The analysis included 137 patients treated through routine care between January 2019 and December 2024 at The Second Affiliated Hospital of Anhui Medical University and Shannan City People’s Hospital in China. Sixty-seven received manipulation under anesthesia followed by intra-articular platelet-rich plasma and a 40 mg triamcinolone acetonide injection, while 70 underwent arthroscopic capsular release. Eligibility required persistent pain and restricted active and passive shoulder motion despite at least three months of conservative treatment, as well as at least 12 months of follow-up. Of 200 screened records, 63 were excluded: 15 did not meet diagnostic criteria, 12 had full-thickness rotator cuff tears, 10 had previous shoulder surgery, 18 had less than 12 months of follow-up and eight had insufficient records for analysis.

Treatment was not assigned randomly. Patients and clinicians selected between the complete pathways through shared decision-making, with factors including symptom duration, imaging findings, patient preference, anticipated invasiveness, recovery, safety, resources and financial circumstances. The manipulation group received general anesthesia, gradual short-lever-arm movement after muscle relaxation and scapular stabilization, and reassessment of passive motion. Autologous platelet-rich plasma was prepared from approximately 8 mL of peripheral blood and 4–5 mL of leukocyte-reduced material was injected into the glenohumeral joint after manipulation. The arthroscopy group underwent radiofrequency ablation and shaver-assisted release of the rotator interval, coracohumeral ligament and anterior and inferior capsule, with posterior release added when posterior contracture was identified. The available procedural summary did not establish whether the corticosteroid was mixed with platelet-rich plasma or injected separately, or record the final injectate volume.

Both groups followed the same rehabilitation principles under the treating surgeon and rehabilitation team. Exercises began after recovery from anesthesia when pain was tolerable, initially emphasizing passive and assisted active forward flexion, abduction, external rotation and internal rotation. Stretching was performed several times daily, with active movement and rotator-cuff and periscapular strengthening added as symptoms and mobility improved. Outcomes were evaluated before treatment and at 1, 3, 6 and 12 months. Pain was measured with the visual analog scale, function with the American Shoulder and Elbow Surgeons score and disability with the Shoulder Pain and Disability Index. Clinicians also measured passive flexion, abduction, external rotation and internal rotation in degrees. The one-month pain comparison was highlighted after data collection rather than prospectively registered, making it an exploratory comparison rather than a prespecified primary outcome.

Both pathways were followed by substantial improvement, but several early measures favored the combined strategy. At one month, the adjusted mean visual analog scale score was 0.57 points lower in the manipulation group, with a 95% confidence interval of −0.75 to −0.38. Its American Shoulder and Elbow Surgeons score was 2.00 points higher, with a 95% confidence interval of 0.88 to 3.12, while its Shoulder Pain and Disability Index score was 2.66 points lower, with a 95% confidence interval of −3.44 to −1.89. The corresponding Holm-adjusted probability values were 0.001 or lower. At three months, the combined group’s American Shoulder and Elbow Surgeons score was 9.09 points higher, with a 95% confidence interval of 7.97 to 10.22 and a Holm-adjusted P value below 0.001. Pain and disability no longer differed significantly at that point, and no later pain comparisons were statistically significant.

The magnitude of the early findings requires caution because statistical significance does not necessarily indicate clinical importance. Contextual reference values came from a separate cohort of nondiabetic patients undergoing arthroscopic capsular release; its distribution-based within-patient minimal clinically important differences at six months were 1.1 points for pain and 8.2 points for function. Those estimates arose from a different population, time point and within-patient construct and are not validated between-group thresholds for the present cohort. The one-month pain and function differences in this study were smaller than those contextual values, whereas the three-month function estimate was numerically larger. A reported 17-point smallest detectable difference for the Shoulder Pain and Disability Index in adhesive capsulitis was not directly comparable, but the one-month difference of 2.66 points was smaller than that reference. The clinical importance of the early estimates therefore remains uncertain.

Passive forward flexion also showed an early difference in favor of manipulation, with an adjusted mean difference of 8.31 degrees at one month and a 95% confidence interval of 5.52 to 11.10. The groups had no significant follow-up differences in abduction or external rotation. At 12 months, the main model identified a 2.10-degree internal-rotation difference favoring the combined strategy, with a 95% confidence interval of 1.01 to 3.20 and a Holm-adjusted P value below 0.001. This result was not confirmed as statistically significant in the inverse probability of treatment-weighted sensitivity analysis. The weighted mean difference was 2.03 degrees, with a 95% confidence interval of 0.02 to 4.03 and an adjusted P value of 0.193. Because the difference was small, lacked a validated disease-specific clinical-importance threshold and was sensitive to the weighting analysis, the authors treated it as uncertain rather than a durable advantage.

By 12 months, the groups had nearly identical outcomes for pain, function, disability, forward flexion, abduction and external rotation. Mean visual analog scale scores were 0.40 in both groups, while mean American Shoulder and Elbow Surgeons scores were 92.72 after the combined strategy and 93.21 after arthroscopic release. Patient satisfaction was 98.5% in the combined group, based on 66 respondents, and 90.0% in the arthroscopy group, based on 63. The difference was not statistically significant, with an odds ratio of 7.33, a 95% confidence interval of 0.88 to 61.31 and P = 0.063. No serious procedure-related complication or reintervention was identified in either group. The zero-event findings had exact upper 95% confidence limits of 5.36% and 5.13%, and the cohort was too small to estimate rare harms precisely. Records also did not systematically capture mild or transient events such as pain flares, short-lived sensory symptoms or recurrent stiffness that did not require another intervention.

The hospital-recorded aggregate treatment amount was lower for the combined pathway. It averaged 7,975.49 Chinese yuan, compared with 14,897.57 Chinese yuan for arthroscopic capsular release. After adjustment for age, sex, dominant-side involvement, symptom duration, diabetes and study site, the mean difference was −6,903.88 Chinese yuan, with a 95% confidence interval of −7,196.76 to −6,611.00 and P below 0.001. This figure should not be treated as a standardized direct medical cost or proof of cost-effectiveness: itemized procedure, hospitalization, consumable and medication charges were unavailable, as were the billing window and price-standardization procedures. Rehabilitation expenses, return to work, quality-adjusted life-years and other indirect costs were not measured. Differences in billing systems and prices between the centers could also remain despite statistical adjustment for study site.

Repeated outcomes were analyzed with mixed-effects models adjusted for baseline values, age, sex, symptom duration, diabetes, dominant-side involvement and study site. These models accounted for repeated observations within patients, while Holm correction was applied across the four postoperative comparisons for each outcome. Inverse probability of treatment weighting was used as a sensitivity analysis for differences associated with treatment allocation. A ridge-penalized propensity model was required because conventional logistic estimation showed near-complete separation. Stabilized weights were truncated at the 2.5th and 97.5th percentiles, improving balance across recorded covariates; all post-weighting absolute standardized mean differences were below 0.10, and the effective sample size was 128.5. Weighted longitudinal estimates were directionally consistent with the primary models for early pain, function, disability and forward flexion, but did not confirm the 12-month internal-rotation finding.

The findings describe two routine-care strategies rather than the independent effects of their components. Manipulation may disrupt adhesions, corticosteroid may reduce early inflammation and platelet-rich plasma was included as a biological adjunct, but the study included no comparison groups receiving manipulation alone, platelet-rich plasma alone or corticosteroid alone. The evidence therefore cannot determine whether any component produced the early association or whether differences in manipulation technique, injection delivery, arthroscopic tissue trauma or postoperative discomfort explain the trajectory. The retrospective design is the central limitation: shared decision-making may have influenced allocation, and neither regression adjustment nor inverse probability weighting can remove unmeasured confounding. Detailed imaging findings, patient preferences, financial circumstances and surgeon judgment were not consistently available, while excluding records with short follow-up or incomplete data may have introduced selection bias. Assessors were not blinded, rehabilitation adherence was not recorded, and one arthroscopy patient had missing postoperative abduction measurements for undocumented reasons. The results can inform shared decision-making, but they do not establish causal superiority, comparative safety, equivalence, noninferiority, component-specific efficacy or cost-effectiveness.

Subject of Research: Comparative early recovery and recorded treatment amounts after combined manipulation and arthroscopic capsular release for refractory frozen shoulder

Article Title: MUA with PRP and corticosteroid injection versus arthroscopic capsular release for refractory frozen shoulder: a retrospective cohort study

Article References: Ye, C., Ciren, L., Wang, Y., Yang, L., Wang, K., Lan, S., Sun, K., Wang, C., Pan, S., & Li, J. (2026). MUA with PRP and corticosteroid injection versus arthroscopic capsular release for refractory frozen shoulder: a retrospective cohort study. Frontiers in Medicine, 13, Article 1957034. https://doi.org/10.3389/fmed.2026.1957034

Image Credits: AI Generated

DOI: 10.3389/fmed.2026.1957034

Keywords: frozen shoulder, adhesive capsulitis, manipulation under anesthesia, arthroscopic capsular release, platelet-rich plasma, corticosteroid injection, retrospective cohort, shoulder function, patient-reported outcomes, treatment amount, corticosteroid, injection

The research team, led by Lin Huang, Ling Cheng, and colleagues at Dianjiang People’s Hospital of Chongqing, reanalyzed three public bulk RNA-sequencing datasets rather than merging them into a single expression matrix. GSE140731, the discovery cohort, contained 22 adhesive capsulitis samples and 26 surgical controls from patients undergoing shoulder-instability repair. Two smaller datasets, GSE190023 and GSE238053, served as independent validation cohorts. The design choice was deliberate: previous studies of frozen shoulder have often relied on small, single-cohort analyses with differing comparators, making cross-study inference fragile. By keeping each cohort separate and adjusting the discovery analysis for the pronounced age and sex imbalance between cases and controls, the mean age was 52.7 years in the adhesive capsulitis group versus 23.9 years in the comparator group, and women accounted for 15 of 22 cases but only 5 of 26 controls, the team aimed to identify which transcriptional features genuinely replicate.

The technical core of the study was differential-expression analysis with PyDESeq2, a count-aware statistical framework that models raw sequencing counts directly. After filtering lowly expressed genes and standardizing age across all samples, the primary design specified the group coefficient as the adhesive capsulitis-versus-control difference after adjustment for age and sex. The adjusted discovery analysis identified 552 genes at a false-discovery rate below 0.05, including 439 upregulated and 113 downregulated genes. Representative upregulated genes included MMP9, a matrix-degrading enzyme, and TPM1, while downregulated genes included AMZ2P1 and OS9. The direction and number of significant genes, the authors note, were not attributable solely to an unadjusted comparison, although residual confounding by the non-healthy comparator could not be excluded.

Pathway-level enrichment told a clearer story. In the age- and sex-adjusted preranked analysis, the KEGG pathway for extracellular matrix-receptor interaction showed a normalized enrichment score of 2.299 and remained strongly significant after false-discovery correction, with a q-value of 0.001. Over-representation analysis of the upregulated genes was dominated by extracellular-structure terms: extracellular matrix organization contained 38 of 176 input genes, collagen fibril organization contained 10 of 42, and extracellular matrix disassembly contained 10 of 44. Leading-edge genes for the enriched pathway included ITGA1, THBS1, COL4A2, COL4A1, and AGRN, all components of the matrix-receptor interface. This is consistent with decades of histopathology showing myofibroblast-rich capsular fibrosis, type-III collagen deposition, and dysregulated matrix metalloproteinases in frozen-shoulder tissue, and with recent single-cell work identifying DKK3-positive and POSTN-positive fibroblast populations alongside inflammatory macrophages in the diseased capsule.

The regulated cell-death results were far more equivocal. The team constructed signature scores from curated gene sets: a nine-gene pyroptosis core including GSDMD, CASP1, NLRP3, IL1B, and IL18; a ferroptosis set including GPX4, SLC7A11, ACSL4, and HMOX1; and a necroptosis set including RIPK1, RIPK3, MLKL, and CASP8. Each score was calculated as the mean of gene-wise z-scores across samples, a summary of relative transcript abundance rather than a direct measurement of gasdermin pore formation, lipid peroxidation, or RIPK3/MLKL-dependent death execution. After adjustment, the pyroptosis score showed no difference between cases and controls, with a delta of -0.105 and a q-value of 0.708. Ferroptosis was lower in adhesive capsulitis but only borderline after correction, with a delta of -0.426 and a q-value of 0.056. Necroptosis was significantly lower, with a delta of -0.320 and a q-value of 0.035, and the core necroptosis gene set was also negatively enriched in the preranked analysis.

Across the three cohorts, the picture grew murkier still. The adjusted and unadjusted point estimates for pyroptosis were -0.10, +0.99, and -0.68 in GSE140731, GSE190023, and GSE238053 respectively, showing clearly different directions across datasets. Ferroptosis and necroptosis point estimates were consistently non-positive rather than directionally conflicting, but the effects were close to zero and imprecise in the small validation cohorts, and formal significance did not replicate. In GSE190023, severity trends across control, mild, and severe adhesive capsulitis for genes such as RIPK3, CASP1, IL1B, and NLRP3 all failed to survive multiplicity correction, with the smallest adjusted value at 0.592. Collectively, the score analyses did not support a claim of uniform regulated cell-death activation in adhesive capsulitis, a conclusion that directly challenges the assumption, common in analogous bioinformatic studies of rheumatoid arthritis and osteoarthritis, that these programs are uniformly switched on in fibroinflammatory joint disease.

Immune marker-gene scoring produced a similar pattern of discovery-cohort promise and validation-cohort failure. Fifteen curated marker panels, assembled from commonly used LM22- and Bindea-derived gene lists, summarized B cells, plasma cells, CD8 and CD4 T cells, regulatory T cells, natural killer cells, monocytes, macrophage-like states, dendritic cells, mast cells, neutrophils, endothelial cells, fibroblasts, and smooth muscle cells. After adjustment, six of the 15 scores met false-discovery significance in the discovery cohort: smooth muscle, endothelial cell, natural killer cell, CD8 T cell, and B cell scores were higher in adhesive capsulitis, while the monocyte score was lower, with the largest positive coefficients at 1.421 for endothelial cells and 1.168 for natural killer cells. But when the same panels were evaluated in the validation cohorts, their directions varied and no panel reached cohort-wise false-discovery significance in either dataset. The authors are careful to note that these scores are marker-gene summaries, not deconvolution-derived cell fractions, and cannot be translated into percentages or absolute numbers of immune or stromal cells.

Cross-cohort concordance statistics quantified the heterogeneity. Gene-wide effects in the adjusted discovery cohort correlated only modestly with GSE238053, with a Spearman rho of 0.383 and 68 genes significant in both cohorts, but were essentially uncorrelated with GSE190023, with a rho of -0.047 and only four shared significant genes. Same-direction proportions across all matched genes were 0.637 for GSE238053 and 0.493 for GSE190023. The near-zero correlation with GSE190023 indicated lack of replication in that small cohort rather than identifying a technical bias or proving either dataset erroneous. Only two regulated cell-death-related genes, PLA2G4A, downregulated, and MAPK12, upregulated, were significant with the same direction in two cohorts. By contrast, MMP9 showed the most stable large positive effect across all three datasets, with log2 fold changes of +8.3, +7.0, and +5.0, while POSTN, SPON2, and PITPNC1 retained generally positive directions.

The team also built an exploratory three-gene classifier from an L1-penalized logistic regression, selecting COL11A1, SPON2, and PITPNC1 as the retained genes. Using pooled out-of-fold predictions, the discovery-cohort area under the curve was 0.820, with a 95 percent confidence interval of 0.684 to 0.930. External-cohort AUCs ranged from 0.750 to 0.812 but carried very wide confidence intervals because of the limited sample sizes, and because the candidate pool was defined before cross-validation, the entire classifier analysis remained non-nested and exploratory. The authors explicitly state that the model provides an exploratory summary of separability in these datasets rather than evidence of clinical utility, and that prospective evaluation in larger, independently recruited populations with prespecified features and fully nested model development would be required before any diagnostic claim could be considered.

A laboratory experiment added a partial, model-specific layer of support. The team stimulated SW982 human synovial sarcoma cells with 10 nanograms per milliliter of recombinant human TGF-beta1 for 24 hours, an operationally defined profibrotic stimulus, and measured four genes by quantitative real-time PCR with GAPDH as the reference. COL11A1 expression rose from a mean relative value of 1.036 in vehicle controls to 1.888 under stimulation, with a P-value of 0.0006. SPON2 rose from 1.016 to 1.518, with a P-value of 0.0040. PLA2G4A fell from 1.013 to 0.700, with a P-value of 0.0065. PITPNC1 showed a smaller numerical increase that was not statistically significant, with a P-value of 0.272. The non-significant PITPNC1 result illustrates that computational feature selection does not guarantee experimental replication, and the authors interpret the qPCR findings as model-specific expression validation rather than proof of regulated cell-death pathway execution, causal relevance to adhesive capsulitis, or clinical validity.

The broader significance of the study lies in its discipline about what the data can and cannot show. Bulk RNA-sequencing cannot resolve whether observed expression differences reflect transcriptional regulation within cells or shifts in cellular composition, and transcript abundance alone should never be read as evidence that a cell-death program has been executed. The discovery comparator was a younger, more male shoulder-instability surgical population rather than a healthy control group, and age and sex adjustment reduces but cannot eliminate confounding. Both validation cohorts were small, limiting statistical power. Future work, the authors argue, should combine independent clinical cohorts with spatial or histologic validation and functional experiments in primary adhesive capsulitis fibroblasts and macrophages using pathway-specific perturbation and rescue assays. Until such evidence is available, the regulated cell-death and immune findings should be regarded as hypothesis-generating associations, while extracellular-matrix remodeling stands as the most reproducible molecular feature of frozen shoulder in the present data, reinforcing an ECM-centered, cohort-aware framework for a condition that affects millions worldwide.

Subject of Research: A three-cohort transcriptomic reanalysis of adhesive capsulitis identifies extracellular-matrix remodeling as the most reproducible molecular feature, while regulated cell-death and immune signatures show cohort-dependent, non-replicating signals.

Article Title: Extracellular matrix remodeling and regulated cell-death-immune associations in adhesive capsulitis: a three-cohort transcriptomic analysis

Article References: Huang, L., Cheng, L., He, J., Zhang, R., Li, X., & Xia, Q. (2026). Extracellular matrix remodeling and regulated cell-death-immune associations in adhesive capsulitis: a three-cohort transcriptomic analysis. Frontiers in Cell and Developmental Biology, 14, Article 1951682. https://doi.org/10.3389/fcell.2026.1951682

Image Credits: AI Generated

DOI: 10.3389/fcell.2026.1951682

Keywords: adhesive capsulitis, frozen shoulder, extracellular matrix, transcriptomics, pyroptosis, ferroptosis, necroptosis, fibrosis, Extracellular, matrix, remodeling, regulated

The research, published in BMC Medical Imaging, was led by Kyu-Chong Lee and Kyung-Sik Ahn of Korea University Anam Hospital in Seoul, together with colleagues from several Korean medical centers. The team set out to answer a deceptively simple question: when a shoulder MRI shows abnormalities of the joint capsule, what do those abnormalities actually mean? Adhesive capsulitis has long been associated with characteristic changes in two specific regions of the shoulder joint, the rotator interval and the axillary pouch. The rotator interval is a triangular space between the supraspinatus and subscapularis tendons through which the long head of the biceps tendon passes, while the axillary pouch is the redundant fold of capsule at the lower part of the joint that allows the arm to lift overhead. In classic frozen shoulder, both regions typically show thickening, edema, and inflammation.

To investigate, the researchers conducted a retrospective analysis of 483 adults who underwent shoulder MRI between January and December 2020. Two musculoskeletal radiologists independently reviewed each scan, assessing abnormalities in the rotator interval and the axillary pouch, as well as tears of four key tendons: the supraspinatus, the infraspinatus, the subscapularis, and the long head of the biceps tendon. The team defined radiologic capsular abnormality, abbreviated RCA, as the presence of abnormalities in both the rotator interval and the axillary pouch simultaneously. They then used univariable and multivariable logistic regression analyses to identify which clinical and imaging factors were associated with RCA, and performed subgroup analyses comparing four patient groups: those with no capsular abnormality, those with isolated axillary pouch abnormality, those with isolated rotator interval abnormality, and those with full RCA, adjusting for age where appropriate.

The headline finding was striking. Of the 483 patients studied, 234, or 48.45 percent, had radiologic capsular abnormality. In other words, nearly one in every two shoulders scanned showed the capsular changes that many radiologists and clinicians associate with frozen shoulder. Yet clinically diagnosed adhesive capsulitis was present in only 45 patients, or 9.32 percent of the cohort. Of those 45 patients, 43 did indeed have RCA, confirming that the imaging finding is sensitive for the disease. But the reverse is emphatically not true: the overwhelming majority of patients with RCA, more than four out of five, did not have a clinical diagnosis of adhesive capsulitis. The imaging finding, in isolation, is simply not specific enough to serve as a diagnosis.

The regression analyses revealed a web of associations that complicate the picture further. Older age was independently associated with higher odds of RCA, with each additional year of age raising the odds by roughly five percent, an odds ratio of 1.05 with a 95 percent confidence interval of 1.03 to 1.07 and a p-value below 0.001. This makes biological sense, since the joint capsule, like every other soft tissue in the body, undergoes degenerative change over time. A capsule that looks thickened or edematous in a 65-year-old may simply reflect the accumulated wear of decades rather than an active inflammatory disorder. Any diagnostic framework that treats capsular abnormality as synonymous with frozen shoulder must therefore account for the age of the patient, or risk labeling normal age-related change as pathology.

Tendon tears added another layer of complexity. Tears of the subscapularis tendon, one of the four muscles that make up the rotator cuff, were positively associated with RCA. Patients with Lafosse type I subscapularis tears, the mildest grade, had 1.82 times the odds of RCA compared with those without such tears, while those with type II or higher tears had 2.15 times the odds, both statistically significant results. The long head of the biceps tendon, which runs directly through the rotator interval, also emerged as relevant: in subgroup analyses, isolated rotator interval abnormality was associated with a higher prevalence of both subscapularis and biceps tendon tears than no capsular abnormality, even after adjusting for age. This suggests that inflammation or degeneration in the rotator interval often reflects pathology of the tendons that traverse it, rather than a primary capsular disease.

Perhaps most intriguingly, tears of the supraspinatus and infraspinatus tendons, the two most commonly torn rotator cuff tendons, showed the opposite relationship: they were negatively associated with RCA. Patients with these tears were less likely to show capsular abnormalities than patients without them. The authors interpret this finding as consistent with the traditional concept of adhesive capsulitis as a diagnosis of exclusion, a condition diagnosed only after other shoulder pathologies have been ruled out. In practical terms, a shoulder dominated by a large supraspinatus or infraspinatus tear appears less likely to harbor the capsular changes of frozen shoulder, perhaps because the two conditions represent distinct biological processes that do not readily coexist, or because the mechanical picture of a cuff tear overshadows and excludes the capsular one.

The clinical implications of the study are considerable. If nearly half of shoulder MRI scans show capsular abnormalities but only about nine percent of patients have frozen shoulder, then any radiology report that flags capsular abnormality without careful qualification invites overdiagnosis. A patient told that their MRI shows findings consistent with adhesive capsulitis may undergo months of stretching programs, corticosteroid injections, or even capsular distension procedures that address the wrong problem, while the true culprit, perhaps a subscapularis tear or biceps tendon pathology, goes untreated. The authors argue that the term radiologic capsular abnormality itself should be used in reports, precisely because it describes an imaging observation without asserting a clinical diagnosis, and that particular caution is warranted in older patients and in those with subscapularis or biceps tendon pathology.

The study does have limitations inherent to its design. It was retrospective, drawing on patients who had already been referred for shoulder MRI at a single Korean institution, which may limit generalizability to other populations. The clinical diagnosis of adhesive capsulitis was extracted from existing records rather than standardized prospectively, and the researchers note that the article was published initially as an early citable version subject to further edits. Still, the size of the cohort, the independent double reading by two musculoskeletal radiologists, the multivariable statistical framework, and the age-adjusted subgroup analyses give the findings substantial weight. The work was supported by a grant from the National Research Foundation of Korea, and the authors declared no competing relationships with companies whose products might relate to the subject matter.

For patients and clinicians alike, the message is ultimately one of humility about what imaging can and cannot tell us. MRI is a magnificent tool for revealing the anatomy of the shoulder in exquisite detail, but anatomy is not destiny, and a thickened capsule on a scan is a finding, not a verdict. Frozen shoulder remains a clinical diagnosis, rooted in a patient’s history of progressive pain and profound restriction of both active and passive motion, and it should be confirmed by examination rather than inferred from a radiology report. As this study makes clear, the capsule that lights up on MRI may be telling a story about age, about a torn subscapularis tendon, or about an inflamed biceps pulley, and only careful clinical correlation can determine which story is true. In an era when imaging findings increasingly drive diagnostic decisions, the humble conclusion that a scan must never replace the physical examination has rarely been more vividly illustrated.

Subject of Research: Radiologic capsular abnormalities on shoulder MRI and their association with rotator cuff and biceps tendon tears in the diagnosis of adhesive capsulitis

Article Title: Radiologic capsular abnormalities on shoulder MRI: associations with rotator cuff and biceps tendon tears and implications for the diagnosis of adhesive capsulitis

Article References: Lee, K.-C., Ahn, K.-S., Kim, S., Kang, C. H., Jeong, W. K., Kang, W. Y., Kim, B. H., & Shim, E. (2026). Radiologic capsular abnormalities on shoulder MRI: associations with rotator cuff and biceps tendon tears and implications for the diagnosis of adhesive capsulitis. BMC Medical Imaging. https://doi.org/10.1186/s12880-026-02895-y

Image Credits: AI Generated

DOI: 10.1186/s12880-026-02895-y

Keywords: shoulder MRI, adhesive capsulitis, frozen shoulder, rotator cuff tear, subscapularis tendon, biceps tendon, rotator interval, axillary pouch, radiologic capsular abnormality, musculoskeletal radiology, overdiagnosis, BMC Medical Imaging