Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The potential role of dietary copper in the development of cartilage defects in foals was investigated. Twenty-one mares were fed rations containing 13 ppm copper (CuC, control) or 32 ppm copper (CuS, supplemented) during the last three to six months of gestation and first three months of lactation. Their foals were fed pelleted concentrate containing 15 or 55 ppm Cu and were destroyed at 90 (5 CuC and 5 CuS foals) or 180 (6 CuC and 5 CuS foals) days. Focal cartilage lesions were found at multiple sites on necropsy. In foals killed at 90 days, there were over twice (9 versus 4) as many lesions of osteochondrosis and more than four times (9 versus 2) as many articular lesions of osteophyte formation or thinning in CuC foals compared with CuS foals. These differences were due predominantly to a higher number of lesions in one CuC foal. Two 90-day CuC foals had osteochondrosis of articular-epiphyseal (A-E) complex, one with thickenings and separation from subchondral bone and one with subchondral fibrosis. One 90-day CuS foal had a cartilage thickening of the A-E complex in the tibiotarsal joint with separation from subchondral bone. In foals killed at 180 days, there were seven times more articular lesions (21 versus 3) of osteophyte formation or thinning, nearly twice as many lesions of osteochondrosis (13 versus 8) [corrected] in the physis and over five times as many involving the A-E complex (11 versus 2) in six CuC foals compared with five CuS foals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of copper supplementation on the prevalence of cartilage lesions in foals. 226 67

A histopathological study on the development of spontaneous osteochondrosis in the humeral head and medial femoral condyle of rats (6-20 weeks old) was carried out. Findings were classified into three types: normal, transitional and osteochondrotic. In the normal type, the articular cartilage at the caudal region of the humeral head and medial femoral condyle was significantly thinned between 6 and 10 weeks of age (generally the caudal region was thicker than elsewhere at all ages). In the transitional type, the thinning of the cartilage was delayed. In the third type, osteochondrotic lesions were detected in the humeral head from 6 weeks of age and in the medial femoral condyle from 10 weeks of age. The thickness of the cartilage had slightly decreased or had not changed at 20 weeks of age. In the early stages, viable chondrocytes and small destructive foci of cartilage were observed in the basal layer of the thick deep zone. These cells were present in pairs or clusters surrounded by matrix in the large lacunae. Cells and destructive foci were also seen in the surface layer of the deep zone as the rats aged. In the advanced stage, a necrotic area or cleft was formed in the basal layer of the articular cartilage and fibrosis was observed in the subchondral bone.
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PMID:Observation on the development of osteochondrosis in young rats. 379 64

The spinal region containing caudal notarium, free thoracic vertebra (T6), and cranial synsacrum was collected from 27 male broiler breeding fowl which were about 60 weeks old when killed. In 12 birds minor abnormalities were detected on gross morphological examination, with minimal scoliotic curvature being the most frequent finding. Particular attention was paid to articulations. Radiological and histopathological examination revealed subchondral defects due to articular osteochondrosis in every spine examined. Such lesions must represent the sequelae of disturbed endochondral ossification in younger birds. Many lesions were severe, showed little evidence of repair and contained clefts and marked cartilage necrosis. Clefts were not always associated with osteochondrosis but were also observed in slightly thickened articular cartilage and that judged to be of normal thickness. In this instance clefts occurred in deep regions of articular cartilage at sites which frequently showed chondrocyte and matrix change. The latter are likely to be the primary lesions. It also seems probable that the same anatomical sites are predisposed to cell death/clefts and osteochondrosis. Clefts in adult articular cartilage, unrelated to lesions of osteochondrosis, are more likely to be progressive leading to segmental cartilage detachment and destructive cartilage thinning.
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PMID:Abnormalities in the axial skeleton of broiler breeding fowl. 1876 84

A number of intra-articular and para-articular defects which occur in the pelvic limb joints of adult male turkeys have been illustrated and described. As in the fowl, the principal patterns of cartilage loss, namely peripheral remodelling and destructive cartilage loss, were identified in turkeys. In addition to cartilage thinning, peripheral remodelling can produce other morphological changes, some of which could be confused with destructive cartilage loss. In some instances, destructive cartilage loss may precede a reparative response which, once established, may be indistinguishable from peripheral remodelling. Defects at tendon or ligament attachments appear to result from traction and a number of pathological changes were observed at such sites. Findings in spinal articulations and distal tibiotarsi with destructive cartilage loss support the concept that regions of cell death and matrix change precede cleft formation which in turn precedes segmental detachment of uncalcified cartilage. Also, as in the fowl, lesions of articular osteochondrosis persist in the spinal articulations of adult birds.
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PMID:Intra-articular and para-articular defects in the pelvic limb and spine of adult male breeding turkeys. 1876 21