Is Obesity a Risk Factor for Adverse Events After Knee Arthroscopy?

PURPOSE: To evaluate how body mass index (BMI) affects rates of 30-day complication, hospital readmissions, and mortality in patients undergoing knee arthroscopy. METHODS: Patients undergoing knee arthroscopy procedures between 2006 and 2013 were identified in the American College of Surgeons National Surgical Quality Improvement Program database. Patient demographics and preoperative risk factors including BMI were analyzed for postoperative complications within 30 days. Cochran-Armitage testing was performed to detect differences in complication rates across BMI categories according to World Health Organization classification. The independent risk of BMI was assessed using multivariate regression analysis. RESULTS: Of 41,919 patients with mean age 48 years undergoing knee arthroscopy, 20% were classified as normal weight (BMI 18.5 to 24), 35% overweight (BMI 25 to 29), 24% obese class I (BMI 30 to 34), 12% class II (BMI 35 to 40), and 9% class III (BMI ≥40). Risk of complication increased significantly with increasing BMI (normal: 1.5%, overweight: 1.6%, obese class I: 1.7%, obese class II: 1.8%, obese class III: 1.9%, P = .043). On multivariate analysis, there was no increased risk of postoperative complication directly attributed to patient BMI. Independent risk factors for medical and surgical complications after knee arthroscopy included American Society of Anesthesiologists (ASA) rating (class 4 v class 1 odds ratio [OR]: 5.39 [95% confidence interval: 3.11-9.33], P < .001), functional status for activities of daily living (dependent v independent OR: 2.13 [1.42, 3.31], P < .001), history of renal comorbidity (presence v absence OR: 5.10 [2.30, 11.29], P < .001), and previously experienced history of wound infection prior to current surgery (presence v absence OR: 4.91 [2.88, 8.39], P < .001). CONCLUSIONS: More than 40% of knee arthroscopy patients qualify as obese. Although univariate analysis suggests that obesity is associated with increased postoperative complications within 30 days of surgery, BMI alone does not predict complications. Independent predictors of complications include patients with high ASA classification, dependent functional status, renal comorbidities, and a recent history of wound infection. LEVEL OF EVIDENCE: Level IV, prognostic case series.

Promoting Endochondral Bone Repair Using Human Osteoarthritic Articular Chondrocytes.

INTRODUCTION: Current tissue engineering strategies to heal critical-size bone defects through direct bone formation are limited by incomplete integration of grafts with host bone and incomplete graft vascularization. An alternative strategy for bone regeneration is the use of cartilage grafts that form bone through endochondral ossification. Endochondral cartilages stimulate angiogenesis and are remodeled into bone, but are found in very small quantities in growth plates and healing fractures. We sought to develop engineered endochondral cartilage grafts using osteoarthritic (OA) articular chondrocytes as a cell source. Such chondrocytes often undergo hypertrophy, which is a characteristic of endochondral cartilages. MATERIALS AND METHODS: We compared the ability of unmodified human OA (hOA) cartilage and cartilage grafts formed in vitro from hOA chondrocytes to undergo endochondral ossification in mice. Scaffold-free engineered chondrocyte grafts were generated by pelleting chondrocytes, followed by culture with transforming growth factor-ß1 (TGF-ß1) and bone morphogenetic protein 4. Samples derived from either primary or passaged chondrocytes were implanted subcutaneously into immunocompromised mice. Grafts derived from passaged chondrocytes from three patients were implanted into critical-size tibial defects in mice. Bone formation was assessed with histology after 4 weeks of implantation. The composition of tibial repair tissue was quantified with histomorphometry. RESULTS: Engineered cartilage grafts generated from passaged OA chondrocytes underwent endochondral ossification after implantation either subcutaneously or in bone. Cartilage grafts integrated with host bone at 15 out of 16 junctions. Grafts variably remodeled into woven bone, with the proportion of bony repair tissue in tibial defects ranging from 22% to 85% (average 48%). Bony repair tissue bridged the tibial defects in half of the animals. In contrast, unmodified OA cartilage and engineered grafts formed from primary chondrocytes did not undergo endochondral ossification in vivo. CONCLUSIONS: hOA chondrocytes can adopt an endochondral phenotype after passaging and TGF-ß superfamily treatment. Engineered endochondral cartilage grafts can integrate with host bone, undergo ossification, and heal critical-size long-bone defects in a mouse model. However, additional methods to further enhance ossification of these grafts are required before the clinical translation of this approach.