Histologically, tendinosis shows loss of the typical linear collagen fiber organization, increased mucoid ground substance, hypercellularity, and increased growth of nerves and vessels (FIGURE 1B).
Tendinosis is not always symptomatic.5,11 When pain is present, experts have proposed that it is neurogenically derived rather than from local chemical inflammation. This is supported by evidence of increases in the excitatory neurotransmitter glutamate and its receptor N-methyl-D-aspartate in tendinotic tissue with nerve ingrowth. Tendinotic tissue also contains substance P and calcitonin gene-related peptide, neuropeptides that are associated with pain and nociceptive nerve endings.2,3,6,10
Patients with tendinosis typically present with an insidious onset of a painful, thickened tendon.11 The most common tendons affected include the Achilles, the patellar, the supraspinatus, and the common extensor tendon of the lateral elbow.2 Lower extremity tendinosis is common in athletes, while upper extremity tendinopathies are more often work-related.3
Paratenonitis: Inflammation surrounding the tendon
Occasionally, tendinosis may be associated with paratenonitis, which is inflammation of the paratenon (tissue surrounding some tendons).2,5,10 Paratendinous tissue contains a higher concentration of sensory nerves than the tendon itself and may generate significant discomfort.10,11
The clinical presentation of paratenonitis includes a swollen and erythematous tendon.5 The classic example—de Quervain disease—involves the first dorsal wrist compartment, in which the abductor pollicis longus and extensor pollicis brevis tendons are encased in a synovial sheath. The term tenosynovitis is commonly used to indicate inflammation of both the paratenon and synovial sheath (TABLE 12,3,5,6,9-11).5
