Knee osteoarthritis (OA) is one of the most prevalent chronic conditions affecting the adult population. OA is no longer thought to come from a purely biomechanical origin but rather one that has been increasingly recognized to include a persistent low-grade inflammatory component. Intra-articular corticosteroid injections (IACSI) have become a widely used method for treating pain in patients with OA as an effective symptomatic treatment. However, as the disease progresses, IACSI become ineffective. FKBP51 is a regulatory protein of the glucocorticoid receptor function and have been shown to be dysregulated in several pathological scenario’s including chronic inflammation. Despite of these facts, to our knowledge, there are no previous studies of the expression and possible role of FKBP51 in OA. We investigated by double and triple immunofluorescence confocal microscopy the cellular and subcellular expression of FKBP51 and its relations with inflammation factors in osteoarthritic knee joint tissues: specifically, in the tibial plateau knee cartilage, Hoffa’s fat pad and suprapatellar synovial tissue of the knee. Our results show co-expression of FKBP51 with TNF-α, IL-6, CD31 and CD34 in OA chondrocytes, synovial membrane cells and adipocytes in Hoffa’s fat pad. FKBP51 is also abundant in nerve fibers within the fat pad. Co-expression of FKBP51 protein with these markers may be indicative of its contribution to inflammatory processes and associated chronic pain in OA.

Throughout history, there has been a fear of open tibial fractures due to the high incidence of infection potentially leading to amputation and death. Before the development of standardized surgical wound treatment and antisepsis, amputations were frequently required to prevent spread of sepsis and risk of death. Even today, this remains a challenging condition to treat. In recent years efforts have been made to develop new techniques and to promote new evidence based guidelines for the management of these injuries. The cooperation between orthopaedic and plastic surgeons together with the use of modern surgical instruments and techniques and modern wound management has resulted in a dramatic reduction in infection rates in many parts of the developed and developing world.

Throughout history, there has been a fear of open tibial fractures due to the high incidence of infection potentially leading to amputation and death. Before the development of standardized surgical wound treatment and antisepsis, amputations were frequently required to prevent spread of sepsis and risk of death. Even today, this remains a challenging condition to treat. In recent years efforts have been made to develop new techniques and to promote new evidence based guidelines for the management of these injuries. The cooperation between orthopaedic and plastic surgeons together with the use of modern surgical instruments and techniques and modern wound management has resulted in a dramatic reduction in infection rates in many parts of the developed and developing world.

A fixed-bearing medial unicompartmental knee arthroplasty (UKA) is a well-established option for the treatment of unicompartmental knee osteoarthritis. Several cohorts, meta-analyses and joint registry studies have shown comparable results to mobile-bearing medial UKA. What is less clear is whether the fixed-bearing all-polyethylene tibia implants provide comparable results to metal-backed versions. It has been suggested that fixed-bearing all-polyethylene tibia UKAs may show early failure due to the loosening of the all-polyethylene tibial component. A historical and narrative review was performed to answer the question: are all-polyethylene tibia implants safe to use and are the postoperative outcomes as good as when using a fixed-bearing metal-back implant? After a thorough review of the all-polyethylene and metal-back UKA philosophy, including the most recent scientific evidence available, we can conclude that all-polyethylene tibia UKA implants achieve similar results to metal back-implants both in terms of survival rates and patient-reported outcomes (PROMS). Both versions, all-polyethylene and metal-back tibia implants are valid treatment options when dealing with a patient presenting with unicompartmental knee osteoarthritis, and the final decision between using one over the other will rely on the surgeon's experience and preference.

Background: Knee osteoarthritis (OA) is traditionally framed as a mechanical “wear-and-tear” disorder. Contemporary evidence supports OA as a whole-joint, immunometabolic and neurosensory disease in which low-grade inflammation modulates tissue homeostasis and pain. In midlife women, the menopause transition coincides with abrupt endocrine changes that plausibly amplify inflammatory tone, alter neuromuscular function, and increase pain sensitisation—often with symptoms disproportionate to imaging. Objective: To synthesise the biological rationale and clinical evidence linking menopausal hormonal decline with OA-relevant inflammatory and neuromuscular mechanisms, and to propose a collaborative orthopaedic model integrating menopause health expertise. Methods: Narrative synthesis of mechanistic, epidemiologic, and clinical trial data on OA inflammation, menopause-related musculoskeletal symptoms, and hormone therapy effects on pain/function and musculoskeletal resilience. Evidence is interpreted with attention to outcome type (symptoms vs structural progression), confounding in observational studies, and timing/continuity considerations. Key Findings: (1) OA pain and disability correlate imperfectly with radiographic severity, consistent with synovitis, adipose-derived mediators, subchondral remodelling, and peripheral/central sensitisation. (2) Perimenopause is associated with increased prevalence of musculoskeletal pain, suggesting a biological inflection period rather than linear age-related decline. (3) Oestrogen decline plausibly shifts immune signalling toward pro-inflammatory pathways (e.g., IL-6/TNF-α/NF-κB), while progesterone and androgen changes may influence sleep quality, recovery capacity, muscle strength, and neuromuscular control—factors strongly linked to knee OA outcomes. (4) Menopausal hormone therapy (when appropriately indicated and supervised) may reduce joint pain in some women and may improve musculoskeletal resilience; however, evidence for disease-modifying structural effects on OA remains limited and confounded. Clinical Implications: Orthopaedic care for midlife women with knee OA should include endocrine-aware phenotyping, screening for menopause-transition symptom clusters, and structured referral pathways to women’s hormonal health specialists. Optimising the systemic biological environment may enhance the durability of rehabilitation, regenerative strategies, and surgical outcomes. Conclusion: Menopause transition biology is a clinically relevant modifier of OA symptom expression and functional decline. Integrating hormonal health expertise into orthopaedic pathways is not scope expansion—it is precision care aligned with modern OA biology.