The aim of this review is to provide an updated review of the epigenetic factors involved in the onset and development of osteoarthritis (OA). OA is a prevalent degenerative joint disease characterized by chronic inflammation, ectopic bone formation within the joint, and physical and proteolytic cartilage degradation which result in chronic pain and loss of mobility. At present, no disease-modifying therapeutics exist for the prevention or treatment of the disease. Research has identified several OA risk factors including mechanical stressors, physical activity, obesity, traumatic joint injury, genetic predisposition, and age. Recently, there has been increased interest in identifying epigenetic factors involved in the pathogenesis of OA. In this review, we detail several of these epigenetic modifications with known functions in the onset and progression of the disease. We also review current therapeutics targeting aberrant epigenetic regulation as potential options for preventive or therapeutic treatment.

Purpose: To compare the outcomes of three sequential surgical techniques used over time for posterior spinal fusion (PSF) in adolescent idiopathic scoliosis (AIS) patients with Lenke 1 & 2 curves. Methods: Three sequential cohorts of Lenke 1 & 2 AIS patients who underwent PSF between 2008 and 2021 were retrospectively identified. Surgical technique, including concave rod derotation (T1), concave en bloc reduction (T2), or convex-first differential rod contouring technique (T3), was recorded. Preoperative, intraoperative, and minimum 2-year postoperative variables were compared. Results: Ninety-three Lenke 1 & 2 AIS patients were evaluated: 30 T1, 25 T2, and 38 T3. No significant differences were noted in demographics or preoperative radiographic measurements. The T3 group utilized higher implant density and more posterior column osteotomies (PCOs). Postoperatively, there was equivalent coronal correction index in all three cohorts. T3 resulted in significantly improved sagittal plane parameters, including final T5-T12 kyphosis (16.8° vs. 13.3° vs. 20.8° p = 0.011), final T2-T12 kyphosis (19.9° vs. 18.8°, 27.0° p = 0.033), delta T2-T12 kyphosis (-1.0° vs. -6.7° vs.1.5° p = 0.005), and delta 3D kyphosis (14.1° vs. 10.5° vs. 15.8° p = 0.034). Significant covariates of postoperative T5-T12 kyphosis included preoperative 3D kyphosis ( p = < 0.001) and number of PCOs ( p = 0.002). There were no differences in complications, readmissions, or unplanned reoperations. Conclusion: Practice evolution using a recent technique, specifically the convex-first differential rod reduction technique (T3), results in superior restoration of thoracic kyphosis compared to older concave rod derotation (T1) or concave en bloc reduction (T2) techniques for Lenke 1 & 2 AIS patients.

Case: Tetanus is a potentially life-threatening infection of Clostridium tetani characterized by painful muscular spasms and hypertonia. Surgical debridement of infected tissue is intended to reduce the number of spores and limit the extent of the disease. We report a case of an unvaccinated 13-year-old adolescent boy who presented with systemic tetanus after stepping on a nail, and we describe the role that surgical debridement of infected tissue plays in optimizing outcomes. Conclusion: Orthopaedic surgeons must remain aware of the role of surgical debridement of wounds potentially infected with C. tetani because it is an important component of proper management.

Background: Pediatric patients with open forearm fractures who undergo operative irrigation and debridement (I&D) are often treated with implant fixation due to concern for delayed healing, nonunion, or loss of alignment. For an open forearm fracture treated with I&D, it is unknown whether reduction and casting alone without implant fixation affects outcomes in young patients. We aim to compare the results of pediatric open forearm fractures treated with I&D and cast immobilization with no implant fixation (NIF) to those treated with implant fixation (IF). Methods: We retrospectively reviewed pediatric patients treated surgically for an open forearm fracture with IF or with casting and NIF from 2010 to 2020. The use of implant fixation was at the discretion of the surgeon. Results: Seventy-seven patients were included (IF 54, NIF 23) without differences between cohorts in sex, fracture type, fracture location, or open grade of fracture. NIF patients were younger (8.2 vs. 10.7 y, P =0.001), as NIF was utilized in 78.3% of patients 10 years or younger. IF was associated with 36 minute longer operative time (77 vs. 41 min, P <0.001), longer length of stay (1.9 vs. 1.6 d, P =0.042), a greater number of radiographic sessions (5.9 vs. 5.1, P =0.038), more follow-up visits (7.1 vs. 5.2, P =0.003), longer time to radiographic healing (110.6 vs. 64.2 d, P =0.003) and longer follow-up (225.8 vs. 80.9 d, P <0.001), as 53.7% underwent elective surgical implant removal. Duration of immobilization was similar (IF 48.9 vs. NIF 55.7 d, P =0.124). There was no difference in incidence of unplanned reintervention (IF 7.4% vs. NIF 4.3%, P =0.999), with 2 deep infections, and 2 refractures requiring reoperation in the IF group and 1 closed reduction and casting in the OR for the NIF group. All fractures were united in satisfactory alignment at final follow-up. Conclusions: Implant fixation may not be necessary for all open forearm fractures, especially in patients 10 years or younger with remodeling potential. This would contribute to shorter operative time, length of stay, fewer follow-up visits, and avoidance of surgical implant removal, all of which would contribute to lower cost of treatment. Level of Evidence: Level III—retrospective cohort study.

Osteoactivin (GPNMB) is a transmembrane protein expressed in multiple cell types with known functions in muscle, bone, and neurons, but the role of GPNMB in chondrocytes and cartilage homeostasis remains unknown. Here we show GPNMB is expressed in human and mouse primary chondrocytes, and that its expression is increased in damaged human cartilage and under pro-inflammatory conditions. We report that recombinant GPNMB treatment inhibits the expression of Mmps (Mmp3, 9, and 13), Adamts-4 and Il-6 following IL-1β-stimulation in vitro. In vivo, GPNMB function was assessed in a post-traumatic osteoarthritis model, destabilization of the medial meniscus (DMM). Transgenic animals lacking functional GPNMB protein (DBA/2J) developed severe cartilage damage and demonstrated significant increases in pro-inflammatory cytokine expression following DMM. To elucidate the mechanism of action, we demonstrate that GPNMB regulates the MAPK signaling pathway via pERK inhibition in primary murine chondrocytes. Taken together, our results identify a novel anti-inflammatory role for GPNMB in cartilage and chondrocytes and identify GPNMB as a potential therapeutic modality for inflammatory joint diseases.