Abstract

Repair of groin hernia is one of the most common operations performed by general surgeons, and mesh repair methods have gained wide acceptance. Chronic pain is the most serious long-term complication that can occur after repair of groin hernia. The development of chronic pain after herniorraphy has been attributed to several mechanisms, including damage to sensory nerves and mesh inguinodynia. Twenty-four rabbits underwent bilateral inguinal dissection and synthetic polypropylene mesh laid on one side. Bilateral inguinal dissection was performed again after 3 months, and samples of nerve tissue were taken from both sides for histological examination. Light microscopic examination of the sections of control group peripheral nerves were in normal appearance, but the nerve fascicles in experimental group operated with mesh showed axonal dilation and mild-to-severe loss of myelinated axons. Examination of semi-thin and ultra-thin sections in control group peripheral nerve fascicles showed normal morphology. Ultrastructural nerve morphology in experimental group operated with mesh exhibited endoneurinal edema with thickening of both endoneurium and perineurium, causing separation of nerve fibers. Myelin sheaths of fibers showed an ondulation toward the axoplasm and the endoneurium. Separation of myelin layers from each other as a prominent feature of myelin degeneration in nerve fibers was also observed. Axoplasms exhibited edema and crystallization. The light microscopic and ultrastructural changes seen in peripheral nerves in experimental group operated with mesh suggested that mechanical compression of peripheral nerves is associated with myelin degeneration, endoneurinal and perineurial edema, fibrosis, axonal loss, and edema that may cause peripheral neuropathy. Chronic groin pain after hernia repair can be possibly caused by the entrapment of peripheral nerves in the scar tissue formed by the mesh.

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