Craniomandibular osteopathy in a bullmastiff

Abstract

A 6-month-old bullmastiff was presented with bilateral painful swellings of the mandible. Craniomandibular osteopathy was diagnosed based on skull radiographs and histological findings from bone biopsies. Treatment consisted of meloxicam to alleviate the pain. Three months later, the dog was pain free without medication or palpable change in the mandible.

A 6-month-old, intact female, 30 kg bullmastiff was referred to the Western College of Veterinary Medicine (WCVM) with a 1-month history of bilateral, painful swellings of the mandible, halitosis, and difficulty eating dry food. The referring veterinarian had submitted blood to the WCVM clinical pathology laboratory. Serum phosphorus and alkaline phosphatase were slightly increased (2.88 mmol/L; reference range 0.63 to 2.41 mmol/L and 131 U/L; reference range 18 to 2.41 U/L, respectively), a mild hypoalbuminemia was present (27 g/L; reference range 28 to 38 g/L), and calcium levels were normal (2.84 mmol/L; reference range 1.91 to 3.03 mmol/L). The referring veterinarian began treatment with cephalexin (Nu-Cephalex; Nu-Pharm, Richmond Hill, Ontario), 25 mg/kg bodyweight (BW), PO, q8h, 6 d prior to the dog's arrival at the WCVM.

A physical examination revealed a dog in good body condition but with bilateral enlargement of the mandibular rami, tense facial muscles, and enlarged submandibular lymph nodes. According to the owner, there had been no change in the dog's condition during the week since the last veterinary examination. Pain was elicited when palpating the jaw, but it was not consistently evident upon opening the mouth. The enlarged, firm mandible was not palpably warm. The dog's body temperature was normal and there were no signs of systemic illness.

The dog was anesthetized and skull radiographs revealed bilateral bony proliferation of the mandible with no interference of the zygomatic arch or the temporomandibular joints (Figure 1). On histopathologic evaluation, biopsies of mandibular bone consisted of interconnected trabecula of woven bone, proliferative endosteal new bone, and abundant osteoclasts on the bone surface. The marrow spaces were filled with loose connective tissue and few foci of dense infiltrations of inflammatory cells (predominantly neutrophils, a few plasma cells, and lymphocytes). There was no evidence of a neoplastic process.

Figure 1. Lateral (A) and ventrodorsal (B) skull radiographs of a 6-month-old bullmastiff with craniomandibular osteopathy illustrating bony proliferation of the mandibles. Note that the temporomandibular joints are not involved.

Figure 1. Continued.

Treatment consisted of pain management to relieve the discomfort when eating. Initially, metacam (Meloxicam; Boerhinger Ingelheim, Burlington, Ontario), 0.1mg/kg BW, PO, q24h, was administered for 14 d. The frequency of dosing was then dropped to q48h for 7 d, and then as needed. On a 3-month follow-up, the owner indicated that the dog had not received metacam for about 1 mo and seemed to be pain free. There did not appear to be any changes in the size of the mandibular swellings at that time.

Craniomandibular osteopathy (CMO), also known as lion's jaw, is a nonneoplastic, proliferative bone disease affecting primarily bones of the head (1) and occasionally long bones (2). Bones commonly involved include those of the skull; namely, the parietal and occipital bones, the tympanic bulla and the mandibular rami, and the temporomandibular joint. It is a self-limiting disease occurring in dogs 3 to 8 mo of age (1). Craniomandibular osteopathy can affect either gender and is seen predominantly in the Scottish terrier, West Highland white terrier, Boston terrier, cairn terrier (2), and other terrier breeds (1). While CMO is rare in large breed dogs, it has been reported in the Labrador retriever (3,4), Great Dane (5), Doberman Pinscher (6), boxer (7), Shetland sheepdog (8), Pyrenean mountain breeds (9), and in an English bulldog (10). There is only 1 previously reported case in a bullmastiff (1).

While the etiology of CMO is unknown, an autosomal mode of inheritance in West Highland white terriers has been suggested (11). The occurrence in nonterrier breeds indicates that other factors may be playing a role, such as bacterial (Escherichia coli) or viral (canine distemper virus) (1) infections. A recent study suggested that distemper virus infection could be the initiating cause of CMO without causing the classical clinical signs associated with the virus infection (12). More recently, a study of 12 Irish setters with canine leukocyte adhesion deficiency (CLAD) showed that 7 of the dogs had radiographic evidence of CMO (13). Since CMO is rare in this particular breed, the study introduced yet another possible association with CMO.

Dogs having CMO are commonly presented to a veterinarian due to their having discomfort while eating, pain upon opening the mouth, intermittent pyrexia, excessive salivation, and bilateral firm swellings of the mandible (14). The clinical signs in the case reported here are typical of the disease. Some dogs have restricted jaw movement and atrophy of the muscles of mastication (1). Differential diagnoses based on clinical findings include osteomyelitis, traumatic periostitis, metabolic disorders, and neoplasia. A diagnosis of CMO can often be made based on lateral and ventrodorsal radiographic views illustrating symmetrically enlarged mandibular bodies due to dense osseous proliferation (2,3). Enlarged tympanic bulla (15), fusion of the temporomandibular joint (14), or auditory canal involvement (1) may also be evident. In large breed dogs, the lesions are usually confined to the mandible (1), while the parietal crest, frontal, lacrimal, and maxillary bones may be affected in small breed dogs (2,4). The radiographic findings in this case were highly characteristic of those reported for large breed dogs.

Histopathologic study of bone biopsies is also useful in confirming a diagnosis of CMO, especially in atypical cases. These results generally indicate early inflammation, osteolysis of the periosteal or subperiosteal region (15), and a generalized thickening of bony trabecula (14).

There are no specific clinical pathologic abnormalities associated with CMO. Complete blood cell counts and serum biochemistry values are usually within the normal reference range. However, there may be an increase in serum alkaline phosphatase (AP), hyperphosphatemia, and an unexplained hypogammaglobulinemia or alpha2 hyper-globulinemia (1,6,7,8). An increase in serum AP and the hyperphosphatemia can be explained as normal findings, since in growing dogs, these values often exceed adult reference ranges (1).

Treatment of CMO generally consists of pain management allowing the dog to eat without much discomfort. Providing IV fluids and nutritional support in patients that are unable to eat properly is critical. Corticosteroids (8,15) have been used but results are inconclusive. Surgical attempts to remove excess bone have been unsuccessful. One report describes a rostral hemimandibulectomy as a salvage procedure when the jaws could not be opened (1).

In itself, CMO usually does not cause death, but animals have been euthanized on account of severe pain and malnutrition resulting from the inability to eat (2). The prognosis is guarded when extensive bone changes involve the temporomandibular joint. Some regression of the bony changes may occur following growth plate closure (7).

A recent study described a condition called calvarial hyperostotic syndrome (CHS) in young bullmastiffs (16). This disease is also a nonneoplastic, proliferative bone disease of the skull with similar clinical, radiographic, and histopathologic characteristics to CMO. The laboratory results are within the normal reference range. However, CHS may have a sex and breed predisposition, having been described only in male bullmastiffs. Skull lesions are frequently not bilateral or symmetric, and the mandible tends to be unaffected. The diagnosis in this dog was CMO, not CHS, because of the signalment and the bilateral mandibular lesions.