Management of Lateral Epicondylitis
(Part 2)
We continue with our discussion on Lateral Epicondylitis (LE) this week.
It is known that increasing shear forces promotes fibrocartilaginous formation at tendon enthesis, which may lead to weakening at the tendon-bone junction and towards the development of tendinosis.
Some studies have shown defects and necrosis inside the tendon fibers within tendons in patients with chronic LE, which is ascribed to strong association with under use of the affected part of the body due toimmobilization because of the pain.
Moreover, inadequate tendon angiogenesis and continuous muscle contraction may lead to tendon ischaemia, which further aggravates tendinosis.
As for the pain mechanism of LE, most research results show the pathogenesis of LE to neurogenic etiology based on several evidence indicating the presence of nerve fibers with reactivity to neuropeptides, including substance P (SP) and calcitonin gene-related peptide (CGRP).
It was observed that in 5 patients with LE and 4 patients with medial epicondylitis (ME) by immunohistochemistry, indicating that the SP/CGRP was present in the pathologic tendon tissues of patients with LE as well as those with ME.
Neurokinin-1 receptor immunoreaction was seen in varicose fibers in the form of a single fiber or nerve bundles.
Other findings present show some evidence for a possible neurogenic pathogenesis of LE and ME.
Experts concluded neuropeptides (SP and CGRP) and cytokines and tumor growth factor-β (TGF-β) might be one of the causes of LE.
However, it should be understood that further studies are needed to fully understand the relationship between neuropeptides and cytokines.
Furthermore, some studies show the mRNA levels of neuropeptides and cytokines in LE with corticosteroid injection treatment.
It was also shown that the expression of SP messenger ribonuclejc acid (mRNA) was maximally restricted by corticosteroid triamcinolone acetonide (TAA) at 24 hours but recovered at 72 hours.
CGRP mRNA and interleukin1 alpha (IL1α) mRNA were restricted at 24 and 3 hours, respectively.
Likewise, the reaction structure of the corticosteroid for alleviating pain in LE patients is mainly through the restriction of neuropeptides and cytokines.
Consequently, a significant positive correlation between CGRP and IL-1α was also seen after 72 hours of TAA treatment, highlighting the role of neurogenic inflammation in LE.
There are patients who often complain of pain or burning around the lateral epicondyle of the humerus, which most often radiates down the forearm and sometimes extends proximally to the upper arm.
This pain is usually exacerbated or triggered by a variety of activities such as grasping objects.
The level of the pain often spans from mild to severe levels and from intermittent to persistent, which seriously affects patients’ quality of life.
This is in addition to the condition where patients often complain of weakness on gripping and difficulty in lifting.
This corner will continue with the discussion on the management of LE next issue.