Aims

This study aimed to define the histopathology of degenerated humeral head cartilage and synovial inflammation of the glenohumeral joint in patients with omarthrosis (OmA) and cuff tear arthropathy (CTA). Additionally, the potential of immunohistochemical tissue biomarkers in reflecting the degeneration status of humeral head cartilage was evaluated.

Aims. Rotator cuff tear (RCT) is the leading cause of shoulder pain, primarily associated with age-related tendon degeneration. This study aimed to elucidate the potential differential gene expressions in tendons across different age groups, and to investigate their roles in tendon degeneration. Methods. Linear regression and differential expression (DE) analyses were performed on two transcriptome profiling datasets of torn supraspinatus tendons to identify age-related genes. Subsequent functional analyses were conducted on these candidate genes to explore their potential roles in tendon ageing. Additionally, a secondary DE analysis was performed on candidate genes by comparing their expressions between lesioned and normal tendons to explore their correlations with RCTs. Results. We identified 49 genes in torn supraspinatus tendons associated with advancing age. Among them, five age-related genes showed DE in lesioned tendons compared to normal tendons. Functional analyses and previous studies have highlighted their specific enrichments in biological functions, such as muscle development (e.g. myosin heavy chain 3 (MYH3)), transcription regulation (e.g. CCAAT enhancer binding brotein delta (CEBPD)), and metal ion homeostasis (e.g. metallothionein 1X (MT1X)). Conclusion. This study uncovered molecular aspects of tendon ageing and their potential links to RCT development, offering insights for targeted interventions. These findings enhance our understanding of the mechanisms of tendon degeneration, allowing potential strategies to be made for reducing the incidence of RCT. Cite this article: Bone Joint Res 2024;13(9):474–484

Aims

Rotator cuff (RC) injuries are characterized by tendon rupture, muscle atrophy, retraction, and fatty infiltration, which increase injury severity and jeopardize adequate tendon repair. Epigenetic drugs, such as histone deacetylase inhibitors (HDACis), possess the capacity to redefine the molecular signature of cells, and they may have the potential to inhibit the transformation of the fibro-adipogenic progenitors (FAPs) within the skeletal muscle into adipocyte-like cells, concurrently enhancing the myogenic potential of the satellite cells.

The sternoclavicular joint (SCJ) is a pivotal articulation in the linked system of the upper limb girdle, providing load-bearing in compression while resisting displacement in tension or distraction at the manubrium sterni. The SCJ and acromioclavicular joint (ACJ) both have a small surface area of contact protected by an intra-articular fibrocartilaginous disc and are supported by strong extrinsic and intrinsic capsular ligaments. The function of load-sharing in the upper limb by bulky periscapular and thoracobrachial muscles is extremely important to the longevity of both joints. Ligamentous and capsular laxity changes with age, exposing both joints to greater strain, which may explain the rising incidence of arthritis in both with age. The incidence of arthritis in the SCJ is less than that in the ACJ, suggesting that the extrinsic ligaments of the SCJ provide greater stability than the coracoclavicular ligaments of the ACJ.

Instability of the SCJ is rare and can be difficult to distinguish from medial clavicular physeal or metaphyseal fracture-separation: cross-sectional imaging is often required. The distinction is important because the treatment options and outcomes of treatment are dissimilar, whereas the treatment and outcomes of ACJ separation and fracture of the lateral clavicle can be similar. Proper recognition and treatment of traumatic instability is vital as these injuries may be life-threatening. Instability of the SCJ does not always require surgical intervention. An accurate diagnosis is required before surgery can be considered, and we recommend the use of the Stanmore instability triangle. Most poor outcomes result from a failure to recognise the underlying pathology.

There is a natural reluctance for orthopaedic surgeons to operate in this area owing to unfamiliarity with, and the close proximity of, the related vascular structures, but the interposed sternohyoid and sternothyroid muscles are rarely injured and provide a clear boundary to the medial retroclavicular space, as well as an anatomical barrier to unsafe intervention.

This review presents current concepts of instability of the SCJ, describes the relevant surgical anatomy, provides a framework for diagnosis and management, including physiotherapy, and discusses the technical challenges of operative intervention.

Cite this article: Bone Joint J 2013;95-B:721–31.

Frozen shoulder is commonly encountered in general orthopaedic practice. It may arise spontaneously without an obvious predisposing cause, or be associated with a variety of local or systemic disorders. Diagnosis is based upon the recognition of the characteristic features of the pain, and selective limitation of passive external rotation. The macroscopic and histological features of the capsular contracture are well-defined, but the underlying pathological processes remain poorly understood. It may cause protracted disability, and imposes a considerable burden on health service resources. Most patients are still managed by physiotherapy in primary care, and only the more refractory cases are referred for specialist intervention. Targeted therapy is not possible and treatment remains predominantly symptomatic. However, over the last ten years, more active interventions that may shorten the clinical course, such as capsular distension arthrography and arthroscopic capsular release, have become more popular.

This review describes the clinical and pathological features of frozen shoulder. We also outline the current treatment options, review the published results and present our own treatment algorithm.

We describe a technique of soft-tissue reconstruction which is effective for the treatment of chronic lunotriquetral instability. Part of extensor carpi ulnaris is harvested with its distal attachment preserved. It is passed through two drill holes in the triquetrum and sutured to itself. This stabilises the ulnar side of the wrist.

We have reviewed 46 patients who underwent this procedure for post-traumatic lunotriquetral instability with clinical signs suggestive of ulnar-sided carpal instability. Standard radiographs were normal. All patients had pre-operative arthroscopy of the wrist at which dynamic lunotriquetral instability was demonstrated. A clinical rating system for the wrist by the Mayo clinic was used to measure the outcome. In 19 patients the result was excellent, in ten good, in 11 satisfactory and in six poor. On questioning, 40 (87%) patients said that surgery had substantially improved the condition and that they would recommend the operation. However, six (13%) were unhappy with the outcome and would not undergo the procedure again for a similar problem. There were six complications, five of which related to pisotriquetral problems. The mean follow-up was 39.1 months (6 to 100). We believe that tenodesis of extensor carpi ulnaris is a very satisfactory procedure for isolated, chronic post-traumatic lunotriquetral instability in selected patients. In those with associated pathology, the symptoms were improved, but the results were less predictable.