Analysis Tools
cellular
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• at 9 months, histology of mutant femoral and tibial joint cartilage and subchondral bone revealed increased chondrocyte proliferation
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skeleton
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• at 9 months, histology of mutant femoral and tibial joint cartilage and subchondral bone revealed increased chondrocyte proliferation
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• seven days following tooth extraction, wild-type mice exhibit well organized trabecular bone restoration in the healing site; in contrast, the extraction socket of homozygous mutant mice shows remarkable variability in alveolar bone wound healing: it often appears as a thick cortical-bone-like tissue formed directly on the bony wall that is lined by a layer of osteoblast-like cells
• in addition, the restored trabecular bones frequently exhibit unusual shapes: some sockets display minimal bone formation activity and are filled with dense fibrous tissues with large cells
• at day 14, the sockets of wild-type mice are healed with more matured trabecular bone, whereas the healing alveolar bone of mutant mice is composed of disorganized bone structure
• histology of mandibular condyles revealed that the primary spongiosa of adult mutant mice display an abnormal trabecular bone structure associated with aberrant immunostaining with the hypertrophic cartilage specific type X collagen antibody
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• homozygotes are viable, fertile, and of normal size with no apparent abnormalities in the vertebral column
• at 4-8 weeks, homozygotes do not display observable growth retardation or defects in skeletal size and shape, including craniofacial bones (e.g. mandible)
• at 4 months or older, homozygotes develop a progressive degenerative joint disease resembling human osteoarthritis, with pronounced changes in the knee joints
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• at 9 months of age, anatomy and histology of mutant knee joint articular cartilage revealed major morphological changes of articulating surfaces and surrounding bones in the absence of observable inflammatory or immune responses
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• at 9 months, the mutant femoral condylar surfaces appear uneven and in some cases exhibit eroded areas with fibrous material
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• at 9 months, the mutant tibia appears wider, and the tibial joint cartilage surfaces appear either flattened or concave
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• at 9 months, the femoropatellar groove is abnormally deep and V-shaped, with loss of cartilage in the center of the groove, fibrillation and areas of increased chondrocyte proliferation
• at 9 months, the articular surface of the patella is also abnormally V-shaped and shows extensive fibrillation
• at 9 months, the mutant subchondral bone appears thinner and disorganized, and shows fibrillation and areas of increased chondrocyte proliferation
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• increased cartilage and bone formation at the periphery of mutant joints with increasing age, leading to morphological changes, esp. in the knee joints
• at 9 months of age, anatomy and histology of mutant knee joint articular cartilage revealed major morphological changes of articulating surfaces and surrounding bones in the absence of observable inflammatory or immune responses
• in contrast to joint cartilage, other hyaline cartilages display no apparent histological alterations
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• at 12 months, homozygotes show total loss of cartilage in certain areas of the femoral and tibial joint surfaces
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limbs/digits/tail
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• at 9 months of age, anatomy and histology of mutant knee joint articular cartilage revealed major morphological changes of articulating surfaces and surrounding bones in the absence of observable inflammatory or immune responses
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• at 9 months, the mutant femoral condylar surfaces appear uneven and in some cases exhibit eroded areas with fibrous material
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• at 9 months, the mutant tibia appears wider, and the tibial joint cartilage surfaces appear either flattened or concave
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• at 9 months, the femoropatellar groove is abnormally deep and V-shaped, with loss of cartilage in the center of the groove, fibrillation and areas of increased chondrocyte proliferation
• at 9 months, the articular surface of the patella is also abnormally V-shaped and shows extensive fibrillation
• at 9 months, the mutant subchondral bone appears thinner and disorganized, and shows fibrillation and areas of increased chondrocyte proliferation
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immune system
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• homozygotes are viable, fertile, and of normal size with no apparent abnormalities in the vertebral column
• at 4-8 weeks, homozygotes do not display observable growth retardation or defects in skeletal size and shape, including craniofacial bones (e.g. mandible)
• at 4 months or older, homozygotes develop a progressive degenerative joint disease resembling human osteoarthritis, with pronounced changes in the knee joints
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hearing/vestibular/ear
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• homozygotes display a crooked tectorial membrane but a normal organ of Corti
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• the striated-sheet matrix is abnormally loose and only aggregated and fused fibers without a cross-striated pattern course among the striated-sheet matrix
• antibody against type II collagen fails to detect type II collagen in mutant tectorial membrane
• however, collagen fibrils in the spiral ligament remain morphologically unchanged
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• at 12 months, ABRs indicate an average increase in auditory threshold of 276.7 dB
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• at 12 months, homozygotes exhibit a mild to moderate hearing impairment, as assessed by ABRs
• at 12 months, wild-type mice maintain normal hearing (35[?]0 dB) while homozygotes display hearing loss (62[?]6.7 dB)
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vision/eye
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• eye histology revealed no obvious abnormalities even in mice with severe articular cartilage alterations
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homeostasis/metabolism
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• seven days following tooth extraction, wild-type mice exhibit well organized trabecular bone restoration in the healing site; in contrast, the extraction socket of homozygous mutant mice shows remarkable variability in alveolar bone wound healing: it often appears as a thick cortical-bone-like tissue formed directly on the bony wall that is lined by a layer of osteoblast-like cells
• in addition, the restored trabecular bones frequently exhibit unusual shapes: some sockets display minimal bone formation activity and are filled with dense fibrous tissues with large cells
• at day 14, the sockets of wild-type mice are healed with more matured trabecular bone, whereas the healing alveolar bone of mutant mice is composed of disorganized bone structure
• histology of mandibular condyles revealed that the primary spongiosa of adult mutant mice display an abnormal trabecular bone structure associated with aberrant immunostaining with the hypertrophic cartilage specific type X collagen antibody
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