Physiopathology of intratendinous calcific deposition

Kalsium ansamlinger i sener eller andre strukturer i bevegelsesapparatet kan bidra til smertetilstander. Denne studien går igjennom hvordan disse oppstår slik at vi kan få en bedre forståelse av hva vi kan gjøre med det. Store ansamlinger kan sees på røntgen, men man kan også ha mikroskopiske ansamlinger som bidrar til plager uten å være synling på røntgen.

Det er spesielt vanlig blant de med diabetes (30%) og assosieres ofte med tyroidea problemer eller andre hormonproblemer. Genetisk predisposisjon er også en viktig faktor.

Ofte starter det med en skade, hvor det så skjer en kursendring i helbredelsesprosessen som gjør at kalsiumavleiringer eller andre problemer fremtrer og bidrar til smerteproblematikk.

In calcific tendinopathy (CT) calcium deposits in the substance of the tendon. CT is particularly common in the rotator cuff tendons (RCTs) and supraspinatus tendon, and Achilles tendon and patellar tendon. CT of the rotator cuff is common in Caucasian populations, with a reported prevalence of 2.7% to 22%, mostly affecting women between 30 and 50 years. The most frequently involved tendon is the supraspinatus tendon, and in 10% of patients the condition is bilateral (Figure 1[1].

(kalsiumansamlinger vises ytterst og øverst på humerus)

(kalsiumansamling vises i ackillesenen)

Clinical manifestations of the calcific process within the tendons include chronic activity-related pain, tenderness, localized edema and various degrees of decreased range of motion (ROM). CT of the rotator cuff shows a tendency toward spontaneous resorption of the deposits and symptoms often resolve spontaneously, although some authors described persistent pain at long time follow-up and persistent reduction of ROM [5,6].

Microscopic calcifications which are not detectable at plain radiography can also occur in chronic tendinopathy. A histological study showed high incidence of small calcium deposits in tendinopathic supraspinatus tendons [8]. Microscopic calcium deposits are frequent also in diabetic patients [9].

Specimens of RCTs obtained during surgery consist of a gritty mass of sandy material or a toothpaste-like fluid, and the deposits were described as a white amorphous mass composed of many small round or ovoid bodies. Later, X-ray diffraction and infrared spectrometry and other techniques identified the material of calcific deposits as calcium carbonate apatite [1820].

Uhthoff and coworkers hypothesized that a favorable environment permits an active process of cell-mediated calcification, usually followed by spontaneous phagocytic resorption [28]. They describe four stages in the calcifying process of the rotator cuff: precalcific phase, calcific phase, resorptive phase, and repair phase. All phases may occur concomitantly in the same tendon.

Finally, bone is deposited and the spur is formed. No inflammatory cells or microtears were identified. The authors believe that the increased surface at the tendon-bone junction may represent an adaptive mechanism to increased mechanical loads.

An association between CT and diabetes and thyroid disorders has been shown, but the precise mechanism is still unknown [1]. Patients with associated endocrine disorders present earlier onset of symptoms, longer natural history, and they undergo surgery more frequently compared to a control population [61,62]. More than 30% of patients with insulin-dependent diabetes have tendon calcification [63]. The exposure of proteins to high levels of sugar moieties cause the glycosylation of several extra-cellular matrix proteins, which can modify the extracellular matrix by cross-linking proteins.

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