Do Focal Chondral Defects of the Knee Increase the Risk for Progression to Osteoarthritis? A Review of the Literature.

backgroundFocal chondral defects (FCDs) of the knee are believed to contribute to the development of osteoarthritis (OA), resulting in pain and dysfunction. PURPOSE: To investigate whether untreated FCDs of the knee progress to radiographically evident OA over time. STUDY

designSystematic review; Level of evidence, 3.

methodsA literature review was performed by searching the PubMed, Embase, and Cochrane Library databases to locate studies evaluating clinical and/or radiological outcomes of patients with FCDs that were diagnosed by arthroscopic surgery or magnetic resonance imaging (MRI) and were left untreated with a minimum 2-year follow-up. Additionally, studies were included if there was a radiographic assessment of OA. Search terms used were "knee," "focal," "isolated," "chondral," "cartilage," and "osteoarthritis." Studies were evaluated based on clinical/radiological outcomes and OA risk factors. The study methodology was assessed using the modified Coleman Methodology Score.

resultsEight studies comprising 1425 knees met the inclusion criteria. All studies were of level 3 evidence. The risk of incident cartilage damage (enlargement of original FCDs or incidence of additional FCDs) at latest follow-up was assessed in 3 studies, while 1 study only reported the incidence of cartilage damage at follow-up. All 4 studies noted an increased progression of cartilage damage at follow-up. The progression of cartilage damage was most commonly seen in the patellofemoral joint and medial femoral condyle but was not associated with the development of knee OA based on the Kellgren-Lawrence grade. MRI of the FCDs revealed increased water content, cartilage deterioration, and proteoglycan loss within the medial and lateral compartments.

conclusionPatients with untreated FCDs of the knee joint are more likely to experience a progression of cartilage damage, although the studies included in this review did not demonstrate the development of radiographically evident OA within 2 years of follow-up.