Nedim Mujanovic

Objective: To compare patient-reported outcomes and reintervention rates after open vs arthroscopic fusion of the ankle (TT—tibiotalar) or subtalar (ST) joint over a 10-year period in a cohort of patients from a single center. Methods: In total, 129 patients (142 joints) underwent surgery for isolated TT or ST osteoarthritis between 2010 and 2020: 40 TT fusions (11 arthroscopic, 29 open) and 102 ST fusions (25 arthroscopic, 77 open). The course of treatment was followed clinically using patient-reported outcome measures (PROMs) for ankle function: Foot and Ankle Outcome Score—FAOS, general quality of life (European Quality of Life in Five Dimensions 3-level time-trade-off—EQ-5D 3L-TTO) and activity level (Tegner Activity Scale—TAS), and by tracking revision procedures. Results: The median follow-up time was 8 (3–13) years. The mean age at the time of surgery was 52 (14) years. Most subjective scores showed significant improvement; cumulative FAOS improved from 41 to 57 in the TT group and from 41 to 67 in the ST group and EQ-5D from 0.40 to 0.55 (TT group) and from 0.38 to 0.60 (ST group), while TAS remained at 2. The ST fusion patients had better subjective outcomes than TT fusion patients. There were no significant differences in PROMs between arthroscopic and open procedures. Older age and preoperative FAOS pain were found to be negative predictors for the postoperative FAOS subscales. Overall, there was an 18% revision rate: 17 non-unions and 8 infections. In addition, 20 hardware removals were performed. Conclusion: Isolated TT or ST fusions performed open or arthroscopically were safe and significantly improved function and quality of life and reduced joint-related pain but did not increase patients’ activity levels. Patients with ST fusion had a better subjective outcome. Older age and lower preoperative FAOS pain were associated with a worse postoperative subjective outcome. Level of Evidence: Level III

A genetically diverse condition called osteogenesis imperfecta (OI) is characterized by low bone mass and fragility. Over the past few decades, OI has evolved from an illness lacking a known etiology to one with a well-defined and well-mapped genetic background. Pathogenic mutations in COL1A1/COL1A2 with autosomal-dominant inheritance are linked to most cases of OI. The pathophysiology of OI is now well understood thanks to recent gene discoveries, which has opened up new opportunities for treatment development. The main characteristics of OI patient include short stature, bone abnormalities, and repeated fractures. Joint hypermobility, dentinogenesis imperfecta, blue sclera, hearing loss, and, less frequently, muscle weakness, pulmonary, and cardiovascular problems are examples of extraskeletal symptoms. In addition to pharmaceutical therapy, OI requires interdisciplinary care from orthopedic management, rehabilitation, nutrition, dentistry, and other subspecialties. Although the current pharmacologic therapy for OI does not address the matrix defect that is the main cause of bone fragility, it may enhance bone mass and morphology. To develop treatments that will target the genetic flaw and mechanism causing OI, research is still being done.