Aims

Arthroplasty is being increasingly used for the management of distal humeral fractures (DHFs) in elderly patients. Arthroplasty options include total elbow arthroplasty (TEA) and hemiarthroplasty (HA); both have unique complications and there is not yet a consensus on which implant is superior. This systematic review asked: in patients aged over 65 years with unreconstructable DHFs, what differences are there in outcomes, as measured by patient-reported outcome measures (PROMs), range of motion (ROM), and complications, between distal humeral HA and TEA?

Deep gluteal syndrome is an increasingly recognized disease entity, caused by compression of the sciatic or pudendal nerve due to non-discogenic pelvic lesions. It includes the piriformis syndrome, the gemelli-obturator internus syndrome, the ischiofemoral impingement syndrome, and the proximal hamstring syndrome. The concept of the deep gluteal syndrome extends our understanding of posterior hip pain due to nerve entrapment beyond the traditional model of the piriformis syndrome. Nevertheless, there has been terminological confusion and the deep gluteal syndrome has often been undiagnosed or mistaken for other conditions. Careful history-taking, a physical examination including provocation tests, an electrodiagnostic study, and imaging are necessary for an accurate diagnosis.

After excluding spinal lesions, MRI scans of the pelvis are helpful in diagnosing deep gluteal syndrome and identifying pathological conditions entrapping the nerves. It can be conservatively treated with multidisciplinary treatment including rest, the avoidance of provoking activities, medication, injections, and physiotherapy.

Endoscopic or open surgical decompression is recommended in patients with persistent or recurrent symptoms after conservative treatment or in those who may have masses compressing the sciatic nerve.

Many physicians remain unfamiliar with this syndrome and there is a lack of relevant literature. This comprehensive review aims to provide the latest information about the epidemiology, aetiology, pathology, clinical features, diagnosis, and treatment.

Cite this article: Bone Joint J 2020;102-B(5):556–567.

Objectives. Emerging evidence indicates that tendon disease is an active process with inflammation that is critical to disease onset and progression. However, the key cytokines responsible for driving and sustaining inflammation have not been identified. Methods. We performed a systematic review of the literature using MEDLINE (U.S. National Library of Medicine, Bethesda, Maryland) in March 2017. Studies reporting the expression of interleukins (ILs), tumour necrosis factor alpha (TNF-α) and interferon gamma in diseased human tendon tissues, and animal models of tendon injury or exercise in comparison with healthy control tissues were included. Results. IL-1β, IL-6, IL-10, and TNF-α are the cytokines that have been most frequently investigated. In clinical samples of tendinopathy and tendon tears, the expression of TNF-α tended not to change but IL-6 increased in tears. Healthy human tendons showed increased IL-6 expression after exercise; however, IL-10 remained unchanged. Animal tendon injury models showed that IL-1β, IL-6, and TNF-α tend to increase from the early phase of tendon healing. In animal exercise studies, IL-1β expression showed a tendency to increase at the early stage after exercise, but IL-10 expression remained unchanged with exercise. Conclusions. This review highlights the roles of IL-1β, IL-6, IL-10, and TNF-α in the development of tendon disease, during tendon healing, and in response to exercise. However, there is evidence accumulating that suggests that other cytokines are also contributing to tendon inflammatory processes. Further work with hypothesis-free methods is warranted in order to identify the key cytokines, with subsequent mechanistic and interaction studies to elucidate their roles in tendon disease development. Cite this article: W. Morita, S. G. Dakin, S. J. B. Snelling, A. J. Carr. Cytokines in tendon disease: A Systematic Review. Bone Joint Res 2017;6:656–664. DOI: 10.1302/2046-3758.612.BJR-2017-0112.R1