Pathological features of the lateral joint capsule and lateral retinaculum in lateral patellar compression syndrome: a retrospective case-control study.

BACKGROUND: Lateral patellar compression syndrome (LPCS) is characterized by abnormal pressure elevation in the lateral patellofemoral joint. The histopathological basis of LPCS, particularly regarding microvascular and inflammatory changes in the lateral joint capsule and lateral retinaculum, remains unclear. This study aimed to systematically compare the histological characteristics of these tissues between patients with LPCS and controls to characterize tissue-level features associated with LPCS and to explore the potential implications of these findings for understanding pathophysiology and informing future research on surgical strategy selection. METHODS: This retrospective case–control study included 26 patients with LPCS and 23 control patients (with meniscal injuries, patellar dislocation, patellofemoral osteoarthritis, or synovial cyst). Intraoperative tissue specimens of the lateral joint capsule and lateral retinaculum were obtained. Histological evaluation was performed using immunohistochemical staining for Factor Ⅷ (F8, microvessels), CD3 (T cells), CD20 (B cells), and CD68 (macrophages). Microvessel density and inflammatory cell density were quantified and compared between groups. RESULTS: Microvessel density was significantly higher in both the lateral joint capsule (48.84 ± 14.12/mm2 vs. 34.72 ± 15.40/mm2, P = 0.002) and the lateral retinaculum (27.50 ± 11.33/mm2 vs. 17.13 ± 9.26/mm2, P = 0.007) of patients with LPCS compared to controls, with large effect sizes (Cohen's d > 1.0). Within both groups, microvessel density was significantly higher in the joint capsule than in the retinaculum (both P < 0.001). In contrast, no statistically significant between-group differences were detected in the densities of CD3 + T cells, CD20 + B cells, or CD68 + macrophages in either tissue. However, in multivariate regression models adjusting for age and sex, the between-group differences in microvessel density were attenuated and no longer statistically significant; interaction terms were also not significant. CONCLUSIONS: Unadjusted analyses showed increased microvessel density in the lateral joint capsule and lateral retinaculum of patients with LPCS while no statistically significant between-group differences were detected in classical inflammatory cell densities (CD3 + , CD20 + , CD68 +) under the current immunohistochemical panel. Because the association with microvessel density was not statistically significant after adjustment for age and sex, these findings should be interpreted as hypothesis-generating and potentially influenced by demographic factors. Larger age- and sex-matched studies, ideally with clinical correlation, are needed to determine whether angiogenesis is an independent pathological feature of LPCS and whether it relates to outcomes.