Initial site of calcifications in rotator cuff tendons: A sonographic observational study

Abstract

Background

This study aimed to investigate the initial site of calcification development in rotator cuff tendons using serial ultrasonographic evaluations.

Methods

A total of 21 patients with de novo calcifications were included. Ultrasonography was used to assess calcifications in the rotator cuff tendons. The distance from the tendon insertion on the humerus to the calcification site was measured, along with the long and short diameters and the long-to-short diameter ratio.

Results

In 19 patients (90%), calcifications were in direct contact with the tendon insertion on the humerus. In the remaining two patients (10%), the calcifications were located 1 mm proximal to the tendon insertion site. The mean long and short diameters of the calcifications were 9.4 ± 4.6 and 2.7 ± 1.2 mm (range: 3.0–17.0 and 1.0–4.5 mm), respectively. The mean long-to-short diameter ratio was 2.4 ± 2.2 mm (range: 1.8–10.0 mm). Regarding shoulder disorders, 1, 7, and 13 patients had a rotator cuff tendon tear, calcific tendinitis, and adhesive capsulitis, respectively.

Conclusions

Calcifications in the rotator cuff tendons appear to originate at the tenoperiosteal junction or in close periosteal proximity and extend along the tendon axis.

Introduction

Rotator cuff calcific tendinopathy is a common disorder characterized by the deposition of calcium crystals within the rotator cuff tendons or the subacromial–subdeltoid bursa. ¹ Calcifications within the rotator cuff tendons have been observed in 2.5%–7.5% of asymptomatic adult shoulders, with approximately 70% of cases occurring in women, particularly those aged 40–50 years. ¹ This condition commonly presents with shoulder pain and functional limitation. ¹ Despite extensive research, the precise pathophysiological mechanisms underlying calcification formation and progression remain unclear, with proposed explanations including mutations in fibroblasts or osteoblast-like cells, tendon degeneration, and mechanical stress.^2–4

Calcifications in the rotator cuff tendons are most frequently located 1.5–2 cm proximal to their humeral insertion. ⁵ However, this represents the site where calcifications are most commonly observed, not necessarily their point of initial formation. Determining the initial site of calcification provides valuable insight into its formation and progression within the rotator cuff tendons.

This study aimed to investigate the initial site of calcification in the rotator cuff tendons in patients with calcifications identified at early stages of formation. The findings could enhance our understanding of the precise origin of calcifications in the rotator cuff tendons, providing further insight into the mechanisms underlying their development.

Methods

Participants

This retrospective study reviewed the medical records of 3954 consecutive patients who underwent shoulder ultrasonography (US) at a local pain clinic between March 2022 and March 2025. Patients were included if they met the following criteria: (a) had undergone two or more shoulder US examinations; (b) demonstrated new-onset calcifications in the rotator cuff tendons on US examinations conducted between March 2022 and March 2025; and (c) had at least one prior US confirming the absence of calcification in the rotator cuff tendons. Calcification was defined as a focal echogenic structure within the tendon, with or without posterior acoustic shadowing (Figure 1).

Figure 1.

Longitudinal ultrasound images of the SST tendon. (a) Baseline image showing a normal-appearing SST tendon without evidence of calcification and (b) follow-up image obtained 20 months later at the same location reveals a newly developed hyperechoic focus (arrow) abutting the bony cortex of the greater tuberosity, consistent with de novo calcification originating at the tenoperiosteal junction. SST: supraspinatus.

The study was approved by the Institutional Review Board of a University Hospital (2025-07-034). The need for written informed consent was waived owing to the retrospective nature of the study.

Outcomes

The variables collected included age, sex, affected side, interval between the initial and follow-up examinations, the specific tendon in which calcification developed—supraspinatus (SST), subscapularis (SCT), or infraspinatus (IST)—and the distance from the tendon insertion on the humerus to the calcification site (bone-to-calcification distance), calcification dimensions (long and short axis), the long-to-short axis ratio, and any associated shoulder disorder.

At the initial US examination (before the development of calcifications), many tendons demonstrated a normal structural appearance without hypoechogenicity, thickening, or partial tears. This finding confirms that de novo calcifications can form in structurally normal tendons and are not necessarily preceded by degenerative tendinopathy.

Measurement of calcifications in rotator cuff tendons

US evaluations were conducted using a high-frequency (12–15 MHz) linear-array transducer on GE LOGIQ E10 or GE LOGIQ E9 systems (GE Healthcare, USA). For calcifications measured using the LOGIQ E10 system, dimensions were measured directly using integrated INFINIT PACS software (Video 1) with on-screen caliper tools. The bone-to-calcification distance was defined as the shortest perpendicular distance from the humeral tendon insertion to the nearest margin of the calcification. The long and short diameters—defined as the greatest length of the calcification along its longitudinal axis and the maximum width perpendicular to the long axis, respectively—were measured.

In the GE LOGIQ E9 system, direct PACS-based measurement was not available; therefore, calcification size was measured using ImageJ software (National Institutes of Health, Bethesda, MD, USA). High-resolution still US images were exported in JPEG format for analysis. Pixel-to-length calibration was conducted using the Set Scale function: the 1 cm reference bar was traced using the straight-line tool, and the known distance (“1 cm”) was entered into the dialog box to define pixel resolution. Subsequently, the bone-to-calcification distance, long diameter, and short diameter were measured using the same tool.

All measurements were recorded in millimeters (mm) with one-decimal-point precision. In cases of poorly defined margins, measurements were repeated, and the average value of two readings was recorded. All US examinations and measurements were conducted by a single musculoskeletal ultrasound specialist with 30 years of clinical experience.

Results

Of the 3954 patients reviewed, 254 underwent ≥2 shoulder US examinations. Among these, 21 patients (mean age: 59.1 ± 8.8 years; range: 41–77 years; male:female = 4:17; affected side right:left = 13:8) demonstrated newly developed calcifications in the rotator cuff tendons that were absent on previous examinations and were ultimately included in this study (Table 1). The mean interval between the initial and follow-up US examination was 1637.6 ± 961.9 days (range: 521–2717 days). Calcification developed in the SST, SCT, and IST in 12, 3, and 6 patients, respectively.

Table 1.

Summary of study findings.

Variable	Value (range)
Total patients (n)	21
Mean age (years)	59.1 ± 8.8 (41–77)
Sex (male:female)	4:17
Affected side (right:left)	13:8
Interval between initial and follow-up US (days)	1637.6 ± 961.9 (512–2717)
Tendon involved (SST:IST:SCT)	12:6:3
Bone-to-calcification distance (mm)	0.1 ± 0.3 (0–1)
Calcifications directly abutting the humerus	19 (90%)
Calcifications 1 mm from the humerus	2 (10%)
Calcification long diameter (mm)	9.4 ± 4.6 (3.0–17.0)
Calcification short diameter (mm)	2.7 ± 1.2 (1.0–4.5)
Long-to-short diameter ratio	2.4 ± 2.2 (1.8–10.0)
Associated shoulder disorders (calcific tendinitis: adhesive capsulitis: rotator cuff tear)	7:13:1

IST: infraspinatus; SCT: subscapularis; SST: supraspinatus; US: ultrasonography.

Regarding calcification characteristics, the mean distance from the tendon insertion point to the calcification was 0.1 ± 0.3 mm (Table 1). In 2 patients, the calcification was located 1 mm proximal to the humerus, whereas in the remaining 19 patients, it was in direct contact with the humerus (0 mm). The mean long and short diameters of the calcifications were 9.4 ± 4.6 and 2.7 ± 1.2 mm (range: 3.0–17.0 mm and 1.0–4.5 mm), respectively. The mean long-to-short diameter ratio was 2.4 ± 2.2 (range: 1.8–10.0).

Regarding shoulder disorders, 1, 7, and 13 patients had a rotator cuff tendon tear, calcific tendinitis, and adhesive capsulitis, respectively. In this study, the term “calcific tendinopathy” was used to describe the structural presence of calcium deposition within the rotator cuff tendons, irrespective of symptoms. In contrast, calcific tendinitis was used only for cases demonstrating acute inflammatory symptoms clinically consistent with a resorptive or rupture phase, supported by US features such as heterogeneous deposits, surrounding hyperemia, or bursal fluid. Therefore, calcific tendinopathy reflects a broad pathologic condition, whereas calcific tendinitis refers specifically to the symptomatic inflammatory stage. ¹ Adhesive capsulitis was diagnosed based on clinical criteria rather than US findings. Patients were classified as having adhesive capsulitis if they demonstrated a characteristic capsular pattern, including global limitation of passive range of motion with proportional restriction in abduction, external rotation, and internal rotation. ⁶ US examinations in these patients were primarily performed to exclude other structural abnormalities, such as rotator cuff tears or bursopathy, rather than to establish the diagnosis of adhesive capsulitis.

Most patients did not report new or worsening shoulder symptoms at the time when calcifications first appeared. This finding is consistent with the known behavior of encapsulated calcifications, which typically remain asymptomatic unless rupture or resorptive inflammation occurs. ⁷

Discussion

In this study, calcification development in the rotator cuff tendons initiated at or near the tenoperiosteal junction. Among the 21 patients, 19 (90%) showed calcifications in direct contact with the humerus cortex. In the remaining two patients (10%), calcifications were located 1 mm from the tendon insertion site. These findings indicate that calcifications typically originate at or near the bone–tendon interface. This pattern was observed across different shoulder pathologies, including adhesive capsulitis, calcific tendinitis, and rotator cuff tendon tear. Because calcifications initially occur at or near the tenoperiosteal junction and are most commonly located 1.5–2 cm proximal to their humeral insertion, calcific deposits appear to originate at the tenoperiosteal junction and subsequently extend along the tendon axis (Figure 2).

Figure 2.

Schematic illustration of the proposed pathogenesis of rotator cuff tendon calcification. Calcific deposits are shown to originate at the tenoperiosteal junction and subsequently extend distally along the tendon axis (A → B → C), a process likely influenced by mechanical stress. Blue: subacromial–subdeltoid bursa.

Unlike previous studies that focused on locations where calcifications are most frequently detected, this study identified the true initial site of calcification formation.^1,4,5 By including only patients with prior US confirming the absence of calcification, de novo calcifications were captured at their earliest detectable stage. Notably, all calcifications developed at or within 1 mm of the tenoperiosteal junction. This finding reflects the true origin of calcification rather than a commonly observed detection site, providing novel insight into the pathogenesis of rotator cuff calcific deposition.

These findings align with existing theories proposing a cellular origin for ectopic mineralization, particularly implicating mutant or dysregulated tendon-derived cells as key contributors to the de novo formation of calcification in rotator cuff tendons.^8,9 Fibroblasts—the predominant cell type in tendinous tissue—and osteoblast-like cells arising through pathological transdifferentiation are considered central mediators of this process.^10,11 Under mechanical stress, including repetitive loading, these cells may undergo phenotypic changes, ¹² including aberrant expression of osteogenic markers such as Runt-related transcription factor 2 (Runx2), alkaline phosphatase, and osteocalcin. This dysregulated differentiation promotes inappropriate deposition of calcium hydroxyapatite within the tendon matrix.^13,14

The location of newly formed calcification provides key etiologic insight. In this cohort, all de novo calcifications originated at or within 1 mm of the tenoperiosteal junction, supporting the concept that pathological osteogenic transformation of fibroblasts and osteoblast-like cells begins at the tendon–bone interface. As calcifications subsequently elongate along the tendon axis, their position reflects the evolutionary stage of the process: bone-attached deposits indicate early formation, whereas more distal intratendinous or musculotendinous deposits likely represent long-standing, migrated, or postrupture remnants rather than the primary origin. Thus, the spatial distribution of calcification is not only anatomical but also provides meaningful clues to the underlying biological mechanism and temporal progression of calcific tendinopathy.

The consistent proximity of calcifications to the tenoperiosteal junction suggests that biomechanical tension at the tendon–bone interface may serve as a localized trigger for pathological mineralization. Furthermore, this phenomenon was observed regardless of the clinical diagnosis—adhesive capsulitis, calcific tendinitis, or rotator cuff tear—supporting a common molecular mechanism rather than distinct disease-specific pathways.^2,15 This finding raises the possibility that individuals with rotator cuff tendon calcifications may have a pre-existing cellular susceptibility that manifests clinically under conditions of cumulative stress or impaired healing.

This study has several limitations. Continued longitudinal observation was not performed. To better understand the calcification development and progression in rotator cuff tendons, longitudinal studies with close-interval follow-ups from the initial onset of calcification are required. Additionally, studies involving tendon biopsy, gene expression profiling, and in vivo tracking of fibroblast differentiation are warranted to clarify etiopathogenesis and identify potential therapeutic targets for modulating or reversing ectopic mineralization.

The findings of this study, highlighting the tenoperiosteal junction as the principal site of de novo calcification, have meaningful clinical implications. This region corresponds to the area where dysregulated fibroblast- and osteoblast-like cell activity occurs, suggesting a potential target for therapeutic modulation. ¹¹ In this context, focal extracorporeal shockwave therapy may exert beneficial effects by modulating the aberrant reparative response at the tendon–bone interface. ¹⁶

The repeat ultrasound examinations in this study were performed as part of routine clinical care in a specialized pain management practice rather than for screening or research purposes. Ultrasound was used to differentiate the causes of shoulder pain, guide interventions, and monitor treatment response. Accordingly, this study does not advocate routine or unnecessary repeat imaging; instead, serial ultrasound data acquired during usual clinical management were analyzed.

In conclusion, this study provides valuable insight into the de novo formation of calcific tendinopathy, reinforcing the tenoperiosteal junction as the primary site of origin. The consistent proximity of calcific deposits to the tendon insertion site—regardless of clinical diagnosis—strongly supports the existence of a common mechanistic pathway underlying calcification development. These findings suggest that calcific tendinopathy should not be viewed merely as a degenerative or idiopathic process but as a dysregulated reparative response at the cellular level—driven by tendon-resident cells, particularly fibroblasts and osteoblast-like cells—which have aberrantly acquired osteogenic functions under mechanical or metabolic stress.