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Updated: Mar 15, 2026

Treatment Protocol for Rotator Cuff Calcific Tendinitis Using a Single-Crystal Piezoelectric Focused Shock Wave Source

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Published on: December 23, 2022

Pathogenesis of Shoulder Calcific Tendinopathy.

Rami Kaplan¹, Micaela Berni², Laura Caliogna²

¹Department of Orthopedics, University of Cattolica Del Sacro Cuore, 00168 Rome, Italy.

International Journal of Molecular Sciences

|March 14, 2026

Summary

Shoulder calcific tendinopathy involves hydroxyapatite crystal deposition in rotator cuff tendons, often linked to metabolic and inflammatory factors. Research explores pathogenesis and new therapies targeting inflammation and calcium balance for shoulder calcification.

Keywords:

calcific tendinopathy pathogenesis shoulder

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A Protocol to Acquire the Degenerative Tenocyte from Humans

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A Protocol to Acquire the Degenerative Tenocyte from Humans

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Published on: June 9, 2018

Area of Science:

Orthopedics
Biochemistry
Pathology

Background:

Shoulder calcific tendinopathy is a prevalent condition characterized by hydroxyapatite crystal deposition within rotator cuff tendons.
It affects adults, particularly women, and involves tenocyte transformation into chondrocyte-like cells due to metabolic, inflammatory, and mechanical factors.

Purpose of the Study:

To review the multifactorial pathogenetic mechanisms of shoulder calcific tendinopathy.
To highlight emerging therapeutic strategies for shoulder calcification.

Main Methods:

Literature review of recent studies on shoulder calcific tendinopathy pathogenesis.
Analysis of risk factors, including hyperlipidemia, diabetes, and thyroid dysfunction.
Exploration of the role of metalloproteinases, oxidative stress, BMPs, and genetic alterations.

Main Results:

Pathogenesis involves metabolic and inflammatory changes, mechanical stress, and tenocyte-to-chondrocyte transformation.
Key contributing factors include hyperlipidemia, advanced age, diabetes, female gender, and thyroid dysfunction.
Metalloproteinases, oxidative stress, inflammatory mediators, BMPs, and genetic factors are significant contributors.

Conclusions:

Understanding the complex pathogenesis is crucial for developing effective treatments.
New therapies modulating inflammation, osteogenic differentiation, and calcium homeostasis show promise, particularly in preclinical settings.