Patellofemoral osteoarthritis (PFOA) is a degenerative joint condition specifically affecting the knee, where the kneecap, or patella, meets the thighbone, or femur. This articulation is known as the patellofemoral joint, where the patella glides within a groove on the femur called the trochlea. PFOA involves the gradual breakdown of the articular cartilage, the smooth, protective tissue covering the ends of these bones. When this cartilage wears down, the joint surfaces rub against each other, causing pain and inflammation.
Anatomical and Developmental Factors
The physical structure of the patellofemoral joint can inherently predispose an individual to developing PFOA. These fixed factors are often present from birth or develop during skeletal maturation, creating chronic mechanical stress. One such condition is trochlear dysplasia, where the trochlear groove on the femur is abnormally shallow or flat, rather than a deep, stabilizing channel. This shallow groove provides inadequate bony restraint, allowing the patella to shift laterally and track improperly during knee movement.
Patellar malalignment is a related issue, often influenced by the Q-angle, which is the angle formed between the line of pull of the quadriceps muscle and the patellar tendon. An increased Q-angle, particularly common in individuals with wider hips or a “knock-kneed” (valgus) alignment, exerts a greater sideways pull on the kneecap. This lateral force vector pushes the patella against the outer edge of the trochlear groove, leading to uneven pressure distribution and accelerated wear on the lateral aspect of the joint cartilage.
Another structural abnormality is patella alta, a condition where the patella sits higher than normal in the trochlear groove. Because of its high position, the kneecap does not properly engage with the groove until the knee is bent to a greater degree. This delayed engagement means the patella is less stabilized during the initial range of motion, increasing joint instability and the potential for premature cartilage wear from poor tracking.
Acquired Biomechanical Stress and Trauma
While inherent structure plays a role, external forces and specific injuries are often the direct cause or accelerator of PFOA. Acute trauma, such as a direct blow to the kneecap or a patellar dislocation, can instantly damage the articular cartilage surface. Even if the bone heals, the cartilage surface may be left irregular, creating friction and an environment for arthritis to develop over time.
Repetitive, high-impact activities constitute a form of chronic overuse that significantly loads the joint. Activities involving deep knee bending, running, or jumping subject the patellofemoral joint to compressive forces several times the body’s weight. Over years, this consistent, high-magnitude loading can exceed the cartilage’s capacity for repair, leading to microtrauma and progressive degeneration.
Muscle imbalances further destabilize the joint, amplifying the stress on the cartilage. Weakness in the quadriceps muscles, particularly the vastus medialis obliquus (VMO), can compromise the patella’s dynamic stability. The VMO helps to keep the kneecap centered in the groove, and its functional deficiency allows the patella to track laterally, reproducing the effect of a structural malalignment.
Similarly, weakness in the hip abductor and external rotator muscles can lead to abnormal lower-limb mechanics, increasing hip adduction and internal rotation during activities like walking or running. This altered kinetic chain transfers excessive rotational stress to the knee joint, forcing the patella to track incorrectly and causing accelerated wear.
Systemic and Biological Risk Accelerants
Beyond the mechanics of the joint, broader biological and systemic factors can accelerate the progression of PFOA. Age is a factor, as the cumulative effects of decades of joint use naturally lead to wear and tear. Advancing age demonstrates a strong correlation with joint degeneration.
Excess body weight, or obesity, contributes to PFOA through a dual mechanism of increased load and biological inflammation. Greater body mass results in increased compressive forces on the cartilage. However, fat tissue (adipose tissue) is also metabolically active and releases pro-inflammatory molecules called adipokines. These systemic inflammatory markers circulate in the bloodstream and can directly promote cartilage degradation within the joint, independent of the physical load.
Genetic predisposition also influences susceptibility, as a family history of osteoarthritis increases an individual’s risk. Specific genes may affect the composition or resilience of the articular cartilage, making it more vulnerable to breakdown from mechanical stresses. Generalized inflammatory conditions, such as rheumatoid arthritis, can create a highly inflammatory environment in the joint. This inflammatory state accelerates the destruction of cartilage, speeding up the progression to end-stage osteoarthritis.