tendinopathy/phosphatase

Hyperuricemia is a well-known consequence of glucose-6-phosphatase (G6Pase) deficiency, the enzymatic abnormality that characterizes glycogen storage disease (GSD) Type Ia. However, acute gout as the presenting manifestation of GSD Type Ia has been reported in only a few patients. We report a new

Calcifying tendinitis of rotator cuff tendons is a common and painful condition caused by ectopic calcification in humans. To examine the involvement of osteopontin (OPN), a potent regulator of calcium deposition on connective tissues, localization and expression of OPN protein and messenger (m)RNA

Calcific tendonitis of the rotator cuff is due to apatite deposits in the shoulder tendons. Patients affected by calcific tendonitis have chronic shoulder pain and disability. Although the disease is frequent, about 10 to 42% of painful shoulders, mechanisms leading to this pathological

A group of 170 patients having functional renal allografts were evaluated at least six months after renal transplantation. They were assessed for symptoms and signs of tendinitis in the Achilles and Supraspinatus tendons. Of the 170 patients, 34 had tendinitis. Four patients (11.8%) had spontaneous

Calcific tendonitis is a frequent cause of chronic shoulder pain. Its cause is currently poorly known. The objectives of this study were to better characterize the cells and mechanisms involved in depositing apatite crystals in human tendons. Histologic sections of cadaveric calcified tendons were

We hypothesized that altered fate of tendon-derived stem cells (TDSCs) might contribute to chondro-ossification and failed healing in the collagenase-induced (CI) tendon injury model. This study aimed to compare the yield, proliferative capacity, immunophenotypes, senescence, and differentiation

Pathologic calcification usually is initiated by the biologic membranes of mitochondria or matrix vesicles. Mitochondria frequently initiate intracellular calcification. Matrix vesicles, derived from the outer membrane of cells by budding or cell disruption, initiate extracellular calcification in

Tendon calcification is a common but intractable problem leading to pain and activity limitation when injury or tendinopathy progresses into the late stage. This is because tendon stem/progenitor cells (TSPCs) can undergo aberrant osteogenic differentiation under inflammatory conditions. This study

Tissue calcification is a typical histopathological feature of tendinopathy. The osteogenic differentiation of tendon stem cells (TSCs) induced by inflammatory mediators is believed to play a key role in this process. Previous studies showed that the major inflammatory mediator prostaglandin E2

The causative mechanism of tendon calcification ('calcifying tendinitis') is unknown. In this report, pathological human tendon samples were examined to give morphological and ultrastructural detail of the calcified regions and these findings were compared with those from normal tendon. Selected