hypertension and began treatment with medication to lower her blood pressure and improve her symptoms.
Word class: Noun phrase / medical condition
The exact cause of myositis ossificans is not fully understood, but it is thought to be related to an abnormal repair process within the muscle tissue. The condition can be diagnosed through a combination of physical examination, imaging studies such as X-rays or MRIs, and biopsy.
Treatment for myositis ossificans usually focuses on relieving pain and improving mobility. This may include rest, physical therapy, anti-inflammatory medications, and in some cases, surgery to remove the abnormal bone growth. The condition can take several months to resolve, and in rare cases, it may recur.
Myositis ossificans is a relatively rare condition, but it can have a significant impact on an individual's quality of life, particularly if left untreated. It is important for healthcare providers to be aware of this condition and its symptoms in order to provide accurate diagnosis and appropriate treatment.
* American Academy of Orthopaedic Surgeons. (2019). Myositis Ossificans. Retrieved from
* MedlinePlus. (2020). Myositis ossificans. Retrieved from
* UW Health. (n.d.). Myositis Ossificans. Retrieved from
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.
Note: The medical information provided here is for general purposes only and should not be considered a substitute for professional medical advice, diagnosis, or treatment. If you suspect that your child may have a congenital limb deformity, it is important to consult with a qualified healthcare provider as soon as possible.
There are two types of brachydactyly:
1. Postaxial brachydactyly: This type affects the little finger side of the hand, causing the corresponding finger to be shorter than the others.
2. Preaxial brachydactyly: This type affects the thumb side of the hand, causing the corresponding finger to be shorter than the others.
Brachydactyly can be caused by a variety of genetic mutations or chromosomal abnormalities, such as Turner syndrome, Noonan syndrome, and Down syndrome. It can also be caused by environmental factors, such as maternal diabetes during pregnancy.
The symptoms of brachydactyly may include:
* Shortened fingers or toes
* Limited range of motion in the affected digits
* Difficulty grasping or manipulating objects
* Aesthetic concerns
Treatment for brachydactyly depends on the underlying cause and severity of the condition. In some cases, surgery may be necessary to lengthen the affected fingers or toes. Physical therapy and occupational therapy can also help improve range of motion and function.
It's important to note that brachydactyly is usually a congenital condition, meaning it is present at birth. However, in some cases, it may not be diagnosed until later in childhood or adulthood. If you suspect your child or yourself may have brachydactyly, it's important to consult with a healthcare professional for proper evaluation and treatment.
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.
There are different types of fractures that can occur in cartilage, including:
1. Fissure fractures: These are small cracks or splits in the cartilage.
2. Fracture-linear fractures: These are longer, more linear cracks in the cartilage.
3. Fracture-bucket handle fractures: These are fractures that have a central crack with two smaller cracks radiating from it, resembling a bucket handle.
4. Fracture-segmental fractures: These are fractures that involve the entire thickness of the cartilage and can be complete or incomplete.
Fractures, cartilage can be caused by a variety of factors, including trauma, sports injuries, degenerative conditions such as osteoarthritis, and systemic diseases such as rheumatoid arthritis. Symptoms of fractures, cartilage can include pain, stiffness, limited mobility, and locking or catching sensations in the affected joint.
Diagnosis of fractures, cartilage is typically made through a combination of physical examination, imaging studies such as X-rays, CT scans, and MRI, and arthroscopy, which involves inserting a small camera into the joint to visualize the cartilage directly.
Treatment for fractures, cartilage depends on the severity of the injury and can include conservative measures such as rest, physical therapy, and medication, or surgical interventions such as repair or replacement of the damaged cartilage. In severe cases, fractures, cartilage may require joint fusion or replacement with an artificial joint.
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.
1. Skull deformities: Synostosis can lead to abnormal growth and shape of the skull, which can cause visual disturbances, hearing loss, and other complications.
2. Respiratory problems: Fused bones in the skull can reduce the size of the nasal passages and sinuses, making it harder to breathe properly.
3. Neurological issues: Synostosis can press on the brain and spinal cord, leading to headaches, seizures, and other neurological symptoms.
4. Vision problems: The fusion of bones can cause double vision or other visual disturbances, which can affect a child's ability to learn and develop normally.
5. Hearing loss: In some cases, synostosis can lead to hearing loss due to the abnormal growth of the bones in the middle ear.
6. Sleep apnea: Synostosis can cause the airway to be narrowed or blocked, leading to sleep apnea and other breathing problems.
7. Dental problems: Fused bones in the skull can affect the alignment of teeth and lead to dental problems such as crowding, misalignment, or tooth loss.
8. Speech difficulties: Synostosis can cause speech difficulties due to the abnormal growth of the bones in the mouth and throat.
9. Feeding difficulties: Fused bones in the skull can make it harder for a child to eat properly, leading to feeding difficulties and malnutrition.
10. Emotional and social challenges: Children with synostosis may experience emotional and social challenges due to their appearance or difficulty with basic functions such as eating and breathing.
Treatment for synostosis usually involves a combination of surgery, physical therapy, and other supportive care to help manage the symptoms and improve quality of life.
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.
The tumor is typically made up of compact, densely packed osteoblastic cells that resemble normal bone tissue. However, unlike normal bone tissue, osteoblastoma has a markedly increased number of blood vessels and can be quite large before it penetrates the surrounding bone.
The exact cause of osteoblastoma is not known, but it is believed to arise from genetic mutations that occur during fetal development. There are several types of osteoblastoma, including:
* Cartilage-forming osteoblastoma: This type of tumor is composed of both osteoblastic and chondrocytic cells and is typically found in the long bones of the arms and legs.
* Fibrous dysplasia: This is a related condition that also arises from abnormalities in the development of bone, but it is not classified as a tumor.
Osteoblastoma is usually diagnosed with imaging tests such as X-rays, CT scans, or MRI scans, and a biopsy may be performed to confirm the diagnosis. Treatment typically involves surgery to remove the tumor, followed by radiation therapy to prevent recurrence. In rare cases, the tumor may be malignant and require more aggressive treatment.
Prognosis for osteoblastoma is generally good if the tumor is diagnosed and treated early, but it can be challenging to distinguish benign from malignant tumors based on imaging studies alone. Therefore, biopsy and careful follow-up are essential to ensure that any recurrences are detected and treated promptly.
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.
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.
Synonyms: cartilage tumor, chondroid tumor, chondromatosis.
Etymology: From the Greek words "chondros," meaning cartilage, and "oma," meaning tumor.
Examples of Chondroma in a sentence:
1. The patient was diagnosed with a chondroma in their knee joint, which was causing pain and stiffness.
2. The surgeon removed the chondroma from the patient's lung, which had been compressing the bronchus and causing difficulty breathing.
3. The chondroma in the patient's heart was monitored with regular imaging studies to ensure it did not grow or cause any further complications.
4. The patient was advised to avoid heavy lifting or bending to prevent exacerbating their chondroma in the spine.
Tibial fractures can range in severity from minor cracks or hairline breaks to more severe breaks that extend into the bone's shaft or even the joint. Treatment for these injuries often involves immobilization of the affected leg with a cast, brace, or walking boot, as well as pain management with medication and physical therapy. In some cases, surgery may be necessary to realign and stabilize the bone fragments.
Note: A malunited fracture is sometimes also referred to as a "nonunion fracture" or "fracture nonunion".
The word "holoprosencephaly" comes from the Greek words "holos," meaning "whole," "prosencephalon," meaning "front part of the brain," and "-ly," indicating a condition or characteristic. The term was first used in the medical literature in the late 19th century to describe this specific type of brain malformation.
In individuals with holoprosencephaly, the two hemispheres of the brain do not properly separate, leading to various abnormalities and impairments. Depending on the severity and location of the defect, symptoms can range from mild to severe and may include:
1. Facial abnormalities, such as a single eye or no nose.
2. Cognitive impairments, including intellectual disability and developmental delays.
3. Motor difficulties, such as weakness or paralysis on one side of the body.
4. Seizures and other neurological problems.
5. Delayed speech and language development.
6. Behavioral challenges, including autism and anxiety.
The exact cause of holoprosencephaly is not fully understood, but it is thought to be related to genetic mutations or environmental factors during early fetal development. Diagnosis is typically made through a combination of prenatal imaging, such as ultrasound or MRI, and postnatal examination, including physical examination and neuroimaging studies.
There is no standard treatment for holoprosencephaly, and management of the condition usually involves a multidisciplinary approach involving neurosurgeons, neurologists, developmental pediatricians, and other specialists. Treatment may include surgery to correct physical abnormalities, medication to control seizures or other neurological symptoms, and various forms of therapy to address cognitive, motor, and behavioral challenges.
The prognosis for holoprosencephaly varies depending on the severity of the condition and the presence of any additional birth defects or medical issues. Some individuals with holoprosencephaly may have a relatively mild form of the condition and can lead active, fulfilling lives with appropriate support and management, while others may experience significant cognitive and physical challenges that require ongoing care and support.
Some common types of eye abnormalities include:
1. Refractive errors: These are errors in the way the eye focuses light, causing blurry vision. Examples include myopia (nearsightedness), hyperopia (farsightedness), astigmatism, and presbyopia (age-related loss of near vision).
2. Amblyopia: This is a condition where the brain favors one eye over the other, causing poor vision in the weaker eye.
3. Cataracts: A cataract is a clouding of the lens in the eye that can cause blurry vision and increase the risk of glaucoma.
4. Glaucoma: This is a group of eye conditions that can damage the optic nerve and lead to vision loss.
5. Macular degeneration: This is a condition where the macula, the part of the retina responsible for central vision, deteriorates, leading to vision loss.
6. Diabetic retinopathy: This is a complication of diabetes that can damage the blood vessels in the retina and lead to vision loss.
7. Retinal detachment: This is a condition where the retina becomes separated from the underlying tissue, leading to vision loss.
8. Corneal abnormalities: These are irregularities in the shape or structure of the cornea, such as keratoconus, that can cause blurry vision.
9. Optic nerve disorders: These are conditions that affect the optic nerve, such as optic neuritis, that can cause vision loss.
10. Traumatic eye injuries: These are injuries to the eye or surrounding tissue that can cause vision loss or other eye abnormalities.
Eye abnormalities can be diagnosed through a comprehensive eye exam, which may include visual acuity tests, refraction tests, and imaging tests such as retinal photography or optical coherence tomography (OCT). Treatment for eye abnormalities depends on the specific condition and may include glasses or contact lenses, medication, surgery, or other therapies.
People with HHT have abnormal blood vessels in their skin, mucous membranes, and organs such as the liver, spleen, and lungs. These abnormal vessels are weak and prone to bleeding, which can lead to nosebleeds, bruising, and other complications.
HHT is usually diagnosed based on a combination of clinical symptoms and genetic testing. Treatment typically involves managing symptoms with medications, lifestyle changes, and in some cases, surgery or other interventions to prevent bleeding episodes.
Some of the main symptoms of HHT include:
* Recurring nosebleeds
* Easy bruising
* Petechiae (tiny red spots on the skin)
* Purpura (larger purple spots on the skin)
* Gingival bleeding (bleeding from the gums)
* Epistaxis (nosebleeds)
* Hematuria (blood in the urine)
* Gastrointestinal bleeding
HHT is a relatively rare disorder, affecting about 1 in 5,000 to 1 in 10,000 people worldwide. It can be inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by spontaneous mutations and not be inherited.
There are several types of HHT, including:
* Type 1: The most common type, characterized by recurring nosebleeds and other bleeding episodes.
* Type 2: Characterized by a milder form of the condition with fewer bleeding episodes.
* Type 3: A rare and severe form of HHT that is often associated with other medical conditions such as liver disease or pulmonary hypertension.
HHT can be diagnosed based on clinical findings and laboratory tests, including:
* Physical examination: To look for signs of bleeding and to assess the size and shape of the nose and ears.
* Imaging studies: Such as CT or MRI scans to evaluate the nasal passages and sinuses.
* Blood tests: To check for abnormalities in blood clotting and platelet function.
* Genetic testing: To identify mutations in the genes associated with HHT.
Treatment for HHT is focused on managing symptoms and preventing complications. It may include:
* Nasal decongestants and antihistamines to reduce bleeding and swelling.
* Corticosteroids to reduce inflammation.
* Antifibrinolytic medications to prevent blood clots from breaking down.
* Surgery to repair or remove affected blood vessels.
* Regular monitoring of blood counts and platelet function.
Early diagnosis and treatment can help improve the quality of life for people with HHT. It is important to seek medical attention if symptoms persist or worsen over time.
The exact cause of osteoarthritis is not known, but it is thought to be due to a combination of factors such as genetics, wear and tear on joints over time, and injuries or trauma to the joint. Osteoarthritis can affect any joint in the body, but it most commonly affects the hands, knees, hips, and spine.
The symptoms of osteoarthritis can vary depending on the severity of the condition and which joint is affected. Common symptoms include:
* Pain or tenderness in the joint
* Stiffness, especially after periods of rest or inactivity
* Limited mobility or loss of flexibility
* Grating or crackling sensations when the joint is moved
* Swelling or redness in the affected joint
* Muscle weakness or wasting
There is no cure for osteoarthritis, but there are several treatment options available to manage the symptoms and slow the progression of the disease. These include:
* Pain relief medications such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)
* Physical therapy to improve mobility and strength
* Lifestyle modifications such as weight loss, regular exercise, and avoiding activities that exacerbate the condition
* Bracing or orthotics to support the affected joint
* Corticosteroid injections or hyaluronic acid injections to reduce inflammation and improve joint function
* Joint replacement surgery in severe cases where other treatments have failed.
Early diagnosis and treatment of osteoarthritis can help manage symptoms, slow the progression of the disease, and improve quality of life for individuals with this condition.
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 types of hypertrophy, including:
1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).
Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.
In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.
Bone morphogenetic protein 2
Bone morphogenetic protein 8B
Bone morphogenetic protein 4
Bone morphogenetic protein
Bone morphogenetic protein 6
Bat wing development
BMP binding endothelial regulator
TGF beta signaling pathway
Bone morphogenetic protein 5
Stem cell marker
Bone morphogenetic protein 1
Bone morphogenetic protein 3
Bone morphogenetic protein 7
Bone morphogenetic protein 10
Bone morphogenetic protein receptor
Bone morphogenetic protein 15
Laminin, alpha 3
Sp7 transcription factor
Collagen, type IV, alpha 2
Index of biochemistry articles
Interbody fusion cage
Development of the endocrine system
Daniel S. Greenspan
Tubulin beta-4A chain
MRC Laboratory of Molecular Biology
Phenolic content in wine
bone morphogenetic protein-2
Dental implants in humans using recombinant bone morphogenetic protein -2
Radix Dipsaci total saponins stimulate MC3T3-E1 cell differentiation via the bone morphogenetic protein-2/MAPK/Smad-dependent...
Romidepsin hepatocellular carcinoma suppression in mice is associated with deregulated gene expression of bone morphogenetic...
The effect of a bone morphogenetic protein (BMP)-2 and/or mesenchymal stromal cell (MSC)-based treatment for canine...
Quantative effect of improving osteoinductive property of a material due to applicationof recombinant morphogenetic bone...
BMPR2 gene: MedlinePlus Genetics
negative regulation of cardiac muscle cell differentiation - Ontology Report - Rat Genome Database
Bmp8b bone morphogenetic protein 8b [Mus musculus (house mouse)] - Gene - NCBI
Dynamics of BMP signaling and distribution during zebrafish dorsal-ventral patterning - PubMed
NanoBiomechanics Lab | Drexel BME
Iemura S et al. (1998), Direct binding of follistatin to a complex of b... - Paper
Browse in Surgery | AVMA
Will YODA End Debate Over rhBMP-2?
Thieme E-Books & E-Journals - Veterinary and Comparative Orthopaedics and Traumatology / Issue
Pulmonary arterial hypertension associated with fenfluramine exposure: report of 109 cases | European Respiratory Society
Junichi Kushioka, MD, PhD's Profile | Stanford Profiles
Lab-Grown Human Pituitary Cells Work in Rats
Recombinant Human Bone Morphogenetic Protein-7 | ScienCell Research Laboratories
Ignacio Valentin Fernandez Monzon | - CCMAR
Frontiers | Epithelial Bone Morphogenic Protein 2 and 4 Are Indispensable for Tooth Development
Director's Report to Council: September 2015 | National Institute of Dental and Craniofacial Research
Seed Funding for Public Health Genomics Research | CDC
Craniofacial Biology : The University of Western Australia
- At present, novel osteoinductive materials containing recombinant bone morphogenetic proteins (rhBMPs) are actively being developed for «regenerative medicine», traumatology and orthopedics. (genescells.ru)
- 8. Neuroforaminal chondrocyte metaplasia and clustering associated with recombinant bone morphogenetic protein-2 usage in transforaminal lumbar interbody fusion. (nih.gov)
- We developed an optimized protocol that included modulating the sonic hedgehog homolog gradient with bone morphogenetic proteins (BMP2) and addition of activin to the culture medium, which shortened the time to generate Lmx1A and FoxA2 immunoreactive cells by 4-6 days. (nih.gov)
- Bone Morphogenic Protein-2 (BMP2) is a driver of epicardial cell migration. (nih.gov)
- The BMPR2 gene provides instructions for making a protein called bone morphogenetic protein receptor type 2. (medlineplus.gov)
- Bone morphogenetic protein receptor type 2 spans the cell membrane, so that one end of the protein is on the outer surface of the cell and the other end remains inside the cell. (medlineplus.gov)
- About half of the mutations involved in this condition disrupt the assembly of bone morphogenetic protein receptor type 2, reducing the amount of this protein in cells. (medlineplus.gov)
- Other mutations prevent bone morphogenetic protein receptor type 2 from reaching the cell surface or alter its structure so it cannot receive or transmit signals. (medlineplus.gov)
- 19. Bone morphogenetic protein receptor signal transduction in human disease. (nih.gov)
- Direct binding of follistatin to a complex of bone -morphogenetic protein and its receptor inhibits ventral and epidermal cell fates in early Xenopus embryo . (xenbase.org)
- Nine (22.5%) out of 40 patients evaluated resulted positive for the presence of germline bone morphogenetic protein receptor ( BMPR) type 2 mutations. (ersjournals.com)
- Germline mutations of the gene encoding bone morphogenetic protein receptor ( BMPR ) type 2 are certainly clear examples of established risk factors for PAH development 4 . (ersjournals.com)
Ectopic bone formation4
- The model of ectopic subcutaneous implantation to rats is very convenience test system to detect increase in osteoinductivity of materials caused by application of rhBMP-2, and to identify features of ectopic bone formation in these materials. (genescells.ru)
- 17. Symptomatic ectopic bone formation after off-label use of recombinant human bone morphogenetic protein-2 in transforaminal lumbar interbody fusion. (nih.gov)
- Axial ( A ) and coronal ( B ) CT scans demonstrating ectopic bone formation in the intervertebral foramen (white arrows) following a transforaminal lumbar interbody fusion performed with the use of rhBMP-2. (aaos.org)
- Harms are common in both (rhBMP-2 and ICBG) groups, but except for cancer at 24 months, the increased risks for retrograde ejaculation, urine retention, and ectopic bone formation (with rhBMP-2) were not statistically significant. (aaos.org)
- A class of osteogenic regulatory molecules, the bone morphogenetic proteins (BMPs), have been isolated, cloned and characterized as potent supplements to augment bone regeneration. (nih.gov)
- This review will discuss the current status of BMPs in bone regeneration and specifically will present the potential for a clinical therapeutic role of recombinant human BMP-2 sustained release carrier systems. (nih.gov)
- The importance of drug delivery to optimize the effects of bone morphogenetic proteins during periodontal regeneration. (nih.gov)
- Arosarena O.A., Collins W.L. Bone regeneration in the rat mandible with bone morphogenetic protein-2: a comparison of two carriers. (genescells.ru)
- We are very excited about the potential for the heparin microparticle technology to improve the safety and efficacy of recombinant protein delivery for tissue regeneration clinical applications. (materialstoday.com)
- Bone regeneration in inflammation with aging and cell-based immunomodulatory therapy. (stanford.edu)
- Chronic inflammation impairs the initiation of bone regeneration in elderly patients. (stanford.edu)
- This review examines current knowledge of the bone regeneration process and potential immunomodulatory therapies to facilitate bone healing in inflammaging.Aged macrophages show increased sensitivity and responsiveness to inflammatory signals. (stanford.edu)
- In aging, persistent chronic inflammation resulting from the failure of M1 to M2 repolarization leads to increased osteoclast activation and decreased osteoblast formation, thus increasing bone resorption and decreasing bone formation during healing.Inflammaging can impair the ability of stem cells to support bone regeneration and contributes to the decline in bone mass and strength that occurs with aging. (stanford.edu)
- Mesenchymal stem cells (MSCs) possess immunomodulatory properties that may benefit bone regeneration in inflammation. (stanford.edu)
- Resolution of inflammation via local delivery of anti-inflammatory cytokines is also a potential therapy for bone regeneration in inflammaging. (stanford.edu)
- MSC exosomes can increase the migration of MSCs to the fracture site and enhance osteogenic differentiation and angiogenesis.In conclusion, inflammaging can impair the proper initiation of bone regeneration in the elderly. (stanford.edu)
- Bone tissue engineering has been emerging as a valid approach to the current therapies for bone regeneration. (who.int)
- Tissue engineering has been emerging as life science towards the development of biological a valid approach to the current therapies for bone substitutes for restoring, maintaining, or improving regeneration. (who.int)
- Firstly, the term engineering concepts in the area of skin, cartilage, "tissue engineering" was derived from an organization and bone regeneration was based on the isolation, of an endothelium-like structure on the surface of expansion, and implantation of cells from the patient's polymethylmathacrylate prosthesis . (who.int)
- BMP-2 also maintained its bioactivity as it was released from microparticles during an in vitro assay. (materialstoday.com)
- The use of bone morphogenetic proteins (BMPs) for cleft lip and palate reconstruction delivered. (dentistrytoday.com)
- A potent osteoinductive protein that plays a critical role in the differentiation of osteoprogenitor cells into OSTEOBLASTS. (bvsalud.org)
- Bone tissue engineering requires a scaffold conducive to cell attachment and maintenance of cell function, together with a rich source of osteoprogenitor cells in combination with osteoinductive growth factors. (who.int)
- Efforts have the growth of chondrocytes on the bioresorbable been made to develop osteoconductive, osteoinductive polymers of polyglycolic acid mesh  and the culture and osteogenic bone materials. (who.int)
- CoCl(2) -simulated hypoxia potentiates the osteogenic differentiation of fibroblasts derived from tympanosclerosis by upregulating the expression of BMP-2. (nih.gov)
- Fig. 1 Three major components in bone tissue cells that can be induced to differentiate into osteogenic engineering: cells, scaffolds, and growth factors. (who.int)
- 4. Transforaminal lumbar interbody fusion with rhBMP-2 in spinal deformity, spondylolisthesis, and degenerative disease--part 2: BMP dosage-related complications and long-term outcomes in 509 patients. (nih.gov)
- 5. Transforaminal lumbar interbody fusion with rhBMP-2 in spinal deformity, spondylolisthesis, and degenerative disease--part 1: Large series diagnosis related outcomes and complications with 2- to 9-year follow-up. (nih.gov)
- 14. Complications with the use of bone morphogenetic protein 2 (BMP-2) in spine surgery. (nih.gov)
- 15. Complications with recombinant human bone morphogenetic protein-2 in posterolateral spine fusion associated with a dural tear. (nih.gov)
- 19. Dose Adjustment Associated Complications of Bone Morphogenetic Protein: A Longitudinal Assessment. (nih.gov)
- The complications typically associated with plating of radial fractures in small-breed dogs cannot be ascribed to an overly stiff bone-plate construct. (avma.org)
- This was one of the complications identified as an increased risk with rhBMP-2. (aaos.org)
- editor-in-chief Eugene J. Carragee, MD, wrote that the studies underreported complications and overstated efficacy as compared with a conventional autograft procedure using iliac crest bone graft (ICBG). (aaos.org)
- Furthermore, the YODA groups found that the study authors underreported complications for both on-label and off-label indications and that they "selected analyses and results that favored rhBMP-2 over ICBG. (aaos.org)
- Current national patterns as a function of patient-, hospital-, and procedure-related factors, and complication rates in the use of recombinant human bone morphogenetic protein-2 (rhBMP-2) as an adjunct to the practice of pediatric spine surgery have scarcely been investigated. (northwestern.edu)
- Evaluate clinically and radiographically the conditions of bone density around the experimental bioactive implants that are covered with Bone Morphogenetic Protein recombinant human type-2 (rhBMP-2) (IE) and to compare it to that obtained whit rough- surface implants (IC). (bvsalud.org)
- McKay W.F., Peckham S.M., Badura J.M. A comprehensive clinical review of recombinant human bone morphogenetic protein-2 (INFUSE Bone Graft). (genescells.ru)
- 7. Mutual regulation of follicle-stimulating hormone signaling and bone morphogenetic protein system in human granulosa cells. (nih.gov)
- 9. Role of Smad1 and Smad4 proteins in the induction of p21WAF1,Cip1 during bone morphogenetic protein-induced growth arrest in human breast cancer cells. (nih.gov)
- 14. The bone morphogenetic protein pathway is active in human colon adenomas and inactivated in colorectal cancer. (nih.gov)
- 7. Recombinant human bone morphogenetic protein-2-induced radiculitis in elective minimally invasive transforaminal lumbar interbody fusions: a series review. (nih.gov)
- 9. Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages. (nih.gov)
- 10. Effectiveness and safety of recombinant human bone morphogenetic protein-2 versus local bone graft in primary lumbar interbody fusions. (nih.gov)
- 13. Allogeneic morphogenetic protein vs. recombinant human bone morphogenetic protein-2 in lumbar interbody fusion procedures: a radiographic and economic analysis. (nih.gov)
- The word is in from the Yale Open Data Access (YODA) project: recombinant human bone morphogenetic protein (rhBMP-2), the product marketed as Infuse® by Medtronic, Inc., offers no appreciable benefit over autograft in spinal fusion surgery. (aaos.org)
- Infuse Bone Graft, which is manufactured by Medtronic Inc., contains recombinant human Bone Morphogenetic Protein (rhBMP-2), a protein released naturally by the body. (yourlawyer.com)
INFUSE Bone Graft5
- Infuse Bone Graft Study Probe Heats Up. (yourlawyer.com)
- A Senate investigation into a bogus Infuse Bone Graft study is heating up. (yourlawyer.com)
- According to The Wall Street Journal, the Senate Committee on Armed Services has asked the U.S. Army to provide it with the results of an investigation into the Infuse Bone Graft study, which was conducted at Walter Reed Army Hospital by former Army surgeon Timothy Kuklo. (yourlawyer.com)
- Last July, the Food & Drug Administration (FDA) warned that the use of Infuse Bone Graft and similar products had caused serious problems when they were used off-label in cervical spine (neck) surgeries. (yourlawyer.com)
- Need Legal Help Regarding Infuse Bone Graft? (yourlawyer.com)
- Bone morphogenetic protein (BMP)2, BMP4, and secreted frizzled related protein 2 were identified as principal effectors of the anti-proliferative effects on RSCs. (bvsalud.org)
- 15. A comprehensive expression survey of bone morphogenetic proteins in breast cancer highlights the importance of BMP4 and BMP7. (nih.gov)
- The growth factor, called bone morphogenetic protein-2 (BMP-2), also remained bioactive after long periods of time spent bound to the microparticles. (materialstoday.com)
- Bone tissue engineering needs to overcome term tissue engineering indicates combinations of cells, major challenges to allow clinical applications with scaffold materials, and bioactive molecules used to predictable outcomes. (who.int)
- The BMPR2 gene belongs to a family of genes originally identified for its role in regulating the growth and maturation (differentiation) of bone and cartilage. (medlineplus.gov)
RhBMP-2 in spinal1
- It concluded that "on the basis of the currently available evidence, it is difficult to identify clear indications for rhBMP-2 in spinal fusion. (aaos.org)
- The encoded preproprotein is proteolytically processed to generate each subunit of the disulfide-linked homodimer, which plays a role in bone and cartilage development. (nih.gov)
- This review aims at outlining the role of stem cells and growth factors in scaffolds, focusing on the use of mesenchymal stem cells and bone morphogenetic proteins as applied to the research and practice of bone tissue engineering. (who.int)
- Mesenchymal stem cells reside in contact with the hematopoietic progenitors in the bone marrow cavity. (who.int)
- Their reports, published in the June 18, 2013, issue of Annals of Internal Medicine, state that rhBMP-2 "provided little or no benefit compared with bone graft and may be associated with more harms, possibly including cancer. (aaos.org)
Stimulated bone formation1
- These findings suggest that rhBMP-2-coated implants can stimulated bone formation around dental implants and may be an alternative in treatment for low bone density sites. (bvsalud.org)
- 11. Nerve injury and recovery after lateral lumbar interbody fusion with and without bone morphogenetic protein-2 augmentation: a cohort-controlled study. (nih.gov)
- It is also approved for use in two dental bone grafting procedures: sinus augmentation and localized alveolar ridge augmentation. (yourlawyer.com)
- The Journal of clinical endocrinology and metabolism 2010 Feb 95 (2): 714-21. (cdc.gov)
- Genetic analyses of bone morphogenetic protein 2, 4 and 7 in congenital combined pituitary hormone deficiency. (cdc.gov)
- 18. Protein associated with SMAD1 (PAWS1/FAM83G) is a substrate for type I bone morphogenetic protein receptors and modulates bone morphogenetic protein signalling. (nih.gov)
- Bone homeostasis is a dynamic process involving a myriad of cells and substrates modulated by regulatory signals such as hormones, growth and differentiating factors. (nih.gov)
- Bone morphogenetic proteins and secreted frizzled related protein 2 maintain the quiescence of adult mammalian retinal stem cells. (bvsalud.org)
- 4. Bone morphogenetic protein 2 is expressed by, and acts upon, mature epithelial cells in the colon. (nih.gov)
- 6. Bone morphogenetic protein activities are enhanced by 3',5'-cyclic adenosine monophosphate through suppression of Smad6 expression in osteoprogenitor cells. (nih.gov)
- The encoded protein may play a role in the generation of primordial germ cells, and has been shown to stimulate thermogenesis in brown adipose tissue. (nih.gov)
- The protective role of bone morphogenetic protein-8 in the glucocorticoid-induced apoptosis on bone cells. (nih.gov)
- BMP-2-loaded microparticles in physical contact with cell culture also stimulated an increase in the number of cells. (materialstoday.com)
- Exposure to these proteins triggered the stem cells to turn into different types of functional pituitary cells that released hormones important for bone and tissue growth (i.e., growth hormone), the stress response (i.e., adrenocorticotropic hormone), and reproductive functions (i.e., prolactin, follicle-stimulating hormone, and luteinizing hormone). (genengnews.com)
- 6. Revision surgery after interbody fusion with rhBMP-2: a cautionary tale for spine surgeons. (nih.gov)
- Reproduced from Rihn JA, Gates C, Glassman SD, Phillips FM, Schwender JD, Albert TJ: The Use of Bone Morphogenetic Protein in Lumbar Spine Surgery. (aaos.org)
- As we've reported previously, Kuklo's study, which claimed to show that wounded soldiers' leg injuries healed better when Infuse was used, was published in the Journal of Bone & Joint Surgery last August, but retracted in March. (yourlawyer.com)
- 2. Mitochondrial aldehyde dehydrogenase activation by Alda-1 inhibits atherosclerosis and attenuates hepatic steatosis in apolipoprotein E-knockout mice. (nih.gov)
- Immunohistochemical markers shown to be useful in identifying/confirming mesonephric/mesonephric-like differentiation (MLD markers) include thyroid transcription factor (TTF1), GATA-binding protein 3 (GATA3), and cluster of differentiation 10 (CD10). (bvsalud.org)
- The net result is more efficient and spatially controlled delivery of this very potent and very valuable protein," said Todd McDevitt, an associate professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University. (materialstoday.com)
- Bone morphogenetic protein 8B promotes the progression of non-alcoholic steatohepatitis. (nih.gov)
- In recent years, the understanding of PAH pathophysiology has allowed the recognition of multiple risk factors and associated conditions that trigger and/or worsen the progression of the disease 2 , 3 . (ersjournals.com)
- 2. Comparison of transforaminal lumbar interbody fusion outcomes in patients receiving rhBMP-2 versus autograft. (nih.gov)
- 12. Comparison of TLIF with rhBMP-2 versus no TLIF and higher posterolateral rhBMP-2 dose at L5-S1 for long fusions to the sacrum with sacropelvic fixation in patients with primary adult deformity. (nih.gov)
- But recently an NIH-funded team of chemical engineers at MIT developed a special coating for implants that promotes a stronger connection to new bone. (nih.gov)
- These microparticles can localize high concentrations of protein therapeutics in an area of tissue damage without introducing large amounts of biomaterial that may take up space and prevent new tissue formation. (materialstoday.com)
Lumbar interbody fusion3
- 1. RhBMP-2-induced radiculitis in patients undergoing transforaminal lumbar interbody fusion: relationship to dose. (nih.gov)
- 3. Clinical sequelae after rhBMP-2 use in a minimally invasive transforaminal lumbar interbody fusion. (nih.gov)
- 18. The use of RhBMP-2 in single-level transforaminal lumbar interbody fusion: a clinical and radiographic analysis. (nih.gov)
- 12. Role of RUNX3 in bone morphogenetic protein signaling in colorectal cancer. (nih.gov)
- Instead of mimicking the complex 3D organization of the developing pituitary gland, Dr. Zimmer's team exposed hPSCs to a few precisely timed cellular signals, specifically, proteins known to play an important role during embryonic development. (genengnews.com)
- Many bony deficits that are excessively traumatic will not result in complete recovery and require therapeutic intervention(s) such as autografting or grafting from banked bone. (nih.gov)
- Traumatic bone injuries such as blast wounds are often so severe that the body can't effectively repair the damage on its own. (materialstoday.com)
- There are 2 forms of osteonecrosis: traumatic (the most common form) and atraumatic. (medscape.com)
- Traumatic and atraumatic osteonecrosis are essentially 2 distinct problems. (medscape.com)
- The traumatic form has a definitive causal event and is isolated to the particular injured bone. (medscape.com)
- Here we see the host bone (red and blue) growing in a cavity of the implant (brown and sliver). (nih.gov)
- Bone defects represent a challenge for guide tissue formation ( Fig. 1 ). (who.int)
- bioartificial bone tissues may help to overcome the Nowadays, tissue engineering is an interdisciplinary problems related to donor site morbidity and size field that applies the principles of engineering and of limitations. (who.int)
- The requirement for new bone to replace or restore the function of injured, damaged, or lost bone is a major clinical and socioeconomic need. (who.int)
- This gene encodes a secreted ligand of the TGF-beta (transforming growth factor-beta) superfamily of proteins. (nih.gov)
- 1. Bone morphogenetic protein signaling and growth suppression in colon cancer. (nih.gov)
- In early development of Xenopus laevis, it is known that activities of polypeptide growth factors are negatively regulated by their binding proteins. (xenbase.org)
- Those trials became the subject of controversy in 2011 when the Senate Finance Committee expressed concerns that researchers with financial ties to the Minneapolis-based company failed to report adverse events in their published research, including sterility in men and harmful bone growth. (aaos.org)
- To aid the recovery, clinicians inject patients with proteins called growth factors. (materialstoday.com)
- The growth factors also disperse, creating unwanted bone formation in the area around the injury. (materialstoday.com)
- A new technology under development at the Georgia Institute of Technology could one day provide more efficient delivery of the bone regenerating growth factors with greater accuracy and at a lower cost. (materialstoday.com)
- The researchers found that heparin microparticles bound BMP-2 with high affinity, exceeding the maximum reported growth factor binding capacity of other heparin-containing biomaterials by greater than 1,000-fold. (materialstoday.com)
- The researchers were also able to control the relative composition of different hormonal cell types simply by exposing hPSCs to different ratios of two proteins-fibroblast growth factor 8 and bone morphogenetic protein 2. (genengnews.com)
- Current BMP-2 delivery techniques use a collagen sponge, which releases large amounts of the drug in an initial burst. (materialstoday.com)
- This positioning allows the protein to receive and transmit signals that help the cell respond to its environment by growing and dividing (cell proliferation) or by undergoing controlled cell death (apoptosis). (medlineplus.gov)
- Mono-(2-ethyl-5-carboxypentyl) phthalate, mono-(2-ethyl-5-hydroxyhexyl) phthalate, mono-(2-ethyl-5-oxohexyl) phthalate, mono-n-butyl phthalate (MBP), mono-n-benzyl phthalate (MBzP), and total phthalates (∑phthalates) levels, and creatinine-adjusted levels of MBP, MBzP, and ∑phthalates were significantly higher on exposure day than on control day. (bvsalud.org)
- B) Expression of molecular markers in dorsal marginal explants of embryos that were uninjected (lane 1), injected with 500 pg of mRNA for CA-ALK2 alone (lane 2), and coinjected with 500 pg of CA-ALK2 and 200 pg of follistatin (lane 3). (xenbase.org)