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

Abstract

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 ...

Fibrous osteodystrophy due to secondary renal hyperparathyroidism in a senile dog

“…Regarding the systemic clinical signs presented by the reported patient, they corroborated those described in the eight-month-old young dog by Castro et al (2007), as well as in the two elderly dogs specified by Alves et al (2014) and Freitas et al (2017), including the osteopenic disorder, characterized by osteoclastic reabsorption of bone trabeculae associated with proliferation of fibrous connective tissue and deficient mineralization of osteoids (Polzin et al, 2011;Waller et al, 2019). In the patient of the present report, the severity of fibrous osteodystrophy could be observed by mandibular and maxillary radiographic images, since the bone demineralization is only detected radiographically when there is a loss of 30% to 50% of bone mass (Lazaretti et al, 2006).…”

“…The kidneys play a key role in maintaining the organic system, and eventual imbalances interfere with homeostasis, directly affecting the quality of life and survival of those affected. In this context, chronic kidney disease (CKD) is the most diagnosed nephropathy in senile dogs (Castro et al, 2007;Waller et al, 2019), characterized by the progressive and irreversible loss of structural and/or functional capacity of one or both kidneys, in a course of more than three months (Bartges, 2012;Dunaevich et al, 2020).…”

“…In this sense, although unusual in dogs (Alves et al, 2014) and cats seniles (Nagode et al, 1996), the exacerbated increase in PTH can mobilize calcium from the bones, causing fibrous osteodystrophy, also known as renal osteodystrophy (Alves et al, 2014;Waller et al, 2019), characterized by an osteopenic disorder with intense proliferation of fibrous connective tissue. Also, in CKD there is a decrease in calcitriol levels, further contributing to hypocalcemia, increasing the release of PTH (Alves et al, 2014).…”

“…Fibrous osteodystrophy can also be caused by nutritional disorders such as a diet rich in phosphorus and low in calcium (Polzin, 2011;Freitas et al, 2017;Silva et al, 2020). This condition mainly affects the bones of the face, in particular the maxillary and mandibular region ("rubber jaw") of growing animals (Rusenov, 2010;Polzin, 2011;Alves et al, 2014;Waller et al, 2019) due to incomplete skeletal maturation in this age group (Rusenov, 2010;Polzin, 2011), causing facial deformity (Freitas et al, 2017). Oral bone resorption probably occurs due to excess PTH combined with increased concentration of fibroblast growth factor 23 (FGF 23), which increases renal phosphorus excretion and suppresses the synthesis of 1,25calcitriol by decreasing the activity of 1αhydroxylase enzyme in the kidneys (Polzin, 2011;Waller et al, 2019).…”

“…This condition mainly affects the bones of the face, in particular the maxillary and mandibular region ("rubber jaw") of growing animals (Rusenov, 2010;Polzin, 2011;Alves et al, 2014;Waller et al, 2019) due to incomplete skeletal maturation in this age group (Rusenov, 2010;Polzin, 2011), causing facial deformity (Freitas et al, 2017). Oral bone resorption probably occurs due to excess PTH combined with increased concentration of fibroblast growth factor 23 (FGF 23), which increases renal phosphorus excretion and suppresses the synthesis of 1,25calcitriol by decreasing the activity of 1αhydroxylase enzyme in the kidneys (Polzin, 2011;Waller et al, 2019). According to Nagode et al (1996), so far, there are no scientific explanations for the mandibular and maxillary bones being predisposed to diffuse density loss.…”