Calcific tendonitis is a condition defined by the deposition of calcium crystals within a tendon, leading to pain and dysfunction. These deposits are made of hydroxyapatite, a type of calcium phosphate that is the primary mineral component of bone tissue. While the exact trigger remains elusive, the condition is understood to be a cell-mediated response rather than a simple consequence of mechanical injury or wear and tear. This deposition follows a specific, predictable pathway of cellular transformation.
Where Calcific Tendonitis Occurs
The shoulder is the most commonly affected area, accounting for the majority of cases seen in clinical practice. Within the shoulder, the rotator cuff tendons are the usual site, with the supraspinatus tendon involved in approximately 80% of occurrences. The deposits typically form slightly away from the tendon’s attachment point on the upper arm bone, known as the greater tuberosity.
Calcific tendonitis can develop in tendons throughout the body. Other sites include tendons around the hip and knee joints, which are the second and third most common locations, respectively. Documentation also exists for the Achilles tendon, the elbow, and the wrist.
The Cellular Mechanism of Deposit Formation
The formation and resolution of calcific tendonitis is described as a three-phase process. The process begins with the formative phase, where the tendon tissue undergoes a fundamental change at the cellular level. Tenocytes, the normal cells of a tendon, transform into chondrocyte-like cells, which are cells that typically form cartilage.
This transformation is known as fibrocartilaginous metaplasia, which creates an environment conducive to mineralization. Within this new cellular matrix, calcium phosphate crystals begin to precipitate and aggregate, forming deposits of hydroxyapatite. This initial phase is highly organized and is mediated by these transformed cells, often occurring with few, if any, painful symptoms.
Once the deposits are formed, the condition enters the resting phase, which can last for an unpredictable time. During this period, the deposits are stable and inactive, and the individual often experiences little to no pain. This phase highlights the self-limiting nature of the condition, as the body prepares for resolution.
The final and most symptomatic stage is the resorptive phase, where the body attempts to clear the calcium deposits. The deposits become softer and are invaded by new blood vessels and specialized cells, including macrophages. These cells actively break down and absorb the crystalline material in a process called phagocytosis.
This aggressive cellular cleanup triggers a significant inflammatory response, which is the source of the intense, acute pain many individuals experience. Although the resorptive phase signals that the body is successfully resolving the condition, this biological action causes the most severe discomfort. Following resorption, the area is slowly remodeled back into healthy tendon tissue.
Identifying Key Contributing Factors
While the cellular mechanism explains how the deposits form, systemic factors are thought to predispose certain individuals to the condition, acting as the initial trigger. The condition is most frequently diagnosed in middle-aged adults, typically affecting those between the ages of 30 and 60. There is also a slightly higher incidence reported in women compared to men.
Unlike many other tendon problems, calcific tendonitis is often not primarily caused by repetitive mechanical strain or overuse injuries. Instead, a reduced oxygen supply, or hypoxia, to a specific area of the tendon is suspected of initiating the cellular transformation. This localized lack of oxygen may trigger the metaplasia that begins the deposition cycle.
Various metabolic and endocrine disorders have also been identified as contributing factors. Individuals with conditions like diabetes, thyroid disorders, and hyperlipidemia appear to have a higher risk of developing calcific tendonitis. These systemic conditions may affect the body’s ability to regulate calcium metabolism or influence tendon tissue health, making it more susceptible to the initial cellular changes.