Masticatory Muscles Myositis (MMM, Atrophic Myositis or Eosinophilic Myositis)
The main masticatory muscles are the temporalis and masseter muscles. These are the large muscles on the top and sides of the head which act to close the jaw. These muscles have a unique muscle protein composition. Masticatory muscles are predominantly composed of fibers designated as Type 2M. Disorders of the muscles of mastication occur relatively commonly in clinical practice and can be of myopathic or neuropathic origin. Masticatory muscle myositis/disorders (MMM/MMD) can be diagnosed by the assay of serum from affected animals to see if there are autoantibodies against Type 2M fibers.
What is masticatory muscle myositis?
Masticatory muscle myositis (MMM) or masticatory muscle disorder (MMD) is an inflammatory disorder that involves (primarily or exclusively) the muscles of mastication (chewing). It is also known as atrophic myositis or eosinophilic myositis. MMM is the most common inflammatory myopathy in dogs. The actual cause of masticatory myositis is unknown, but is suspected to be an immune-mediated mechanism. This disorder can affect any dogs of any breed, but it seems to be seen most commonly in large breed dogs. German Shepherds, Cavalier King Charles Spaniels, retrieving breeds and other large breed dogs. German Shepherd Dogs are highly predisposed. It is seen most commonly in young or middle-aged animals and there is no gender predisposition. This has not been recognized in cats.
MMM is caused by the presence of 2M fibers in the muscles of the jaw. 2M fibers are not found elsewhere in the body, but they are close in structure to proteins found on the surface of bacteria. The immune system recognizes these proteins as foreign to the body and attacks them, resulting in inflammation.
Acute form: Masticatory myositis is generally bilateral (both sides are affected). The acute form of masticatory myositis is characterized by painful swelling of the muscles of mastication, particularly the temporal and masseter muscles. Ophthalmic signs may include third eyelid protrusion, red eyes, and exophthalmos (protrusion of the eye from the socket) may be present, caused by pressure on the back of the eye from the swollen muscles. This can cause inflammation of the optic nerve and can produce vision disorders. Fever, enlarged lymph nodes, and inflammation of the tonsils may also be found. Dogs with the acute form are reluctant to eat and may drool excessively. They are painful on palpation of the muscles of mastication and on attempts to open the mouth.
Chronic form: The chronic form of masticatory myositis is the more common form. It may occur after repeated bouts of the acute form or without any history of acute episodes. Affected dogs have severe, progressive atrophy of the jaw muscles (the temporal and masseter muscles), accompanied by replacement of muscle tissue with fibrous connective tissue (scarring) of the masticatory muscles due to fibrosis. This results in a sunken appearance to their cheeks and the top of their head. They have decreased ability to open their mouths (trismus), but are otherwise bright and alert. The affected muscles include the temporalis, masseter, and pterygoid muscles. The disease is usually bilateral.
A diagnosis of masticatory myositis is suspected based on clinical signs. The acute form must be differentiated from other disorders affecting the teeth, eyes, mouth, and temporo-mandibular joint. The chronic form must be differentiated from trigeminal neuropathy (a disorder of the nerve which innervates the muscles of mastication).
Diagnosis of MMM can also be done through either biopsy of the temporalis or masseter muscles or the 2M antibody assay, in which blood serum of the possible MMM-dog is reacted with temporalis tissue of a normal dog, or both. False negatives by the 2M antibody assay may be obtained if MMM is end-stage with destruction of type 2M fibers and marked fibrosis.
A complete blood count may show a mild decrease in red blood cells and increased white blood cells (primarily neutrophils, but occasionally an increase in eosinophils is seen). A biochemistry panel may show increased creatine kinase (CK), aspartate aminotransferase (AST) and globulin (antibody) concentrations, especially in the acute phase of the disorder. CK and AST are commonly increased with any muscle disorder. In a few dogs, protein may be seen in the urine.
Electromyography (EMG) measures the electrical activity in muscles and can help confirm the presence of muscle disease. However, this can be normal in some dogs, especially those with chronic disease. EMG can help with selection of sites for muscle biopsy. Muscle biopsy is used to make the definitive diagnosis of masticatory myositis.
Treatment is usually with immunosuppressive doses of corticosteroids such as prednisone, often with decreasing doses for up to 4–6 months, and in the case of trismus, manual opening of the mouth under anesthesia. This should result in clinical remission of masticatory myositis. The dose of corticosteroids is gradually reduced over that time period of 4 – 6 months, starting two weeks after therapy is initiated.
Feeding very soft or liquid food during this time is usually necessary. The ultimate degree of recovery of jaw function and muscle mass will depend upon the extent of damage to the muscle tissue.
Some dogs may relapse after treatment is discontinued or each time the dose of corticosteroids is decreased. These cases may warrant the use of additional immuno-suppressive drugs.
Recovery is usually rapid and complete if treatment is begun early. Dogs with the chronic form of masticatory myositis, who have extensive fibrosis, may not respond well to therapy.
Recurrence of MMM may occur. Misdiagnosis of MMM as a retro-orbital abscess based on physical examination and finding of trismus leads to inappropriate treatment with antibiotics, which will not impede the progress of MMM.
Last Updated (Wednesday, 23 November 2011 13:39)
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