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.7,8 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 been reported to exhibit seasonality, with its onset being less frequent in the winter and more frequent in the spring to summer seasons.9-14 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.14 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.11, 14, 15
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.6, 13, 16 Furthermore, diffusion of apatite crystals from calcification into the subacromial bursa causes acute severe pain.17 While the function of macrophages can be regulated by various factors, transient receptor potential melastatin 2 (TRPM2), a thermosensitive channel expressed in a wide range of immunocytes including macrophages, has also been identified to regulate macrophages.18 TRPM2 contributes to enhancing the phagocytic activity of macrophages when body temperature is elevated.18 When the ambient temperature is elevated in the summer, the opportunity of increasing skin temperature also increases, which may predispose the activation of phagocytosis in macrophages. This mechanism 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. In this study, 17.4% of patients developed the symptoms due to trauma, heavy work, or sports. This finding supports the possibility that increased physical activities may also affect the onset of acute calcific tendinitis. However, further studies are needed to clarify the mechanism of the seasonal variation of acute resorption of calcific tendinitis.
In contrast, the results of our study did not suggest a correlation between the season of pain onset and the disappearance of symptoms. One previous study reported that 90% of symptomatic calcific tendinitis of the rotator cuff is relieved by conservative treatment,19 and in this study, similar results were obtained, where the symptoms disappeared in 95.5% of patients by conservative treatment. In a previous study, multivariate analysis identified female gender as a significant risk factor against conservative treatment20; however, the prognostic factors of treatments for acute calcific tendinitis remain largely unknown. The results of our study suggested that the season of pain onset may not have affected the symptom course, but younger age may be a negative prognostic factor of conservative treatment.
In addition, the results of our study also suggested that the epidemiology of the calcific tendinitis in resorptive phase does not necessarily match the epidemiology of calcific tendinitis overall. In a previous study that investigated 6061 volunteers,21 calcific deposits in the rotator cuff were observed in 2.7% of them, but among those with calcific deposits, 34.6% were symptomatic, and in particular, only 8.9% exhibited acute shoulder pain. In this study, only patients in the calcium resorptive phase exhibiting acute shoulder pain were included. Thus, even though calcific tendinitis is a common disease, the number of subjects who developed this disease in this study was smaller for the study period of 13 years. Calcific tendinitis has been reported to be associated with diabetes and thyroid disorders.3-6 However, in this study, patients with a history of diabetes and thyroid disorders were 10.7% and 2.1%, respectively, and these were almost the same as the incidence of diabetes (11.2%22) and thyroid disorders (up to 10%23) among the Japanese, suggesting no correlation between the onset of calcific resorption in calcific tendinitis and history of these diseases. In addition, 21.3-46.4% of patients were reported to exhibit bilateral calcific deposits,20, 21 but in this study, no patient developed bilateral calcific resorption during the study period. In terms of age, calcific tendinitis of the rotator cuff occurred commonly in the patients aged 30 to 50 years,21 but the mean age of patients in this study was slightly older, at 62.8 ± 14.2 years, suggesting that calcific resorption may have developed after a certain period of time after the formation of calcium. These findings suggest that the epidemiology of calcific tendinitis in the resorptive phase is not representative of the epidemiology of calcific tendinitis overall.
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 the 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 and emergency hospital in Tokyo, there were more patients in need of surgery and more acute diseases compared to medical practitioners, which might have resulted in selection biases and a smaller sample population. In addition, the ethnicity was limited to the Japanese population. Thus, the present results may not represent the general population.