The thyroid gland produces hormones that regulate metabolism across nearly every cell and tissue in the body. Hypothyroidism, or an underactive thyroid, occurs when the gland does not produce sufficient amounts of these hormones, slowing metabolic functions. Tendonitis refers to the pain and dysfunction of a tendon, the tough cord connecting muscle to bone. While often attributed to overuse, a direct clinical association exists between hypothyroidism and various tendon issues. Low thyroid hormone levels significantly impact musculoskeletal health, meaning unexplained or persistent tendon pain can sometimes signal underlying thyroid dysfunction.
The Clinical Link Between Hypothyroidism and Tendon Issues
A recognized clinical association exists between low thyroid function and an increased incidence of musculoskeletal complaints, including tendinopathy. These tendon problems are frequently among the earliest symptoms experienced by patients with undiagnosed or poorly managed hypothyroidism. Orthopedic specialists increasingly acknowledge this connection in cases of tendinopathies that appear without a clear traumatic cause.
Musculoskeletal issues are common in individuals with thyroid disease. Carpal tunnel syndrome, which involves tendon sheath inflammation, is notably more prevalent in patients with overt hypothyroidism. The presence of tendon issues can prompt physicians to investigate thyroid hormone levels when localized treatments for tendinopathy fail to provide lasting relief. Treating the underlying metabolic cause is necessary for true resolution of the tendon pathology.
Biological Mechanisms of Connective Tissue Dysfunction
Low levels of thyroid hormones directly disrupt the normal biology of connective tissues, including tendons. Thyroxine, the main hormone produced by the thyroid, plays a significant part in both collagen synthesis and the metabolism of the extracellular matrix that provides the tendon’s structure. Reduced thyroid hormone levels impair the rate of protein turnover and the capacity for tissue repair within the tendons. This reduction in the maintenance cycle makes the tendon structure more vulnerable to degeneration from normal daily stress.
A hallmark of hypothyroidism is the abnormal accumulation of hydrophilic substances, specifically glycosaminoglycans (GAGs), such as hyaluronic acid, within the connective tissues. This build-up, known as myxedema, causes the tendon and its surrounding sheath to swell and thicken. The swelling compromises mechanical integrity, making the tendon stiff, less flexible, and mechanically weaker. Chronic hypothyroidism contributes to tendinopathy, which is a degenerative process.
Thyroid hormone receptors are present in tenocytes, the specialized cells that maintain tendon tissue. Thyroid hormones enhance the growth of these tenocytes and protect them from programmed cell death (apoptosis). When hormone levels are low, this protective and regenerative function is diminished. This contributes to the degeneration and poor healing response characteristic of tendinopathy, making the compromised tendon slower to recover from minor strains or micro-trauma.
Specific Musculoskeletal Manifestations
The systemic effects of hypothyroidism lead to several distinct musculoskeletal conditions. Carpal Tunnel Syndrome (CTS) is a common manifestation, where the abnormal accumulation of GAGs causes the tendon sheaths within the wrist to swell, compressing the median nerve. This tenosynovitis results in the characteristic numbness, tingling, and weakness in the hand. The thickening of connective tissue can also lead to trigger finger, where a flexor tendon sheath becomes too thick to glide smoothly through its pulley.
The shoulder is another common site for injury, where patients may develop rotator cuff tendinopathy or adhesive capsulitis (frozen shoulder). Connective tissue stiffness contributes to the painful restriction of movement seen in adhesive capsulitis. The Achilles tendon is also a frequent site of pain and swelling in hypothyroid patients, sometimes leading to calcific tendinopathy, which involves the deposition of calcium. These specific injuries often represent a physical breakdown that is secondary to the underlying metabolic imbalance.
Treatment Strategies for Thyroid-Related Tendinopathy
The treatment strategy for thyroid-related tendinopathy is optimizing thyroid hormone replacement therapy. Correcting the underlying deficiency with medication such as levothyroxine is the crucial step for the long-term resolution of the tendon issue. Once thyroid hormone levels are normalized, the metabolic environment in the connective tissue returns to normal, allowing the body’s natural repair mechanisms to start working effectively. Symptomatic relief of tendon pain often follows the achievement of a stable euthyroid state.
While the thyroid issue is being addressed, local treatments can provide relief from pain and dysfunction. Physical therapy, focusing on strengthening and controlled loading exercises, is a secondary treatment to restore the tendon’s mechanical function. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used for short-term pain relief, but they do not treat the underlying cause of the tendinopathy. Corticosteroid injections should be approached with caution, as their efficacy is limited if the metabolic dysfunction is uncorrected, and repeated use carries a risk of weakening the compromised tendon structure.
Patients must be aware that tendon healing is a slow process, even after thyroid levels are corrected, because connective tissue has a slow turnover rate. It may take several months following the normalization of thyroid function before the structural integrity and symptoms of the tendon improve. Consistent monitoring of thyroid-stimulating hormone (TSH) levels is necessary to ensure the hormone replacement dosage remains optimal, which is the foundation for a successful and lasting resolution of the tendinopathy.