Maxillomandibular Deformity in a Canine with Fibrous Osteodystrophy Secondary to Chronic Kidney Disease

Background: Cases of renal fibrous osteodystrophy are usually associated with nutritional causes, which of renal causes are considered uncommon in dogs. This disorder is characterized by the intense proliferation of fibrous connective tissue in bones, impairing bone stiffness. The aim of this study was to report a case of fibrous osteodystrophy secondary to chronic kidney disease in a canine with a "rubber jaw" facial deformity.Case: A 4-year-old male unneutered mongrel dog weighing 5.2 kg had a history of apathy, progressive weight loss and vomiting for one month, and polyuria and polydipsia for more than three months. In addition, the owner complained about the deformed appearance in the muzzle region of the animal, which was evidenced flexibility of the same, with a displacement of the mandible and maxilla on physical examination, similar to the "rubber jaw". Blood tests revealed macrocytic anemia, elevated total plasma proteins, and lymphopenia-associated neutrophilia, as well as hyperphosphatemia (24 mg/dL), uremia (283.6 mg/dL) and increased creatinine (8.6 mg/dL), ALT (143.2 UI/L) and alkaline phosphatase (3222.2 UI/L), while calcium (8.8 mg/dL) and albumin (1.9 g/dL) were decreased. A serological test for visceral leishmaniasis was also performed, which was negative. Abdominal ultrasound imaging revealed kidneys with alterations in tissue architecture, increased thickness and complete loss of cortico-medullary relationship, while the parathyroid gland was enlarged and spindle-shaped. Cranial radiography showed marked radiopacity of the bilateral maxillary bones, with destruction of the nasal, turbinate and frontal bones, as well as loosening of the teeth and destruction of the mandibular bone matrix, characterizing an aspect of “rubber jaw”. Based on the history, history and evidence of azotemia, hyperphosphatemia and loss of facial bone density, the diagnosis of fibrous osteodystrophy secondary to chronic kidney disease associated with hyperparathyroidism was concluded.Discussion: The clinical and laboratory findings reported in the present study were similar to those described in dogs with renal fibrous osteodystrophy associated with hyperparathyroidism. In the presence of azotemia, the patient was in stage 4 of chronic kidney disease which, despite investigating the infectious etiology, which was negative, remained unknown. Along with chronic kidney disease, the observation of hyperphosphatemia associated with hypokalemia contributed to the clinical investigation, whose pathophysiological mechanisms of this disorder were discussed in this study. The organic alterations observed in the patient's imaging examination coincided with the pathophysiological processes of renal fibrous osteodystrophy. The findings of renal and parathyroid alterations on ultrasound, as well as the damage to the bone matrix, maxillomandibular deformity and loss of bone support evidenced on cranial radiography, led to the conclusion of the diagnosis of renal fibrous osteodystrophy secondary to hyperparathyroidism. Despite the recommended symptomatic therapy, the patient died within 24 hours of hospitalization, and it was not possible to perform a necropsy. This report is highlighted by the occurrence of bone deformity at the maxillary and mandibular level, as a result of renal dysfunction in a young canine, alerting to the importance of complementary exams for proper diagnosis