Hemarthrosis

BackgroundHaemarthrosis and pain adversely affects the functional outcome of ACL reconstruction, especially in case of DB ACL reconstruction due to more extensive procedure. The purpose of the study was to evaluate the effect of haemarthrosis on the rehabilitation of DB ACL reconstruction versus SB ACL reconstruction.Methods100 patients were divided into two groups, of SB ACL and DB ACL reconstruction consisting of 50 patients each. An intra-articular drain was put in every patient. The pain was evaluated till week 8 using VAS (Visual Analog Scale). The Functional outcomes were evaluated using the Isokinetic Dynamometer at 3 and 6 months in both the groups. Muscle bulk and Range of motion were also noted in each group.ResultsThe results showed that there was statistically significant difference between the drain amount (n=60.3 ml in SB ACL group vs. n=94.2 ml in the DB ACL group) and haemarthrosis (n=0.7 in SB ACL vs n=1.5 in DB ACL) at week 1 post-operatively. Also the pain outcome improved on SB ACL after day 3 (VAS, n=1.8) as compared to the DB ACL group (VAS, n=3.7). The isokinetic muscle strength was found to be statistically significantly (p valueConclusionWe noted that rehabilitation of DB ACL reconstruction group lags behind that of SB ACL reconstruction during the first 3 months due to post-operative haemarthrosis & its effects, but show comparable results after 6 months. The muscle strength measured isokinetically and the muscle bulk were found to be greater in the SB ACL group initially after 3 months but was found to be similar after 6 months.

Permanent joint dysfunction is a devastating complication in patients with septic arthritis. Staphylococcus aureus (S. aureus) lipoproteins (Lpp), the predominant ligands for TLR2, are known to be arthritogenic and induce bone destruction when introduced directly into the joint. Here, we aim to investigate the importance of S. aureus Lpp and TLR2 in a hematogenous septic arthritis model, which is the most common route of infection in humans. C57BL/6 wild-type and TLR2 deficient mice were intravenously inoculated with S. aureus Newman parental strain or its lipoprotein-deficient Δlgt mutant strain. The clinical course of septic arthritis, radiological changes, and serum levels of cytokines and chemokines, were assessed. Newman strain induced more severe and frequent clinical septic polyarthritis compared to its Δlgt mutant in TLR2 deficient mice, but not in wild-type controls. Bone destruction, however, did not differ between groups. Lpp expression was associated with higher mortality, weight loss as well as impaired bacterial clearance in mouse kidneys independent of TLR2. Furthermore, Lpp expression induced increased systemic pro-inflammatory cytokine and neutrophil chemokine release. Staphylococcal Lpp are potent virulence factors in S. aureus systemic infection independent of host TLR2 signalling. However, they have a limited impact on bone erosion in hematogenous staphylococcal septic arthritis.

Bleeding with resultant hemophilic arthropathy constitutes the largest cause of morbidity in patients with hemophilia. It results from repeated bleeding episodes in the joint and is characterized by synovial hypertrophy and cartilage and bony destruction. Hemophilic arthropathy assessment is a continually evolving process and is particularly challenging in children and young adults in whom joint disease may be missed or underestimated as obtaining serial "baseline" magnetic resonance imaging scans of multiple clinically asymptomatic or nearly asymptomatic joints may be unjustifiable and cost-ineffective. Musculoskeletal ultrasound-particularly, point-of-care musculoskeletal ultrasound-has emerged as a promising imaging modality for the early detection and management of hemophilic arthropathy, and for the evaluation of hemarthrosis and painful musculoskeletal episodes in patients with hemophilia. This review summarizes currently available data on the emerging role of this new imaging modality, its limitations, and gaps in knowledge. The review also raises unanswered questions, highlights the need for consolidated research efforts, and delineates future directions expected to advance this technology and optimize its use in this patient population.

Background and Objectives: Osteoarthritis (OA) is the most common degenerative joint disease and a leading cause of pain and disability worldwide. Increasing evidence indicates that dysregulated iron metabolism contributes to joint degeneration by promoting inflammation, oxidative stress, and cartilage damage. Hemophilic arthropathy (HA), a severe complication of hemophilia caused by recurrent hemarthroses, represents a unique model of iron-driven joint degeneration. This narrative review summarizes current evidence on the contribution of iron deposition to the pathogenesis of hemophilic arthropathy and discusses its relevance to knee osteoarthritis (KOA). Materials and Methods: The literature was reviewed using the PubMed, Scopus, and Web of Science databases, focusing on published studies addressing iron deposition, synovial inflammation, angiogenesis, oxidative stress, cartilage degeneration, subchondral bone remodeling, and dysregulated iron metabolism. Results: Current evidence indicates that iron stored primarily as hemosiderin promotes persistent synovial inflammation and progressive joint destruction. Several pathological pathways associated with iron accumulation, including chronic low-grade inflammation, extracellular matrix degradation, and altered bone remodeling, are shared by HA and KOA. Conclusions: These findings suggest that iron-mediated mechanisms may provide important insights into OA pathogenesis and support further investigation of iron as a potential diagnostic and therapeutic target in degenerative joint diseases.