Masticatory muscle myositis (MMM) is an autoimmune disease possibly triggered by recent infection or, while not yet proven, recent vaccination in a susceptible animal (within 30-45 days). Even if vaccination is not a direct cause, it can exacerbate the severity of disease during the active phase.

2M Antibody Assay. Current methodology uses an ELISA that is easier to perform and has similar high sensitivity and specificity to the immunohistochemical method previously used.

Specificity of this test is 100% for masticatory myositis, with no false positives. It will not be positive in cases of polymyositis where the masticatory muscles are also affected. Sensitivity of this test is affected by steroid use (immunosuppressive dosages for >7-10 days) which will therapeutically lower antibody titers. Anti-inflammatory doses of corticosteroids given for weeks to months will likely decrease 2M antibody levels as well. It is always preferable collect the serum sample for this test prior to corticosteroid administration. In end-stage disease, this test may also be negative because all of the Type 2M fibers are destroyed and the antigenic stimulus for antibody production is lost.

Muscle Biopsies. Both muscle biopsy and 2M antibody titers are recommended for the diagnosis of MMM, as the antibody test can give false negatives, as discussed above. Muscle biopsy gives more information about the long-term prognosis, as it indicates how much damage is present, the severity of inflammation and degree of fibrosis. For taking biopsy specimens, the recent review in Compendium (2004) has useful diagrams. Open biopsies are required, as punch biopsies yield inadequate tissue samples. The preferred site is the temporalis muscle (as the masseter muscle has lots of vessels and nerves). The frontalis muscle overlies the temporalis, but it is not involved in MMM, so will appear histologically normal. To obtain a proper temporalis muscle specimen, incise and retract the frontalis muscle, then incise and retract the thick fascia overlying the temporalis muscle. A 5 mm³ piece of muscle is required.

Immunosuppressive doses of corticosteroids should be given initially, and these should not be decreased too quickly or stopped abruptly. Recur-rence of clinical signs is a common problem if treated inappropriately. Return of jaw mobility should be monitored if trismus was a presenting clinical sign, and serum creatine kinase (CK or CPK) can also be checked during the course of therapy. In affected dogs, the CK is usually normal or only mildly elevated (in the range of 1000-2000 IU/L). When elevated, monitoring CK response to therapy is useful.

Once CK and jaw function are normal, slowly decrease the dose of prednisone to the lowest every other day (EOD) dosage that controls clinical signs. Stay at this EOD dose for 4-6 months, and then try to decrease further. Some cases do well on very low doses of steroids, but if dosage is stopped, symptoms may recur. Usually prednisone alone is adequate, although a second choice would be azathioprine. Other treatment choices include mycophenolate and cyclosporine, but experience with these drugs is minimal at present.