In this study, we investigated the seasonality of acute calcific tendinitis onset in Japan. The results of our study indicated that the occurrence of acute calcific tendinitis exhibited a seasonal distribution characterized by a summer peak in July. Additionally, this study suggested that the mean monthly temperature can affect the onset of acute calcific tendinitis.
To date, seasonal variation of calcium resorption in calcific tendinitis has not been clarified. Regarding musculoskeletal pain, some previous studies have reported that cold or humid weather conditions negatively influence the symptoms of patients with chronic pain.3,4 However, our results do not agree with those of previous reports on musculoskeletal chronic pain. This discrepancy suggests that the mechanism of pain associated with the onset of calcium resorption differs from that of musculoskeletal pain. Conversely, acute gout attack, a type of microcrystalline arthritis, has also been reported to exhibit seasonality, with its onset being less frequent in the winter and more frequent in the spring to summer seasons.5–10 These results are similar to those of seasonal distributions in the present study. However, the incidence of acute gout attack has been reported to have no significant association with mean monthly temperature.10 Thus, changes in physical activity, serum uric acid/lipid/cortisol levels, diet, and alcohol consumption associated with seasons were suggested as triggering factors of acute gout attack.7, 10, 11
Based on the results of this study, the mechanism behind seasonal variation of acute calcific tendinitis is unclear; however, several possible hypotheses can be raised. One hypothesis involves the regulation of phagocytic activity of immune cells by body temperature. Pathological findings in the resorptive phase of calcific tendinitis include macrophage and multi-nucleated giant cells surrounding broken-up calcium deposits, and phagocytosis of the calcification by these cells is suspected to cause the calcium resorption.2, 9, 12 Furthermore, diffuse of apatite crystals from calcification into the subacromial bursa causes acute severe pain.13 While the function of macrophages can be regulated by various factors, transient receptor potential melastatin 2 (TRPM2), a thermosensitive channel expressed in wide range of immunocytes including macrophages, has also been identified to regulate macrophages.14 TRPM2 contributes to enhancing the phagocytic activity of macrophages when body temperature is elevated.14 When the ambient temperature is elevated in the summer, the opportunity of increasing the skin temperature also increases, which may predispose the activation of phagocytosis in macrophages. This mechanisms could possibly explain the predominance of the onset of acute calcific tendinitis in the summer. Another hypothesis is that repetitive microtauma owing to increased physical activity in the summer may affect the immune responses in the rotator cuff. However, further studies are needed to clarify the mechanism of the seasonal variation of acute resorption of calcific tendinitis.
This study has several limitations. First, because this is an observational study, it can be influenced by residual confounding owing to bias caused by factors not measured in this study. For example, the concurrence of rotator cuff and adhesive capsulitis can cause to trigger the onset of acute calcific tendinitis, but these factors were not considered in this study. Second, as this study was conducted in a general hospital in Tokyo and the sample population was small, this may have resulted in selection biases, and the ethnicity was limited to the Japanese population. Thus, the present results may not represent general population.