Increased risk of shoulder calcific tendinopathy in diabetes mellitus: A nationwide, population‐based, matched cohort study

Abstract

Background: Calcific tendinopathy of the rotator cuff is a common cause of painful disability in the shoulder with unclear aetiology. Diabetes mellitus (DM) is associated with calcific tendinopathy; however, large epidemiological data are lacking. Thus, we conducted a nationwide population-based matched cohort study to investigate the risk for calcific tendinopathy of the shoulder in diabetic patients. Methods: The National Health Insurance Research Database of Taiwan was used to include 42 915 patients newly diagnosed with DM between 1 January 2000 and 31 December 2015 and randomly extract the data of 171 660 individuals, as a matched control group. All individuals were followed-up until the development of calcific tendinopathy or the end of 2015. Results: Overall, 122 patients from the DM group (0.284%) developed calcific tendinopathy compared with 340 individuals from the non-DM group (0.198%). TheKaplan-Meier analysis indicated that patients with DM had a higher risk of calcific tendinopathy since the eighth year of follow-up (log-rank test, P = .006). Cox proportional hazard regression revealed that the adjusted hazard ratio of calcific tendinopathy in diabetic patients to that in non-diabetic patients was 1.276 (95% confidence interval 1.037-1.571, P = .002). Moreover, the stratified analysis disclosed that DM was a strong independent risk factor for calcific tendinopathy irrespective of the existing comorbidities. Conclusions:This study demonstrated that patients with DM had a 27% increased risk of developing calcific tendinopathy of the shoulder, 8 years after initially being diagnosed with DM.

Risk Factor Analysis for Predicting the Onset of Rotator Cuff Calcific Tendinitis Based on Artificial Intelligence

“…A national population study by Su et al confirmed that the risk of secondary calcific tendonitis in patients diagnosed with either type 1 or type 2 diabetes was about 27%. Their hypothesis for this was that diabetes-induced vascular compromise and hyperglycemic exposure; the former may reduce the supply of nutrients and oxygen to connective tissue, thus causing degeneration and promoting calcification deposits, and the latter may lead to glycosylation of extracellular proteins, thus altering the biomechanical environment and possibly promoting calcification of connective tissue [ 30 ]. Furthermore, distinguishing between symptomatic and asymptomatic RCCT, after searching the literature, we found that Siu et al reported elevated subacromial fluid IL-1 β levels in diabetic patients with shoulder pain and shoulder stiffness, which may be strong evidence to support the diagnosis of symptomatic RCCT [ 31 ].…”

Untargeted metabolomics reveals dynamic changes in metabolic profiles of rat supraspinatus tendon at three different time points after diabetes induction

“…Among these, diabetes mellitus is a major factor affecting tendon quality and leading to tendinopathy ( 2 ). In recent years, the increasing number of people with diabetes has prompted a large number of studies ( 3 , 4 ) to focus on the adverse effects of diabetes on tendons. Some studies have shown that diabetes alters the physical and chemical properties of tendons and the arrangement of collagen fibers, extracellular matrix composition, and biomechanics in a high-glucose microenvironment ( 5 ).…”

Hyperoxia promotes osteogenic differentiation of diabetic tendon stem/progenitor cells via ROS/HIF-1a signaling axis

“…Diabetic tendinopathy is a common disease of the musculoskeletal system in patients with diabetes mellitus (DM) (Giha et al 2022;Cai et al 2018) that causes chronic pain, movement restriction, tendon micro-damage and rupture, and seriously affects patients' quality of life (Lui 2017; Mavrikakis et al 1989). Calci c tendinopathy is a serious type of diabetic tendinopathy (Su et al 2021;Lu et al 2020)mainly caused by calcium deposition in tendons, aggravating the clinical manifestations of diabetic tendinopathy (Oliva et al 2012). Currently, effective means of clinical prevention and treatment of calci c tendinopathy are limited because the pathogenesis remains unclear.…”