Anterior disc displacement without reduction can cause acute functional limitations and may coexist with inflammatory and early degenerative changes in young patients. We report a 22-year-old woman with right preauricular pain, a closed lock, and a maximum unassisted interincisal opening of 19 mm. Cone-beam computed tomography and magnetic resonance imaging confirmed Stage II osteoarthritis of the right temporomandibular joint, right anterior disc displacement without reduction with limited opening, left anterior disc displacement with reduction, and bilateral joint effusion consistent with synovitis. Hormonal testing showed values discordant with the expected follicular-phase ranges after recent discontinuation of injectable contraception; this finding was interpreted as a potential modulatory factor rather than evidence of causation. Management included bilateral temporomandibular joint arthrocentesis, intra-articular administration of betamethasone and sodium hyaluronate, a stabilization splint, pharmacological therapy, physical therapy, and behavioral modification. Pain decreased markedly within the first week. At the 3-month follow-up, maximum unassisted mouth opening was 42 mm, with a straight opening path, pain-free function, and resolution of the right masseter spasm. This case highlights the value of early imaging-based diagnosis and individualized multimodal management in young patients with concomitant mechanical, inflammatory, and early degenerative temporomandibular joint changes.

ObjectiveEnhanced glycolysis is a metabolic hallmark of chondrocytes in osteoarthritis (OA); however, the roles of the glycolytic rate-limiting enzyme hexokinase 2 (HK2) in cartilage remain poorly understood.MethodsMice and cell models involving HK2 knockout in Col2a1-expressing chondrocytes and 3-bromopyruvate (3-BrPA) treatment are utilized to assess the potential impact of HK2 blockage on cartilage ex vivo and in vivo. Additionally, we analyzed published single-cell RNA sequencing (scRNA-seq) datasets from human articular cartilage and integrated these with bulk RNA-seq data from HK2-deficient chondrocytes to characterize HK2 expression features across conditions. The in vivo effects of HK2 inhibition on OA progression were evaluated using a destabilization of the medial meniscus (DMM)-induced model, through both chondrocyte HK2 deletion and 3-BrPA administration.ResultsBoth pharmacological inhibition and genetic deletion of HK2 impair chondrocyte differentiation ex vivo and suggest a promoted calcification-like process. Through pseudotime analysis of published single-cell RNA sequencing (scRNA-seq) datasets from human articular cartilages, we further identified that HK2 is differentially expressed across conditions, with a feature of a relatively high expression level at terminal stages of chondrocyte differentiation in the context of OA. We next confirmed HK2 deficiency in chondrocytes significantly exacerbated OA progression but having no impact on skeletal development in mice.ConclusionsOur findings reveal a novel, critical role for HK2 in regulating chondrocyte differentiation both ex vivo and in vivo, likely by preserving cartilage function under stress. Consequently, targeting HK2 as a therapeutic strategy for OA requires careful consideration of potential risks.

Bone marrow lesions (BMLs) of the knee are a common magnetic resonance imaging finding, defined as an alteration of the bone marrow detectable as a high signal on fluid-sensitive sequences. A wide range of pathologies can present with BMLs, including traumatic lesions, osteoarthritis, subchondral insufficiency fractures and osteonecrosis. Several treatment options have been proposed to address BML, from conservative to surgical approaches. If nonoperative treatments fail, operative treatments are indicated. These procedures include intraosseous injections, unloading procedures and meniscus implants. In detail, intraosseous injections may be performed with biomaterials like calcium phosphate, or with orthobiologics like platelet-rich plasma or mesenchymal stromal cells. Aim of these interventions is either to stabilise the microtrabecular tissue or to promote a healing response. Good results have been reported in the literature for many of the available surgical options, but the level of evidence is still suboptimal, and the best approach has not yet been identified. Level of Evidence: Level V, expert opinion.