Calcific tendonitis is a common and often severely painful shoulder condition resulting from the accumulation of calcium deposits within the tendons. While the precise trigger remains unknown (often classified as idiopathic), the condition involves a distinct biological process that explains the formation and eventual resolution of the calcium buildup. Understanding this process, along with demographic and systemic factors, provides the current scientific explanation for how and why this condition occurs in the shoulder.
Defining Calcific Tendonitis and Affected Anatomy
Calcific tendonitis is characterized by the formation of calcium phosphate crystals, specifically hydroxyapatite, within the substance of a tendon. This condition is distinct from standard tendinosis, which involves non-calcified degeneration of the tendon fibers, though both cause shoulder pain. The deposits have a characteristic chalk-like consistency during formation and a toothpaste-like consistency when the body attempts to break them down.
The shoulder is the most common site for this condition, with deposits overwhelmingly occurring within the rotator cuff tendons. The supraspinatus tendon is involved in the majority of cases due to its function in lifting the arm away from the body. The rotator cuff is a group of four tendons and muscles that surround the shoulder joint, providing stability and allowing the arm to rotate and lift.
When calcium hydroxyapatite crystals build up in the supraspinatus tendon, they reduce the space available for the tendon to glide smoothly under the acromion bone. This mechanical obstruction, combined with inflammation caused by the deposits, restricts the shoulder’s range of motion and generates pain. The physical presence of the deposits, which are visible on an X-ray, is the defining feature distinguishing calcific tendonitis from other common shoulder injuries.
The Three Stages of Calcium Formation
The formation and subsequent removal of calcium deposits follow a predictable, self-limiting biological course known as reactive calcification. This process is understood as a cellular or metabolic event rather than one primarily driven by mechanical wear and tear. It is divided into three main stages: formative, resting, and resorptive.
Formative Stage
The process begins with the precalcific stage, where specific areas of the tendon tissue undergo a cellular transformation called fibrocartilaginous metaplasia. During this transformation, tenocytes (the specialized cells of the tendon) change their behavior to resemble chondrocytes, or cartilage cells. These transformed cells then create a matrix conducive to calcification, similar to the process of bone formation.
This cellular change leads directly into the formative phase, where calcium hydroxyapatite crystals are actively deposited into the prepared matrix within the tendon. The deposit forms a dense, well-defined mass with a dry, chalky texture. This phase is often painless or only mildly uncomfortable because the body is actively building the deposit without triggering an inflammatory response.
Resting Stage
Once the calcium deposit is fully formed, the process enters a resting stage where the deposit remains stable within the tendon tissue. The body is neither actively creating nor removing the calcium mass during this time. Pain is highly variable; some individuals experience no symptoms, while others may have chronic, low-grade discomfort or mechanical pain if the deposit impinges on surrounding structures.
Resorptive Stage
The most painful phase is the resorptive stage, which begins when the body attempts to clear the calcium deposit. Macrophages, a type of immune cell, infiltrate the area to begin dissolving and engulfing the crystals. This aggressive cellular activity triggers a massive inflammatory response, causing the deposit to liquefy into a softer, toothpaste-like consistency under pressure.
The combination of increased pressure from the inflamed and swollen tissue, along with chemical irritation from the dissolved calcium, leads to the sudden onset of severe, acute pain. This intense pain signals that the body is actively attempting to resolve the condition. Pain typically subsides once the majority of the calcium has been reabsorbed. The final phase, sometimes called the post-calcific stage, involves the remodeling of the tendon tissue back to its original, healthy structure.
Non-Mechanical Risk Factors and Predispositions
The underlying cause of the cellular changes that initiate the formative stage is not fully established. However, several systemic and demographic factors are consistently associated with an increased risk of developing calcific tendonitis. The condition is most commonly diagnosed in adults between the ages of 30 and 50, a demographic not typically associated with the degenerative changes seen in older patients. Women are also affected at a slightly higher rate than men.
Metabolic and endocrine disorders appear to predispose individuals to the condition, suggesting a systemic biological component. People with diabetes mellitus have a higher incidence of calcific tendonitis, as do those with thyroid abnormalities, particularly hypothyroidism. These associations point toward a dysfunction in the body’s overall calcium regulation or a generalized effect on connective tissue health.
A leading theory suggests that the trigger for the initial cellular change is localized tissue hypoxia, or a temporary lack of oxygen in a specific area of the tendon. The supraspinatus tendon is known to be a relatively low-blood-flow area, and this reduced oxygen tension may cause the tenocytes to transform into cartilage-producing cells. This localized environmental change, rather than general athletic overuse or heavy physical labor, is thought to initiate the entire cycle of calcium deposition and reabsorption.