mmm

Masticatory Muscle Mysositis

Jan Elliott-Goin
http://www.curiohoundsigs.com/index.htm

Masticatory Muscle Mysositis (MMM) appears to be a breed problem in many large breed of dogs, including but not limited to:

Bearded Collies

Chinese Sharpei

German Shepherd Dogs

Doberman Pinschers

All Retrievers (Goldens and Labradors make up most reported cases in this group)

Old English Sheepdogs

Sloughis

This immune-mediated, focal inflammatory myopathy selectively affects the muscles of mastication and can occur in dogs less than 6 months of age, although the condition primarily affects young and middle-aged dogs and is unrelated to gender. While most cases occur in large breeds of dogs, it can affect any breed. (The incidence of this in Italian Greyhounds seems to be moderate, based on the information we have. We have found information on only six other affected dogs nationwide. I'm sure the numbers are higher, as many cases go unreported or undiagnosed) **(updated, October 2005...it has been brought to our attention that there are a number of other IGs diagnosed with this condition, including two in one litter. I have spoken with the breeders/owners of several of these dogs soon, so that we can compare information and pedigrees of these dogs to the ones we already know of.)

While most veterinarians are hesitant to say it's an inherited condition, it has been witnessed in lines and in litters of affected individuals.

This condition used to be described as two separate disorders:

(1)eosinophilic myositis

(2) atrophic myositis.

It is currently felt that these are manifestations of the same disease now called masticatory myositis. (MMM) is a canine inflammatory disorder, most likely immune-mediated,selectively involving the masseter, temporal, and pterygoid muscles of mastication. These muscles are used to grind and chew food prior to swallowing.(In layman's terms, these are the muscles in the top and sides of the face, including the cheek muscles, that assist in opening and closing the mouth)

Five muscle groups in the dog are involved in the process of mastication - four muscles are responsible for closing the mouth and one with opening the mouth. The tempoallis muscles and the masseter muscles are primarily the muscles used to powerfully close the jaws.


Fig 1 side view	Fig 2 dorsal view, unaffected	Fig 3 dorsal view, affected

Bear in mind that these muscles must also relax in order for the mouth to open. Since these two muscles are the largest muscles which close the jaw, when they become involved in masticatory myositis, the primary clinical sign is trouble in opening the jaws.

Masticatory myositis can be divided into an acute and chronic form. It must be remembered that one acute attack can lead immediately into the chronic form of the disease, although, more often than not, multiple, recurrent acute attacks are necessary. In a very few cases, the acute attack is not severe enough to be noticable. Clinical signs include some combination of masticatory muscle atrophy or swelling and abnormal jaw function, manifested generally by restricted jaw mobility. The dog's head sometimes appears swollen and larger than normal. The dog will be reluctant or unable to open his mouth. Opening the mouth more than 1 inch or so elicits an extremely painful response. This results in difficulty in eating and often the owner notices increased drooling as well. This swelling may even cause exophthalmia or the eyes to "bug out". Usually a fever is present and the lymph nodes in the head and neck region are enlarged. The tonsils are often enlarged as well, but it is difficult to visualize them due to the inability to open the mouth. The patient is often depressed and may resent palpation of the head musculature.

Laboratory findings are variable, but very often are normal. The white blood cell count may be elevated and often there is an increase in eosinophils (a type of white blood cell often seen with inflammation). Most often there is a dramatic increase in a skeletal muscle enzyme known as Creatine Kinase or Creatine Phosphokinase (CPK-MM). Smaller amounts of this enzyme are also located in the brain (CPK-BB) and in the heart muscle (CPK-MB). This enzyme has a short life span in the serum and is most often elevated in the acute form of the disease due to the magnitude of muscle damage and because the owner usually presents the dog while the disease is present. CPK may not be part of the normal serum enzyme panel your veterinarian uses and may have to be requested separately. Your vet should also request the CPK enzyme be reported in terms of the various isoenzymes (heart, brain and skeletal muscles).

The chronic form usually is evident when the dog's head appears "sunken", especially the top of the head. Sever and recurrent muscle damage leads to scar tissue formation and atrophy or shrinking of the muscle. This scar tissue is non-functional and these dogs often cannot open their mouths more than 1/2-1 inch. The dog's head often appears "skull-like" with a prominent external sagittal crest (the bony ridge on top of the head) and the eyes are sometimes enophthalmic or sunken due to loss of the muscle mass behind them (fig.3). In the chronic form, laboratory findings are often normal. The CPK-MM is usually normal due to the fact that there is little muscle left to produce the enzyme. The dogs are normal otherwise and non-painful, although the mouth cannot be opened.

The cause of masticatory myositis is uncertain, but is thought to be immune-mediated because:

The type of cellular infiltrate in the affected muscles.
The disease is responsive to immunosuppressive doses of corticosteroids.
Laboratory diagnosis is made by detection of circulating antibodies against type 2M fibers, a unique fiber type present only in the muscles of mastication(the temporalis and/or masseter muscles). These antibodies may play a role in the immune system attack on these muscle fibers. Evaluation of a muscle biopsy is necessary for confirmation of the diagnosis and in prognosis for return of jaw function and muscle mass as determined by the amount of myofiber destruction and fibrosis.

Immunosuppressive dosages of corticosteroids should be used until jaw function returns to normal and serum CK is within the reference range. The dosage should then be decreased until the lowest alternate day dosage is reached that keeps the dog free of clinical signs. In some dogs, prone to relapses, this must be maintained on continuous alternate day therapy over the dog's lifetime. This dosage should be continued for an additional 4-6 months since clinical signs will reoccur if treatment is stopped too soon or an inadequate dosage is used initially

Surgery is sometimes necessary to allow some return of jaw function. Often the insertion of the temporal muscle on the lower jaw is surgically incised and released. This may free up the jaw enough for the dog to be functional.

Fortunately, this is not a common disease, but one that veterinarians and owners need to be aware of.

This information was compiled from a number of veterinary sites, as well as newsletters and seminar transcripts.

Ditto's Story

reprinted with kind permission from Jan Elliott-Goin
CURIOHOUNDS Italian Greyhounds since 1987

The above information is simply informational. It's intent is not to replace the advice of a veterinarian nor to assist you in making a diagnosis of your pet. Please consult with your own veterinarian for confirmation of any diagnosis. Your pets life may depend on it.