Extensive expression of markers for acetylcholine synthesis and of M2 receptors in tenocytes in therapy-resistant chronic painful patellar tendon tendonosis - a case study

• We have recently, in a study of a group of patients with chronic painful patellar tendon tendinosis (“jumper’s knee”), obtained evidence favoring the occurrence of an upregulation of a non-neuronal cholinergic system in this condition. Today, there is a new line of treatment of patellar tendinosis in the form of doppler guided sclerosing injections (Polidokanol), a treatment that has turned out to be very successful. However, the mechanisms for this therapy remain somewhat unclear. After an average of three treatments, a majority of the patients experience a significant decrease of pain symptoms. Nevertheless, a few patients seem resistant to this therapy, exhibiting no clear decrease in pain sensation. Therefore, we have in this pilot study investigated biopsies from the patellar tendon of one such therapy-resistant patient (male, exhibiting long duration of pain symptoms and showing radiological findings confirming tendinosis), using immunohistochemical methods examining both chemically fixed and unfixed tissue. The results were compared with our previous findings of both normal and tendinosis tendons. Morphologically, there was hypercellularity in the tendon tissue. The immunohistochemical studies showed that there were marked immunoreactions for choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) (fixed tissue), as well as for the M2 muscarinic acetylcholine receptor (unfixed tissue), in the overwhelming majority of the tenocytes. The levels of immunoreactions were more pronounced than those obtained in the tendinosis tissue of the previously studied patients and clearly more pronounced than those of tendon tissue of controls. In conclusion, our theory is that cases of severe tendinosis, exhibiting therapy-resistance, are related to the occurrence of an excessive local acetylcholine (ACh) production that appears to be even more prominent than in tendinosis in general. This case study emphasizes the need for further investigation regarding the role of non-neuronal ACh in therapy-resistant patellar tendon tendinosis.

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