Deep somatic pain that originates in skeletal muscles, fascial sheaths, and tendons (myogenous pain); in bones and periosteum (osseous pain); in joints, joint capsules, and ligaments (arthralgia pain); and in soft connective tissues (soft connective tissue pain).
Muscle pain is mediated by A delta and C fibers.
Stretch or contraction of a muscle produces sharp pain.
Contraction produces ischemia with the release of algogenic substances such as bradykinin and prostaglandins.
Siegfried Mense described at least three mechanisms for muscle pain:
Peripheral mechanisms. Local pain from muscle is due to the excitation of muscle nociceptors by overuse, trauma, or inflammation. In this type of pain, many substances are involved that are released from the damaged tissue (e.g. potassium ions, prostaglandins, bradykinin, serotonin, ATP) or from the nociceptive nerve ending (e.g. neuropeptides such as substance P (SP), calcitonin gene-related peptide (CGRP) or somatostatin (Mense, 1997; Mense and Simons, 2001).
Spinal mechanisms. One possible mechanism explaining the referral of muscle pain is an expansion of the spinal neuronal population that can be excited by input from the damaged muscle. Among the substances that have been shown to induce an expansion of the neuronal population that responds to a given input are SP acting on NK-1 and glutamate acting on NMDA receptors (Woolf and Thompson, 1991). The lesion-induced expansion of the spinal target area of input from a given muscle is probably due to central sensitization, i.e. overexcitability of dorsal horn neurons which under these circumstances respond to an input that does not normally affect these cells.
Supraspinal mechanims. Besides psychological disorders and pathologic stress reactions, one possible explanation for this condition is that the descending painmodulating systems may be dysfunctional. At present, two such systems are known, an antinociceptive or pain-inhibiting system, which is relatively well known, and a pronociceptive or pain-facilitating system, for which only few data are available (Basbaum and Fields, 1984; Fields et al. 1995; Sandkühler, 1996).
Okeson (2019 ) uses the following categories for muscle pain:
Co-contraction*
Local soreness*
Myofascial Pain*
Chronic centrally mediated pain
*Common in dental settings
The 2014 Diagnostic criteria for temporomandibular disorders for clinical and research applications has 6 categories:
Myalgia
Myofascial pain
Fibromyalgia
Myositis
Spasm myalgia*
Movement disorders
The international classification of Headache disorders (2018) does not have a specific category for masticatory or facial muscle pain, but includes the following:
11.7 Headache attributed to temporomandibular disorder (TMD)
A11.2.5 Headache attributed to cervical myofascial pain
The International Classification of Orofacial Pain (2020) uses a different approach:
Myofascial Orofacial Pain
Primary myofascial orofacial pain (acute or chronic)
Secondary myofascial orofacial pain (tendonitis, myositis or muscle spasm)
*A myospasm might be secondary to soreness, CNS activity, or could be a stand-alone condition. It will present as a reduction in range of motion, but lengthening of the muscle is possible (although painful).