Pathogenesis of Shoulder Calcific Tendinopathy

TL;DR

This review explores the causes and potential treatments for shoulder calcific tendinopathy, a condition involving calcium deposits in shoulder tendons.

Contribution

The paper provides a comprehensive overview of the pathogenesis and emerging therapies for shoulder calcific tendinopathy.

Findings

Calcific tendinopathy involves tenocyte transformation and hydroxyapatite deposition in rotator cuff tendons.

Risk factors include hyperlipidemia, diabetes, and thyroid dysfunction, with women being more affected.

Therapies targeting inflammation and calcium homeostasis show promise in preclinical models.

Abstract

Shoulder calcific tendinopathy is a common condition affecting adults and is has a higher incidence in women. This condition is due to a multifactorial process and is characterized by the deposition of hydroxyapatite crystals in the rotator cuff tendons. The disease shows a phenotypic transformation of tenocytes into chondrocyte-like cells, likely caused by metabolic and inflammatory changes and mechanical stress. Risk factors promoting this pathology include hyperlipidemia, advanced age, diabetes, female gender, and thyroid dysfunction. Recent studies highlight that metalloproteinases, oxidative stress, inflammatory mediators, bone morphogenetic proteins (BMPs), genetic and post-transcriptional alterations play a significant role in the pathogenesis of the disease. New therapeutic strategies are currently available that aim to modulate inflammation, osteogenic differentiation, and calcium homeostasis, showing promising results, especially in preclinical models. The aim of this review is to explore the different pathogenetic mechanisms and highlight future therapeutic developments for the treatment of shoulder calcification.

Figures