Patellofemoral pain syndrome (PFPS) is one of the most common knee disorders experienced by active adults and adolescents (
1,
2). PFPS can be defined as either retropatellar or peripatellar pain (
1,
3) and is the most frequently diagnosed condition in patients under 50 with knee complaints (
4). The cause is thought to be multi-factoral (
4-
6), with some of the main contributing factors being abnormal tracking (
7,
8), lateral patellar malalignments (
9,
10), and decreased patellofemoral joint contact area, such as in patella alta (
11). These factors may induce uneven stresses on both the patella itself and the peripatellar tissues (
12). Abnormal patellar tracking may be due to excessive foot pronation, patellofemoral ligament properties, joint conformity, a large quadriceps angle, and altered muscle recruitment at the hip joint with increased femoral rotation (
13). Under normal conditions, the vastus medialis oblique (VMO) muscle is able to counterbalance the lateral pull of the large vastus lateralis (VL) muscle to ensure patellar stability (
6). The VM and VL muscles are countervail each other to adjust the location of the patella in the patellofemoral joint (
14). Although few studies have found any link between patellar malalignment and PFPS (
8), it has been noted that an imbalance between the VMO and the VL can alter patellar alignment during knee extension, leading to pathological problems in the patellofemoral joint (
15).
Various studies have demonstrated morphological changes, such as significantly smaller VMO volume (
6,
8,
16,
17), insertion volume, and fiber angles in PFPS (
17). Furthermore, there is a significant correlation between decreased VMO fiber angle and patellar malalignment (
8,
18). To understand the involvement of the VL muscle in the pathogenesis of knee dysfunction, precise knowledge of its anatomical structure is essential. However, there is a lack of information on the architecture of the VL muscle (
19,
20). In one study, the authors compared the VMO and VL in individuals with PFPS and found atrophy in both muscles, although no significant difference was found in the amount of atrophy (
16). There is insufficient data to determine if there is greater atrophy of the VMO than of the VL (
6,
16). In addition, tightness of these muscles has been reported to contribute to this dysfunction (
20). Studies about other morphological characteristics of VL, such as fiber angles, are sparse. Most studies only report on healthy groups and not on those with PFPS (
19), thus resulting in a dearth of information (
21).
Investigation of VMO fiber angles, VL fiber angles, and the ratio of VMO fiber angles to VL fiber angles will provide a better understanding of the relationship between the morphological parameters of the VMO and VL to patellar kinematics and the etiology of PFPS.
PFPS patients who possess lower VMO activation compared to VL activation do not necessarily have quadriceps weakness (
22), and the patellar tilt angle has not been reported to change after improvements in quadriceps strength (
11). Nonetheless, there is a gap in determining the effect of quadriceps exercise on the fiber angles of VMO and VL muscles in PFPS.