[Cysts of the jaw bone: origin, development, classification and surgical technic].
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Myositis ossificans traumatica (MOT) is a nonneoplastic, heterotopic ossification of soft tissues i.e. skeletal muscle, tendons, aponeuroses and fascia. It is often encountered in young male athletes participating in contact sports as a result of a single or repeated contusion. MOT tends to be solitary, localized and well circumscribed with a self-limited growth potential that may culminate in regression. The pathogenesis of MOT is still enigmatic. Recent animal experiments have led to a theory that mesenchymal connective tissue cells, undergo metaplasia induced by trauma and probably osteogenic proteins, to fibroblasts and osteoblasts. These cells deposit and structure osteoid centripetally in the lesion. As the lesion matures, cancellous bone develops into mature, lamellar bone in the periphery of the lesion. In its earlier stages MOT is easily cytologically and radiologically confused with osteogenic sarcoma. The management of MOT is largely conservative and the principles are of considerable value to physicians and physiotherapists engaged in the treatment of sports injuries. This article reviews the various forms of myositis ossificans as well as the pathology, diagnosis and treatment options.
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Bone morphogenetic protein-2 is a low molecular weight glycoprotein, classified as a morphogen. The sine qua non of bone morphogenetic protein is consistently reproducible induction of bone development in heterotopic sites. Bone morphogenetic proteins belong to the expanding transforming growth factor-beta superfamily. Bone morphogenetic protein-2 has pleiotropic functions that range from extraskeletal and skeletal organogenesis to bone generation and regeneration. Bone morphogenetic protein induced bone formation in postfetal life recapitulates the process of embryonic and endochondral ossification. Through recombinant gene technology, human bone morphogenetic protein-2 is available in almost unlimited amounts for basic research and clinical trials. Human bone morphogenetic protein-2 induces structurally sound orthotopic bone in a variety of experimental systems, including femoral defects in rats, tibial and ulnar defects in rabbits, femoral defects in sheep, mandibular defects in dogs, spinal fusion in dogs, and porous ingrowth in rats. Human bone morphogenetic protein-2 research extends to the fields of developmental biology, genetics, and evolution. Bone morphogenetic protein has been used successfully at the authors' institution to heal clinical nonunions and to achieve spinal fusion. This report reviews the current understanding of bone morphogenetic proteins in general and BMP-2 in particular and summarizes their potential applications.
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The purpose of the study was to investigate the influence of pamidronate on mechanical properties, growth, and structural changes in bones of rats in which experimental osteopenia was induced by administration of prednisolone. The experiment was carried out on male WAG rats divided into three groups: I. Control, II. Prednisolone (5 mg/kg im daily) and III. Disodium pamidronate (3 mg/kg sc daily) + prednisolone (5 mg/kg im daily). After three weeks of the experiment, the animals were sacrificed and their femoral and tibial bones were prepared. The administration of prednisolone resulted in morphological and metabolic changes in the osseous system, characteristic of osteopenia. The increased osteopsathyrosis was noted, manifesting in lowered resistance to fractures and lesser deformability in comparison with the control group. The administration of pamidronate resulted in the reduction of the destructive action of prednisolone on bones.
Since the introduction of bone scans in 1951, there have been many studies comparing biologic and physical characteristics of new bone-imaging agents and the results of scintigraphy and radiology in large numbers of patients. Relatively speaking, there have been fewer studies detailing the health benefits and financial cost associated with the use of skeletal scintigraphy. This review concerns these aspects in patients with malignancies of various sites and stages. About 2% of patients with stage I or II breast cancer have bone metastases at the time they first present, whereas nearly 28% of patients with stage III disease have bone metastases. A large percentage of patients with initially negative scans develop bone metastases during the first 3--4 yr; many of them develop them within the first 12--18 mo after initial diagnosis. For patients with lung cancer, the use of bone scans in staging their disease is somewhat controversial. Several studies indicate that the yield of positive bone scans may range from as low as 2% to as high as 35%. Data on the use of bone scans in staging prostatic cancer initially are similar to those in patients with breast cancer, that is, yields of 7% in patients with stage I or II disease and a yield of about 20% with stage III disease. Children with osteosarcoma or Ewing's sarcoma rarely have bone disease distant from the site of their primary bone lesion at presentation. However, a large percentage of them (30%--40% or so) develop bone metastases during the follow-up period. As in the case with patients with breast cancer, about half of these bone metastases are evident by 12--18 mo.
Seventy-six patients receiving regular haemodialysis, without biochemical or radiological evidence of renal osteodystrophy, entered a five-year double-blind placebo-controlled trial of calcitriol (1,25-dihydroxycholecalciferol) in the prevention of bone disease. Significantly more patients on placebo developed bone disease as judged by a sustained elevation of plasma alkaline phosphatase or the development of sub-periosteal erosions on hand radiographs. Serum parathyroid hormone fell significantly in the patients receiving calcitriol and was significantly lower than in patients receiving placebo. It is concluded that calcitriol delays and may prevent the development of metabolic bone disease in patients receiving regular haemodialysis therapy.
The cranial lateral-line system, as well as the canal bones are well developed in the African clariid catfish Clarias gariepinus. A generalised cranial lateral-line pattern is present (supraorbital, infraorbital, preoperculo-mandibular, otic, postotic and temporal canals). The supratemporal commissure, however, is missing, although a supraorbital commissure is present (formed through the fusion of the epiphysial branches). In addition to canals, some pit-lines are present which cover both canal regions and non-canal regions (vertical, horizontal, oral, anterior, middle and posterior pit-lines). In this paper, several ontogenetic stages of the canal related bones in C. gariepinus were studied. A description of the canal bones, as well as some considerations concerning their nomenclature are given. All canal bones develop, whereas the parietal bone seems to have fused with the supraoccipital bone during ontogeny, as has been observed in some siluroids. The extrascapulars (= supratemporals) are missing in C. gariepinus, as is the case in many siluroids. The posttemporal and supracleithral bones have fused as well. Surprisingly, some separate splenial bones, enclosing the distal part of the mandibular canal are present. Some secondary modifications indicate the apomorphic features of the Clariidae. The infraorbital bones, from which the antorbital bone has lost the antorbital commissure, and the suprapreopercular bone are enlarged, plate-like bones. The nasal bone has undergone some secondary, plate-like extensions as well.
Indigenously developed bone wax was evaluated for cytogenetic effects of a saline extract of the bone wax. Swiss mice were assigned to 5 groups of 6 animals each. Groups I, II, III were given non-lethal doses of 2.5, 5.0 or 10.0 ml bone-wax saline extract/kg body wt and Groups IV and V received sterile 0.9% saline vehicle or cyclophosphamide ip as controls. After 24 h the mice were sacrificed by cervical dislocation. Bone marrow preparations were stained with Giemsa's stain and examined by light microscopy. Abnormalities such as numbers of chromosome gaps, breaks and translocations were noted. The bone-wax saline extract did not induce chromosomal aberrations in the bone marrow of Swiss mice under our laboratory conditions.
Parathyroid hormone-related protein (PTHrP) participates in the regulation of endochondral bone development. After the cartilage mold is established in fetal life, perichondrial cells and chondrocytes at the ends of the mold synthesize PTHrP. This ligand then acts on PTH/PTHrP receptors on chondrocytes. As chondrocytes go through a program of proliferation and then further differentiation into post-mitotic, hypertrophic chondrocytes, PTHrP action keeps chondrocytes proliferating and delays their further differentiation. Indian hedgehog (Ihh) is synthesized by chondrocytes that have just stopped proliferating and is required for synthesis of PTHrP. The feedback loop between PTHrP and Ihh serves to regulate the pace of chondrocyte differentiation and the sites at which perichondrial cells first differentiate into osteoblasts. Activation of the PTH/PTHrP receptor leads to stimulation of both Gs and Gq family heterotrimeric G proteins. Genetic analyses demonstrate that Gs activation mediates the action of PTHrP to keep chondrocytes proliferating, while Gq activation opposes this action. Downstream from Gs activation, synthesis of the cyclin-cdk inhibitor, p57, is suppressed, thereby increasing the pool of proliferating chondrocytes. PTHrP's actions to delay chondrocyte differentiation are mediated by the phosphorylation of the transcription factor, SOX9, and by suppression of synthesis of mRNA encoding the transcription factor, Runx2. These pathways and undoubtedly others cooperate to regulate the pace of differentiation of growth plate chondrocytes in response to PTHrP.
During puberty, the acquisition of skeletal mass and areal bone mineral density (BMD) mainly reflects an increase in bone size (length and perimeters) and not true volumetric BMD. Sexual dimorphism in bone mass and areal BMD is also explained by differences in bone size (longer and wider bones in males) and not by differences in volumetric BMD. Androgens stimulate skeletal growth by activation of the androgen receptor, whereas estrogens (following aromatization of androgens and stimulation of estrogen receptors) have a biphasic effect on skeletal growth during puberty. Recent evidence from clinical cases has shown that many of the growth-promoting effects of the sex steroids are mediated through estrogens rather than androgens. In addition, skeletal maturation and epiphyseal fusion are also estrogen-dependent in both sexes. Nevertheless, independent actions of androgens in these processes also occur. Both sex steroids maintain volumetric BMD during puberty. Androgens interact with the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis neonatally, resulting in a sexual dimorphic GH pattern during puberty, whereas estrogens stimulate GH and hereby IGF-I in both sexes. Hypogonadism in adolescents impairs not only bone size but also maintenance of volumetric BMD, hereby severely reducing peak areal BMD. Delayed puberty in boys and Turner's syndrome in women impair both bone length and size, reducing areal BMD. Whether volumetric BMD is also reduced and whether fracture risk is increased in these conditions remains controversial. Replacing sex steroids according to a biphasic pattern (starting at low doses and ending at high-normal doses) seems the safest approach to reach targeted height and to optimize bone development.
Bones of the rats flown on Cosmos-1667 were examined histologically and histomorphometrically. It was found that 7-day exposure to weightlessness led to osteoporosis in the spongy matter of proximal metaphyses of tibia and, although to a lesser extent, in the spongiosa of lumbar vertebrae whereas no signs of osteoporosis were seen in the spongy matter of iliac bones. Osteoporosis in the spongy matter of the above bones developed largely due to the inhibition of bone neoformation, which was indicated by a decrease in the number and activity of osteoblasts. Increased bone resorption (as shown by a greater number and activity of osteoclasts) was observed only in the spongy matter of tibial metaphyses. It is emphasized that a reduction of the number of highly active osteoblasts in spongy bones is one of the early signs of inhibition of bone neoformation and development of osteoporosis.