Description: CMO, also known as the lion’s jaw, is a non-neoplastic, proliferative bone disease affecting the primary bones of the head. It is characterized by excessive growth of the jawbone (irregular proliferation of the lower jaw and tympanic bull) and rarely long bones (Huchkowsky, 2002; Taylor et al. 1995). CMO dogs generally exhibit eating problems, mouth opening pain, occasional fever, and severe bilateral jaw swelling (Huchkowsky, 2002). It is also commonly associated with excessive salivation and anorexia resulting from eating pain or mechanical inability to open the mouth (Taylor et al., 1995). Some dogs are affected by limited jaw movement and chewing muscle atrophy. The diagnosis of CMO is based on lateral and ventrodorsal radiographs showing symmetrically enlarged mandibles due to bone proliferation. These manifestations occur between the fourth and eighth month of life. The disease is caused by a mutation in the SLC37A2 gene. SLC37A2 is a glucose-6-phosphate transporter that is expressed in many tissues, particularly bone-related tissues e.g. in osteoclasts. It plays a central role in maintaining glucose homeostasis in major types of cells involved in osteogenesis. The disorder disrupts glucose homeostasis in bone development and leads to hyperostosis.
Inheritance: autosomal dominant with incomplete penetrance
Mutation: c.1332C>T in 15 exon SLC37A2 gene
Sample: EDTA whole blood (1.0 ml) or 2 buccal brushes. For official purposes, the confirmation of the dog’s identity by Veterinarian is recommended.
The analysis is suitable for the following breeds: West Highland White Terriers, Cairn Terriers, and Scottish Terriers, Jack Russel Terriers
Notes: The predicted heredity of CMO was autosomal recessive. However, new studies have confirmed that heterozygotes also suffer from the symptoms described, but the symptoms are milder. Other breeds showing CMO were also tested: Bullterrier, Curly Retriever, Border Collie, Australian Terrier, Basset Hound, German Wirehaired Pointer, and Bobtail. None of them had this mutation (Hytönen et al., 2016).