Gluteus minimus tendinosis (GMT) is a painful, chronic condition affecting the deep muscles of the hip that is increasingly recognized as a primary cause of lateral hip pain. For many years, pain localized to the outer hip was mistakenly attributed to trochanteric bursitis, an inflammation of the fluid-filled sac near the hip bone. We now understand the root cause is usually a degenerative change within the gluteus minimus tendon itself, which is part of a larger diagnosis called Greater Trochanteric Pain Syndrome. GMT is a source of significant discomfort, typically felt as a dull ache or tenderness over the bony prominence of the hip.
Understanding the Gluteus Minimus and Tendinosis
The gluteus minimus is the deepest of the three gluteal muscles, situated beneath the gluteus medius, with its tendon attaching to the greater trochanter of the femur. Its primary mechanical function is to act as a powerful hip abductor, lifting the leg away from the body’s midline, and as an internal rotator. The minimus and medius muscles work together dynamically to stabilize the pelvis during single-leg activities, such as walking or running. This stabilization prevents the pelvis from dropping on the side of the swing leg, making it a continuously working muscle during most daily movements.
The term tendinosis describes the underlying pathology, which is a degenerative process rather than an acute inflammatory one (tendinitis). Tendinosis is characterized by the breakdown and disorganization of the tendon’s collagen fibers, along with a failed healing response at the cellular level. This distinction is important because it explains why anti-inflammatory medications and rest alone often do not resolve the condition. The tendon structure weakens and loses its capacity to handle normal loads, making it susceptible to ongoing microtrauma that perpetuates the cycle of pain and degeneration.
Primary Mechanism: Repetitive Overload
The direct cause that initiates the degenerative process of gluteus minimus tendinosis is chronic, repetitive mechanical overload of the tendon. This mechanism involves microtrauma, where the cumulative stress placed on the tendon exceeds the body’s natural ability to repair the tissue. The tendon’s health depends on a balance between “wear” from activity and “repair” during rest. Overload occurs when the rate of wear significantly outpaces the rate of repair. This imbalance often results from doing “too much, too soon” without adequate conditioning or recovery.
Activities that involve frequent or prolonged single-leg stance disproportionately load the gluteus minimus tendon. Examples include long-distance running without proper training progression, or occupational tasks that require extended periods of standing or repetitive stair climbing. The tendon is particularly vulnerable when subjected to a combination of high tensile (pulling) force and compressive force. Compressive stress occurs when the tendon is pressed against the greater trochanter during certain hip movements or sustained postures.
Common habits and postures can contribute to this detrimental compressive loading. For instance, standing with all weight shifted onto one hip, known as “hip hanging,” compresses the gluteal tendons against the bony prominence. Similarly, sleeping on the affected side can subject the tendon to continuous direct pressure, exacerbating the microtrauma and hindering the restorative process. These constant, low-level stresses prevent the tendon tissue from recovering, leading to the structural changes characteristic of tendinosis.
Underlying Biomechanical Contributors
While repetitive overload is the direct trigger, certain intrinsic factors predispose individuals to gluteus minimus tendinosis, explaining why not everyone engaging in the same activities develops the condition. Muscular imbalances are a major contributor, particularly weakness in the gluteus medius and other core stabilizers. When the gluteus medius is weak, the smaller gluteus minimus is forced to overcompensate to maintain pelvic stability during gait, leading to excessive strain and fatigue of its tendon.
Gait abnormalities further increase the damaging compressive and tensile loads on the tendon. Individuals with poor hip control may exhibit excessive hip adduction or internal rotation when bearing weight, causing the thigh to cross the body’s midline slightly. This movement pattern increases the friction and compression of the gluteal tendons against the greater trochanter, accelerating the degenerative changes. Severe abductor weakness is indicated by the Trendelenburg sign, a distinct pelvic drop on the non-weight-bearing side, which places higher stress on the stance-leg’s gluteus minimus.
Structural and Systemic Factors
Structural and systemic factors also play a significant role in reducing the tendon’s resilience. A leg length discrepancy, even a small one, can alter the mechanics of the hip and pelvis, leading to asymmetrical loading and chronic overuse of the shorter leg’s gluteal tendons. Age-related changes reduce the overall elasticity and regenerative capacity of all tendons, making the condition more prevalent in individuals over the age of 40 to 50. Women, especially peri- and post-menopausal women, are affected up to four times more often than men. Furthermore, the presence of enthesophytes, or bone spurs, on the greater trochanter is often associated with GMT, as these bony growths can mechanically irritate and compress the tendon tissue.