2002
DOI: 10.1093/rheumatology/41.4.474
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Endochondral ossification in Achilles and patella tendinopathy

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Cited by 51 publications
(41 citation statements)
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“…Indeed, the ectopic chondro-ossified deposits in the tendon mid-substance appeared in a process resembling endochondral ossification as shown by immunohistochemical staining of collagen type X in our collagenase-induced failed healing animal model of tendinopathy [63]. This is similar to the endochondral ossification process observed in Achilles and patellar tendinopathies [61]. We also observed an earlier expression of chondrogenic markers (collagen type II and Sox9) in the healing tendon fibroblasts prior to their expression in the chondrocyte-like cells and ossified deposits which appeared later in the tendon midsubstance in our animal model [63].…”
Section: Evidence For Erroneous Differentiation Of Tdscs In the Pathosupporting
confidence: 81%
See 1 more Smart Citation
“…Indeed, the ectopic chondro-ossified deposits in the tendon mid-substance appeared in a process resembling endochondral ossification as shown by immunohistochemical staining of collagen type X in our collagenase-induced failed healing animal model of tendinopathy [63]. This is similar to the endochondral ossification process observed in Achilles and patellar tendinopathies [61]. We also observed an earlier expression of chondrogenic markers (collagen type II and Sox9) in the healing tendon fibroblasts prior to their expression in the chondrocyte-like cells and ossified deposits which appeared later in the tendon midsubstance in our animal model [63].…”
Section: Evidence For Erroneous Differentiation Of Tdscs In the Pathosupporting
confidence: 81%
“…Its underlying pathogenesis is poorly understood and treatment is usually palliative. A change of tendon loading caused by mechanical overload, compression or disuse has been implicated as the possible etiologies [52], but they do not completely explain the failed healing responses, cellular and molecular alternations seen in the diseased tendon, including hypercellularity, hypervascularity, matrix disturbance with an increase in proteoglycan deposition, particularly the oversulfated form, ECM degradation, rounding of cell nuclei and acquisition of chondrocyte phenotypes, occasional adipose and bony metaplasia [53][54][55][56][57][58][59][60][61]. The production of abnormal matrix components (e.g., fatty degeneration, glycosaminoglycan accumulation with cell rounding and acquisition of chondrocyte phenotypes and calcification) in tendinopathic tendons suggested either that non-tenocytes migrated to the injury site; or that endogeneous or exogeneous stem cells possessing multilineage differentiation potential differentiated into nontenocytes.…”
Section: Evidence For Erroneous Differentiation Of Tdscs In the Pathomentioning
confidence: 99%
“…Chondroitin sulphate is the major glycosaminoglycan in tendinosis tissue and the accompanying increase in DNA content has been primarily attributed to fibroblasts and vascular cells (endothelial and smooth muscle cells) (Khan et al 1996;Fenwick et al 2002). Therefore, the excessive chondroitin sulphate found in biochemical assays of tendinosis could be produced by resident fibroblasts (tenocytes) or by vascular cells, or both (Riley 2005).…”
Section: Introductionmentioning
confidence: 99%
“…Calcification secondary to tendon degeneration is encountered in the supraspinatus tendon in particular9 with enchondral ossification of the tendon being important for this condition 2. In various locations neurovascular infiltration is encountered in tendinopathy of the Achilles, the patellar and the supraspinatus tendon, as well as in tennis elbow tendinopathy.…”
mentioning
confidence: 99%