The femorotibial joint is the primary articulation of the knee, functioning as a modified hinge joint where the thigh bone (femur) meets the shin bone (tibia). This complex joint is formed by the distal end of the femur and the proximal end of the tibia. It permits movement in one main plane while accommodating the substantial forces generated during daily activities. As a major weight-bearing structure, the femorotibial joint supports the body’s mass and plays a central role in human locomotion.
Structural Components
The architecture of the femorotibial joint involves a relationship between the rounded, spool-like condyles of the femur and the relatively flatter surface of the tibial plateau. To allow for smooth movement between these mismatched bony surfaces, a layer of articular cartilage covers both the femoral condyles and the tibial plateau. This specialized connective tissue is slick and resilient, acting as a low-friction surface that allows the bones to glide against one another.
Between the femur and tibia sit two C-shaped wedges of fibrocartilage known as the menisci: the medial and the lateral meniscus. These structures function like shock absorbers and space fillers, significantly deepening the shallow tibial surface to improve joint congruence. By distributing the load across a wider area, the menisci transmit between 30% and 70% of the force applied across the joint, protecting the articular cartilage underneath.
The stability of this joint is maintained by a complex network of ligaments, which act like strong, non-elastic ropes. The collateral ligaments—medial and lateral—resist sideways forces, preventing the knee from bending too far inward or outward. Within the joint capsule, the anterior and posterior cruciate ligaments cross over each other, providing front-to-back stability and preventing the tibia from sliding too far forward or backward relative to the femur.
Biomechanics and Primary Function
The primary functions of the femorotibial joint are to facilitate flexion (bending) and extension (straightening) of the leg. These movements are not simple rotation but involve a dynamic combination of rolling and gliding between the femoral condyles and the tibial plateau. For example, during knee flexion, the femur first rolls backward on the tibia, then simultaneously glides forward to prevent the femur from rolling off the back edge of the tibia.
A specific rotational movement, known as the screw-home mechanism, is required to achieve full, stable extension. During the final 15 to 20 degrees of extension, the tibia automatically rotates externally relative to the femur. This slight twist, caused by the unequal size and shape of the femoral condyles, effectively “locks” the knee.
This locking mechanism provides structural rigidity, minimizing the need for constant muscle contraction to maintain an upright stance. The joint’s overarching function is to manage and transmit substantial forces, which can reach three times the body’s weight during walking and higher multiples during activities like climbing stairs. This ability to absorb ground reaction forces, combined with coordinated rolling and gliding, is essential for the joint’s mobility.
Common Sources of Pain and Dysfunction
A frequent cause of chronic pain and disability in the femorotibial joint is osteoarthritis, a degenerative condition involving the wear and tear of the articular cartilage. As the cartilage thins and erodes, the protective layer is lost, causing the underlying bones to rub together, which results in pain, stiffness, and inflammation. The loss of this smooth surface impairs the joint’s biomechanics and progressively limits the range of motion.
Meniscal tears are another prevalent source of dysfunction, arising from either acute trauma, such as a sudden twisting movement, or gradual degeneration over time. When a meniscus tears, its ability to distribute load and absorb shock is compromised, leading to mechanical symptoms like clicking, catching, or a sensation of the knee locking. A tear can also accelerate the progression of osteoarthritis because the impaired meniscus no longer provides adequate protection to the articular cartilage.
Damage to one structure, particularly the menisci, places excessive and abnormal stresses on the remaining cartilage. This altered load bearing initiates a cascade that can quickly lead to widespread joint deterioration, resulting in chronic pain and a significant reduction in mobility.