The correlation between CaT and RCTs has become a bone of contention in recent years. The correlation between the two can be predicted based on four aspects: CaT and RCTs have a similar pathogenesis, RCTs lead to CaT, CaT may cause cuff tears, or there is no correlation between RCTs and CaT [11].
The pathogenesis of CaT remains unknown. Initially, CaT was thought to be caused by the accumulation of hydroxyapatite in the rotator cuff tendon caused by degeneration and local necrosis of the tendon fibers and the increase of calcium phosphate content [13]. Recent studies have shown that the metaplasia mechanism of CaT is that tendon fibers transform into fibrocartilage and are calcified [14]. It has been reported in subsequent studies that metaplasia of tendon fibers, differentiation of tendon stem cells into chondrocytes and osteoblasts [15], endocrine disorders (thyroxine, estrogen, insulin) [16], and genetic factors [17, 18] may also be related to the development of CaT. In this study, the incidence of diabetes and hypothyroidism was high, but this high incidence was not statistically significant in the two groups of patients. Archer et al. found that calcified fibrocartilage in CaT does not have typical immunohistochemical markers formed by chondrocyte-mediated calcium and questioned the metaplasia mechanism of tendon fibers to transform into fibrocartilage and finally calcify [19].
The pathogenesis of RCTs includes both external and internal factors. External factors include trauma, chronic impact, diabetes, and obesity, which can increase tendon damage. Internal factors include inadequate blood perfusion, tendon aging or degradation, apoptosis theory, and modification and calcification of the extracellular matrix [4, 20]. The most common cause of RCTs is tendon degeneration [11, 20]. Tendon degeneration is prevalent in patients with RCTs, and it is related to the reduction of tendon vessels [21]. In the rotator cuff, a relatively avascular region is called the avascular critical zone, a common site for the development of rotator cuff degeneration and tears [21, 22] and is also considered a common site for the development of rotator cuff calcification [21]. Therefore, some scholars believe that CaT is related to rotator cuff degenerative tears [5]. However, in this study, it was found that for the majority (95.7%) of patients with RCTs, the tears were found in different tendons or different areas of the same tendon (Figs. 2, 3, 4, 5, 6, 7).
Clinically, CaT mainly occurs in patients aged 30–60 years [23]. However, as patients age, the incidence of degenerative RCTs increases, too [24]. CaT can be observed, not only in the supraspinatus and subscapular tendon within the “avascular critical zone,” but also in the subscapularis and teres minor tendon outside the “avascular critical zone” [21]. Although CaT primarily occurs in the “avascular critical zone,” it is not uncommon that CaT affects other areas of the rotator cuff, or its calcification is limited to the deltoid muscle, but no tendon is damaged.
Our results also verified that 16% of patients with CaT had calcification in the subscapular tendon, and 0.7% of patients had CaT in the teres minor tendon. At the same time, calcification and tears were found to occur in different tendons or different areas of the same tendon. Calcification could also be seen in tendons outside the avascular critical zone, suggesting that the etiology of CaT was different from that of RCTs.
Although clinical evidence suggests that CaT associated with hydroxyapatite deposition is not a precursor or sequelae of degenerative tendon tears, there is still a significant correlation between rotator cuff tendon calcification and RCTs on histological and macroscopic levels [7]. However, the calcification deposited on the site of the RCTs appears to be histologically different from the calcification in hydroxyapatite deposition. Some scholars have found that 33% of patients with degenerative RCTs have obvious calcification at the site of tendon tears [25]. However, the calcifications associated with degenerative RCTs show different phosphorus concentrations and calcium: phosphorus ratios, suggesting that different calcium compounds may be responsible for the calcification of degenerative RCTs. In contrast, the phosphorus concentration and calcium: phosphorus ratios of all patients with CaT are consistent with hydroxyapatite crystals.
However, some studies suggest that CaT may accelerate the progress of RCTs. Merolla et al. [12] found that previous abnormal calcification may lead to or aggravate RCTs, which requires surgical treatment. Similarly, Ari et al. [5] reported that of 81 CaT patients who underwent arthrography, 27% had partial or complete RCTs. It is worth noting that in the study of Ari et al., the average age of patients was over 61 years old, which is the most common age for getting degenerative RCTs. This indicates that in their studies, the high prevalence of RCTs may be related to the age of the studied population, not just because of the complication of rotator cuff calcification. At the same time, some studies related to rotator cuff surgery have found that RCTs rarely occur even when patients only have CaT [9]. Other studies have shown that 23% of patients with RCTs will suffer CaT [7]. These conclusions are based on the results of research related to rotator cuff surgery, and only patients who fail to be cured with conservative treatment will undergo surgical intervention. Therefore, it is not entirely correct to conclude that CaT is correlated with RCTs. Therefore, for all patients with shoulder pain, MRI evaluation is more objective and accurate for assessing the correlation between CaT and RCTs [12]. The signal intensity of calcification on MRI is low, and the accuracy of identifying calcification with MRI is about 95% [12, 26]. In addition, the studies of Norenberg et al. [27] show that compared with X-ray, MRI boasts a diagnostic sensitivity of 98% and a specificity of 96% for shoulder joint calcification.
In the past, RCTs were rarely associated with CaT in imaging diagnosis. In a study using ultrasound to evaluate 94 rotator cuff CaT patients with an average age of 57 years, no RCTs occurred in the calcified region [10]. Beckmann et al. [11] conducted MRI examinations on 86 patients with CaT and 86 patients with shoulder joint pain in the control group, and the results showed no statistically significant difference in RCTs incidence between the two groups. In addition, in the CaT group, only 3/8 of the patients (3.5% of all CaTs) had calcifications and RCTs on the same tendon, which appeared in the same location of the tendon. In our study, only 4.3% of patients in the CaT group had calcifications and tears in the same area of the same tendon. Therefore, these research results support the view that CaT is not caused by RCTs, and it does not exacerbate RCTs. But there is possibility that CaT can cause tendon rupture indirectly by long-term mechanical change.
At present, this study still has some shortcomings. (1) The sample size is not big enough. For the correlation between CaT and RCTs to be accurately analyzed, the sample size needs to be further expanded. (2) In this study, MRI, rather than surgery, was adopted as the gold standard for diagnosing RCTs. As a result, some tiny tears in the tendon may be ignored. (3) This study evaluated the correlation between CaT and the current and static state of the tendon. It did not assess whether CaT increases the risk of tendinosis or tendon tears over a long period. (4) This study is based on using MRI to diagnose CaT, but calcification is not confirmed on x-ray. However, for all cases with x-rays, calcification can be seen through radiology.
