Background: The etiologic factors, time of development, and extent of the progression of postoperative osteoarthritis (OA) in traumatic shoulder instability remain controversial.
Hypothesis: Most OA seen postoperatively occurs before surgery and progresses very slowly.
Study design: Cohort study; Level of evidence, 3.
Methods: Review of 167 joints of 163 patients undergoing the open Bankart procedure, who had no history of shoulder surgery and were younger than 45 years at follow-up, was done at a mean follow-up of 8.7 years (range, 5-20 years). The shoulders were directly examined and radiographed. A statistical analysis was performed to examine the correlation between OA development/progression and patients' demographic characteristics and various factors, and to evaluate the correlation between these factors.
Results: Recurrence of instability occurred in 8 of 167 joints (4.8%). Preoperative computed tomography (CT) showed OA in 44 shoulders (26.3%), among which 12 shoulders (7.2%) showed OA on the preoperative radiographs. Consequently, CT-proven OA in the remaining 32 shoulders was incipient OA that was not revealed radiographically. Radiographs taken at follow-up revealed OA in 30 shoulders (18.0%), of which 24 (80%) had had OA proven by preoperative imaging. Preoperative CT-proven OA in 20 shoulders never became visible on postoperative radiographs. The severity of OA slightly increased in 14 joints (32%) during the postoperative period. The number of preoperative subluxations and the total number of preoperative dislocations/subluxations were significantly greater, and the percentages of male patients and glenoid bone defect greater than 20% of the anteroposterior diameter were higher for the 30 shoulders with postoperative OA.
Conclusion: Most postoperatively detected OA developed before surgery. The preoperative factors are profoundly involved in the development of OA. The role of surgery in favoring the OA development appears to be inconclusive. The development and progression of OA cannot be prevented by surgical intervention, but the progression of postoperative OA is extremely slow.