Hann, Susan Rachel; (1990) Cellular and molecular changes in calcifying tendinitis. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

Calcifying tendinitis can be a debilitating disease and occurs when mineral becomes deposited in tendon. The tendons situated in the rotator cuff of the human shoulder are particularly vulnerable. The pathogenetic mechanisms of this disease are unknown, but chondrogenic modulation has been proposed by Uhthoff (1975 et seq.) and this particular theory has been investigated. Cellular, molecular and enzymic features of pathological tendon have been compared and contrasted with normal tendon and articular cartilage, in addition to ossifying muscle. Fresh tissue samples were taken in the operating theatre, sub-divided, then processed by several different methods. Pathological specimens showed a variety of morphological changes. Ultrastructural observations in the regions around the deposited mineral enabled a detailed description of the pathological tissue and the associated calcific deposits. Alkaline phosphatase is frequently associated with calcification but in mineralising tendon, enzyme activity was not evident. Immunocytochemistry used to investigate the possible presence of collagen types II, VI, hyaluronic acid binding region protein and chondroitin- 4 and 6- sulphates, molecules that may be associated with a pathological cellular modulation in the tendon. No collagen type II was observed in the calcifying tendon. Thus, we suggest that a chondrogenic modulation is an unlikely causal mechanism of the pathology. Microanalytical studies compared the calcium to phosphorous ratios of mineral found in individual patients. Statistically significant ratios were obtained from hydroxyapatite crystals found in ossified tendon, compared with the less electron dense crystals of cal-cospherites located in the same tissue section. The ratios were all closer to the expected value for hydroxyapatite rather than pyrophosphate. Although it is not yet possible to provide a specific pathological mechanism for calcifying tendinitis, it appears not to be akin to endochondral ossification or primary bone formation, but may have features unique to tendon mineralisation.

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