Causes:  The disease is caused by an autosomal recessive trait. Both parents must be affected or be carriers, i.e. have at least one gene for  CMO, in order to transmit the condition to their offspring.  Carriers and asymptomatic affected dogs can pass the disease to their offspring even if they don’t display clinical signs. 

Symptoms:  The first signs appear usually at three to four months of age but may be present as early as 4 weeks and as late as 9 months.  The affected puppies have difficulty opening their mouths, swallowing and chewing or when their mouth is examined.  The opening of the mouth is reduced.  Radius and ulna are occasionally involved. Some puppies may show considerable amounts of pain. They may at the same time run a fever or show lethargy. Weight loss can occur because of the pain of eating.  On palpation, the bone of the affected area feels dense, hard and rough and sometimes warm to the touch. Some atrophy of the muscles of the head and jaw can occur. 

Diagnosis: The diagnosis is made by radiography of the skull. Only x-rays can detect cases where a dog is affected but only so mildly that the dog never presents symptoms. 

The affected bones will show excessive growth and thickening.  Radiographs should be repeated every three months to monitor the condition. Blood samples may also show increased serum calcium levels and some enzymes such as serum alkaline phosphatase. 

Treatment: There is no known cure for the disease but symptoms can be relieved by the administration of medications such as anti-inflammatory drugs going from simple aspirin to corticosteroids under the supervision of a veterinarian. It might be helpful to use soft food and even tube feeding if there is much pain. Euthanasia might be necessary in very severe cases when the animal is in great pain and cannot eat. Dogs with no symptoms don't require treatments. 

Prognosis: The condition is usually self-limiting and the dog recovers at about one year of age after 4 to 10 months of treatment. Bone growth may even recede to the point where jaw remodelling is nearly total. 

Prevention:  The only way to prevent the disease is to remove all affected dogs and carriers from breeding programs. Unfortunately, it is only when there are affected puppies that we can identify carriers as there is no genetic marker as yet.  To make sure no affected dog is included in a breeding program, the West Highland Anomaly Task Council (WATCH) recommends "that all radiographs be done at the appropriate age because without radiographs, mild cases can and will be missed". 
 

Further reading:

Ackerman, L. Keeping your West Highland White Terrier Healthy.  Project TEACH Course Notes for Westie Breeders. Version 1.05  Pet Health Initiative, 1996.

Guaguere-Luca J, Smal D, Mialot M.  Localisation ulnaire d'un cas d'ostéopathie craniomandibulaire chez un West Highland White Terrier. Prat Méd Chir Anim 1995 30: 385-390.

Gutteling J, Hazewinkel HA. Hyperostosis of the Mandibles in a West Highland White Terrier. Tijdschr Diergeneeskd. 1986 Dec 15 ;111(24) :1246-8. Dutch.

Padgett GA, Mostosky UV : The Mode of Inheritance of Craniomandibular Osteopathy in West Highland White Terrier Dogs. Am J Med Genet 1986 Sep;25(1):  9-13. 

West Highland Anomaly Task Council, Inc. (Watch). Understanding and Reducing Genetic Disease in West Highland White Terriers, 2nd ed., 1991.
 

Useful links:

http://barkbytes.com/medical/med0071.htm

http://www.westieclubamerica.com/health/cmo.html

http://www.vetinfo.com/dcranio.html

http://www.offa.org/ofaothr.html   Database maintained by OFA
 

Author: Monique Courtois
Gailuron Kennel
Revised by Dr Yves Gosselin, D.M.V.