The semimembranosus muscle originates at the lateral ischial tuberosity, and the muscle runs down the posterior medial thigh. The muscle belly ends and the tendon begins just above the knee joint. The tendon then has main insertion on the posteromedial tibial plateau; it also spreads out into different insertion points (eg, one anteriorly on the tibia, one on the popliteus muscle fascia, and one on the posterior medial aspect of femoral condyle). The functions of the semimembranosus muscle are knee flexion, internal rotation, and hip extension. In addition to the semimembranosus muscle, the hamstring muscle group is also made up of the biceps femoris and the semitendinosus muscles. The long head of the biceps femoris and semitendinosus originate from the inferomedial portion of the ischial tuberosity. The biceps femoris inserts at the lateral condyle of the tibia and fibular head, while the semitendinosus inserts at the medial border of the tibial shaft. The biceps femoris is responsible for flexion of the knee, lateral rotation, and extension of the hip. In addition to the semimembranosus tendon, these tendons can also become irritated or inflamed, leading to a more generalized condition called distal hamstring tendonitis.
Classic history and presentation: Patients usually present with a complaint of posterior knee pain, and then pain localized further to the posteromedial knee. Usually, it is a vague pain with insidious onset (described as an ache); onset will be more acute if there was a sudden, dramatic increase in physical activity. Semimembranosus tendonitis / tendinopathy can occur anywhere from origin to insertion of the tendon; there is also a bursa in this region that can become inflamed. Semimembranosus bursitis is a distinct entity from semimembranosus tendonitis, but it will be grouped together here since the approach is similar for a PCP / emergency physician.
Posteromedial knee pain is less common than anterior or lateral knee pain.
Distal hamstring tendonitis can occur in the medial or lateral hamstring tendons. The onset of symptoms is generally insidious; however, a more acute onset can develop as the result of a recent increase in physical activity involving overuse or misuse of the muscle group. Many patients will describe a recent increase in running, dancing, or use of exercise equipment. Patients will complain of a general pain over the posterior aspect of the knee that can be constant and severe. The patient may attempt to protect the inflamed tendon by holding the knee in the flexed position. Additionally, patients may develop decreased functional ability with decreasing range of motion. Other signs and symptoms can consist of crepitus on flexion of the knee or pain on palpation over the tendinous insertion, with the medial portion affected more often than the lateral.
Prevalence: The true incidence of semimembranosus tendinopathy is unknown; it is probably underdiagnosed.
Patients typically fall into 2 categories:
- Relatively young, athletic adults and adolescents
- Middle-aged / elderly patients who are starting a new exercise regiment or increasing activity levels
Pathophysiology: Semimembranosus tendinopathy is frequently an overcompensation injury, as the tendon sees more stress if a patient is overcompensating, eg, because of a medial meniscus tear. Friction and repetitive eccentric loading can lead to degenerative changes within the tendon. The pathophysiology of tendinopathy is often a more degenerative process than an inflammatory one. When tendon fibers are overloaded and repeatedly stretched, the collagen fibers slide on top of each other, breaking crosslinks. Additionally, thermal stresses and hypoxia can lead to an increased expression of molecules such as metalloproteinases, which lead to the degradation of the extracellular matrix and increased production of inflammatory cytokines such as leukotrienes and prostaglandin E2. Thus, when the recovery capacity of the tissue is exceeded due to overload or inadequate recovery time, repair mechanisms of the tendon are lost. Microscopically, collagen fibers become disorganized and lose their parallel arrangement, while there is increase in mucoid material within the extracellular matrix, which can separate collagen fibers. Additionally, there is a marked increase in type III collagen fibers, which have a lower number of cross-links when compared to type I collagen fibers. At the cellular level, it has been cited that there are reported increased numbers of leukocytes, including macrophages and mast cells in chronically painful tendons. However, it should be noted that when compared to more immune-driven pathologies, these numbers are in fact relatively small.
