Fibrous Osteodystrophy Research Articles

Osteodystrophy Fibrosa in a Goat Kid: Clinical Assessment and Management

Fibrous osteodystrophy is a mineral based caprine metabolic disease in which bones are resorbed as a result of prolonged hypersecretion of parathyroid hormone. High phosphorus or low calcium in the diet frequently contributes to fibrous osteodystrophy. This was a case of 8 months old kid presented to the Referral Veterinary Polyclinic of ICAR-IVRI with the history of anorexia and prominent bilateral facial swelling. History-taking revealed that owner was regularly feeding wheat bran and barley to the kid in the diet. On clinical examination, goat kid was found to be dull and depressed with rectal temperature lying within the normal reference range. Haematobiochemical analysis exhibited decreased level of serum calcium (7 mg/dl) and increased level of serum phosphorus (8.2 mg/dl). In dorsovental cephalometric radiography, facial bones appeared radiolucent. Treatment of osteodystrophy began with the administration of injection AD3E at the dose of 1 ml I/M for 5 days, injection pheniramine maleate (AvilTM) at 1 ml I/M for 5 days, syrup CalcimustTM at 5 ml PO for 5 days and injection Calcium sandozTM at 10 ml mixed with 200 ml NSS I/V SD and anabolic steroid Nandrolone at 50 mg SD. Concurrently, the owner was advised to immediately stop feeding wheat bran and barley to the kid. After 5 days of the treatment, kid’s condition started to improve and uneventful recovery was achieved 14 days post-therapy.

A case report of canine kidney dysplasia

The renal dysplasia consists of an abnormal development of the renal parenchyma and stroma, which gives it a whitish appearance and irregular surface, whitish color and firm consistency to the touch. Microscopically, the renal tubules have an adenomatous appearance, with the presence of immature or fetal glomeruli and tubules, primitive mesenchymal tissue with a myxomatous appearance and interstitial fibrosis. The renal dysplasia is considered a congenital and hereditary disease, mainly described in breeds such as Alaskan Malamute, Chow Chow, Golden Retriever, Lhasa Apso, Shih-Tzu, Miniature Schnauzer, Soft-Coated Wheaten Terrier and Standard Poodle. Dogs affected by the disease present polydipsia, polyuria, anorexia, vomiting, lethargy and weight loss. With disease progresses, secondary renal hyperparathyroidism and fibrous osteodystrophy may develop. In this case report, we describe a six-month-old Golden Retriever dog with a history of polydipsia, polyuria and growth retardation. A complete blood count, serum chemistry, urinalysis, abdominal ultrasound and ultrasound-guided percutaneous renal biopsy were requested, which were essential for establishing the diagnosis of renal dysplasia.

Bilateral renal dysplasia with systemic fibrous osteodystrophy in a four-toed hedgehog (Atelerixalbiventris)

A 4-month-old female four-toed hedgehog (Atelerix albiventris) presented with lethargy, anorexia, dyspnoea and weight loss. Following death, post-mortem computed tomography (CT) and an autopsy were performed. CT revealed that the external surfaces of bones, including the cranial bones and vertebrae, were rough and osteolytic lesions were present multifocally in the ribs and some appendicular bones. On gross examination, both kidneys were severely enlarged and, on cut sections, a few cysts (up to 1 mm diameter) were present in the medulla. The cervical, thoracic and lumbar vertebrae were diffusely enlarged with deformation of the intervertebral discs. Histologically, there were immature glomeruli and tubules and adenomatoid/atypical epithelium in the kidneys. These changes were interpreted as renal dysplasia. In the bones evaluated, the trabeculae were thinner than normal, decreased in number and surrounded by many osteoclasts, with abundant fibrous connective tissue between atrophied trabeculae. These changes were consistent with fibrous osteodystrophy. Although kidney diseases are common in four-toed hedgehogs, there are no reports of congenital renal diseases, including renal dysplasia. To the best of our knowledge, this is the first report of the clinical and pathological features of renal dysplasia with fibrous osteodystrophy in a four-toed hedgehog.

Osteodistrofia fibrosa decorrente de hiperparatireodismo secundário renal em cão senil

ABSTRACT Renal hyperparathyroidism stands out among the complications of kidney disease in dogs due to phosphorus retention with a predisposition to hypocalcemia, parathyroid hormone stimulation with mobilization of calcium from the bones, characterizing fibrous osteodystrophy, unusual in the elderly. The objective was to report it in 12-year-old Labrador with polyuria, polydipsia, and emesis for five months due to maxillary and mandibular volume increase, followed by loosely fixed teeth, and facial deformity. Blood tests showed anemia, thrombocytosis, azotemia, hypoalbuminemia and hyperphosphatemia and urinalysis showed low density, glycosuria, proteinuria, and moderate caudate and transitional epithelial cells. Oral x-rays showed loss of dental bone support and decreased bone radiopacity. Chest radiographs showed decreased density in the ribs and costochondral junction; on the other hand, organs of the cardiorespiratory system showed no changes. The electrocardiogram and echocardiogram did not show impairment. Abdominal ultrasound revealed kidneys with asymmetry, increased echogenicity of the cortical and poorly preserved cortico-medullary definition. Oral histopathology showed intense fibroplasia associated with bone reabsorption. Support therapy was instituted, but the patient died ten days after consultation. Thus, although uncommon in the elderly, fibrous osteodystrophy should be investigated in dogs with advanced-stage chronic kidney disease and, even with conservative therapies, the prognosis is unfavorable.

Renal secondary hyperparathyroidism should be considered a differential diagnosis in forensic cases where animal abuse is suspected

This case description reports an adult dog with multiple rib fractures that was initially suspected to be the victim of non-accidental trauma, but eventually was diagnosed with severe chronic interstitial nephritis and renal secondary hyperparathyroidism leading to fibrous osteodystrophy and multiple pathological fractures. The importance of the specific expertise of a dedicated expert panel on animal abuse is discussed. This case illustrates the significance of the identification of normal, pathological, and breed-related variations within an animal in addition to forensic expertise, emphasizing that the presence of multidisciplinary teams in an expert panel on animal abuse is crucial.

Investigating factors of metabolic bone disease in baboons (Papio spp.) using museum collections.

ObjectivesTo assess manifestations of metabolic bone disease (MBD) and their potential environmental and phenotypic factors in captive and non‐captive baboon (Papio spp.) specimens.Materials and methodsOur sample consisted of 160 baboon specimens at the Smithsonian's National Museum of Natural History accessioned from 1890 to 1971. Combining cranial indicators of MBD and the museum's historical data, we examined factors contributing to likely instances of MBD. We used binomial‐family generalized linear models to assess differences in MBD frequency by environment (captive, non‐captive), specimen accession year, and skin color (light, medium, dark).ResultsIndicators of MBD were most frequently observed in captive baboons, with a decrease in MBD frequency over time. Fifteen non‐captive individuals showed indicators of MBD, which are the first published cases of MBD in non‐captive nonhuman primates (NHPs) to our knowledge. The most common MBD indicators were bone porosity (n = 35) and bone thickening/enlargement (n = 35). Fibrous osteodystrophy was observed frequently in our sample, likely relating to nutritional deficiencies. We found no association between exposed facial skin color variation and MBD.ConclusionsOur findings are consistent with historical accounts of MBD prevalence in captive facilities, especially earlier in the 20th century. A decrease in MBD prevalence later in the 20th century likely reflects improvements in housing, diet, and veterinary care in captive settings. Causes of MBD development in non‐captive baboons should be further explored, as understanding the potential health impacts that anthropogenic environments impose on NHPs is imperative as humans increasingly alter the natural world in the 21st century.

Fibrous Osteodystrophy, Chronic Renal Disease, and Uterine Adenocarcinoma in Aged Gray Mouse Lemurs (Microcebus murinus).

The gray mouse lemur (Microcebus murinus, GML) is a nocturnal, arboreal, prosimian primate that is native to Madagascar. Captive breeding colonies of GMLs have been established primarily for noninvasive studies on questions related to circadian rhythms and metabolism. GMLs are increasingly considered to be a strong translational model for neurocognitive aging due to overlapping histopathologic features shared with aged humans. However, little information is available describing the clinical presentations, naturally occurring diseases, and histopathology of aged GMLs. In our colony, a 9 y-old, male, GML was euthanized after sudden onset of weakness, lethargy, and tibial fracture. Evaluation of this animal revealed widespread fibrous osteodystrophy (FOD) of the mandible, maxilla, cranium, appendicular, and vertebral bones. FOD and systemic metastatic mineralization were attributed to underlying chronic renal disease. Findings in this GML prompted periodic colony-wide serum biochemical screenings for azotemia and electrolyte abnormalities. Subsequently, 3 additional GMLs (2 females and 1 male) were euthanized due to varying clinical and serum biochemical presentations. Common to all 4 animals were FOD, chronic renal disease, uterine adenocarcinoma (females only), cataracts, and osteoarthritis. This case study highlights the concurrent clinical and histopathologic abnormalities that are relevant to use of GMLs in the expanding field of aging research.

Non-Renal Lesions of Uraemia in Domestic Cats

Uraemia is a clinical syndrome caused by an increase in uraemia-associated toxins in the bloodstream as a consequence of intrinsic kidney or lower urinary tract diseases. Cats seem to be more affected by urinary tract diseases than dogs, particularly considering that chronic kidney disease (CKD) is one of the most important conditions in cats. Considering the lack of information on the systemic lesions of uraemia in cats, the aim of this study was to investigate the prevalence and clinical and pathological aspects of non-renal lesions in uraemic cats, with special attention to the differences between cats and dogs. Cats necropsied between 2000 and 2019 (n=1,330) were investigated for urinary tract diseases and non-renal lesions of uraemia. The prevalence of uraemic cats with non-renal lesions (n=78) was 5.8%. Adult, elderly and male animals were predominantly affected. Anorexia, apathy and vomiting were the most common clinical signs and CKD was observed in the majority of uraemic cats. Pulmonary oedema was the most frequent non-renal lesion identified. In contrast with previous reports, haemorrhagic and ulcerative gastritis was frequently observed, whereas soft tissue mineralization and parathyroid hyperplasia were uncommon features. Fibrous osteodystrophy was not observed. Cats with urinary tract diseases did not have as wide a variety of non-renal uraemic lesions as uraemic dogs and multisystemic manifestation of uraemia was observed in only 24.4% of cases.

Mineralização vascular associada a distúrbio mineral ósseo em paciente com doença renal crônica - relato de caso

A doença renal crônica (DRC) é uma afecção comum na rotina clínica de animais de companhia e sua presença está associada há alterações polissistêmicas, como distúrbios minerais ósseos relacionados a ação de toxinas urêmicas como o paratormônio (PTH). O desequilíbrio da homeostasia causada pelo excesso do PTH pode cursar com repercussões clínicas como osteodistrofia fibrosa, calcificações teciduais e progressão da doença renal. Objetiva-se com o presente trabalho, descrever o caso de um paciente canino de quatro anos de idade, portador de DRC associada a distúrbio mineral ósseo com repercussões como osteodistrofia fibrosa e alterações cardiovasculares como hipertensão arterial sistêmica, hipertrofia concêntrica do ventrículo esquerdo e calcificações vasculares.

Atypical fibrous osteodystrophy in a lactating mare

Secondary nutritional hyperparathyroidism is a condition caused by increased serum phosphorus levels compared to calcium, which leads to an growth in the production of the PTH, parathyroid hormone of the parathyroid glands, increasing the osteoclastic activity withdrawing calcium from the bones, forming fibrous tissue, known as osteodystrophy, usually in the facial bones. The goal of this paper was to report an atypical case of hyperparathyroidism and fibrous osteodystrophy in a 8-year-old lactating mare, whose face enlargement was focal and nodular, involving of the right nostril and incisor bones, causing breathing and feeding difficulties. In the radiological examination the image was suggestive of osteosarcoma, with Doppler showing superficial circulation to the nodular mass. Treatment with cisplatin and calcium supplementation was performed. The the patient died three days after a temporary tracheostomy and a biopsy procedure. At necropsy parathyroid’s lymphadenomegaly was confirmed by histopathology, and osteodystrophy in the maxillary region was observed. In this case, hyperparathyroidism did not presented itself as a typical form, and there is a need for further studies on possible atypical forms of the disease on tropical countries.

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.

Combined metabolic bone diseases, medullary aplasia and bacterial pneumonia in broad-snouted caiman (Caiman latirostris)

Seven juvenile broad-snouted caiman (Caiman latirostris), bred in captivity and subjected to a diet deficient in minerals and vitamins during the first months of life, developed intense cachexia and generalized loss of bone stiffness. In a histopathological evaluation, the proliferation of stellate elongated cells with scarce and eosinophilic cytoplasm in the middle of a loose fibrillar and eosinophilic extracellular matrix was observed, especially in the long bones, which was compatible with fibrous osteodystrophy. Diffuse disorganization of the chondrocyte columns of the endochondral ossification zones with a light multifocal presence of dilated blood capillaries characterized rickets. The bone marrow of the animals revealed intense replacement of active myeloid tissue with adipose tissue and rare promyelocytes, which were compatible with marrow aplasia. Additionally, caseous lesions were evident in the lungs of three animals and the histopathological findings and microbiological analysis were compatible with a bacterial pneumonia. The present work gives a detailed anatomopathological description of the case.

Relationship between Osteoporosis and Periodontal Diseases after Radiation Therapy

Background: The relationship between osteoporosis and periodontitis was valued gradually, but till now the association between them remains a controversial issue, this correlation and potential mechanisms linking of these two bone-loss diseases are still uncertain (1).Aim: Our study was directed to investigate the association between Osteoporosis and Periodontal diseases after Radiation therapy in animal clinically and histologically.Methods: A total of (63), adult female Albino rats of average age of 6 months and average weight (230-250 gm) provided by(NCRRT) were used. The animals were divided into 7 groups of 9 rats each, in group 1, rats were used as control.While, in group 2, the rats received radiation only. In group 3, the rats for this group were injected by Depo-Medrol subcutaneous in a dose of 7 mg/kg once a week for 8 weeks for induction of osteoporosis. In group 4, periodontitis was induced by for this group by a ligature (3-0 silk suture) were placed around the cervix of mandibular incisors. In group 5, the rats received radiation and osteoporosis was induced for this group. In group 6, the rats received radiation and periodontitis was induced for this group. In group7, radiation was received by rats were suffered from osteoporosis and periodontitis.Results: The radiation+periodontitis+osteoporosis group showed the lowest bone density mean value at different intervals of the study. Osteoporosis and radiation group revealed more inflammatory and focal fibrous osteodystrophy than other groups. Osteoporosis and radiation group showed more osteoclasts and more fibrous and thinner trabeculae than osteoporotic group.

Fibrous osteodystrophy in a Lavradeira filly associated with Brachiaria humidicola ingestion

Fibrous osteodystrophy in horses is due to low calcium ingestion, high phosphorus ingestion, high oxalate ingestion, or a combination of these. Tropical forages usually have high levels of oxalates, which prevents calcium absorption and results in calcium deficiency. The present study reports a case of fibrous
 osteodystrophy in a filly associated with Brachiaria humidicola ingestion. A 1-year-old filly of the Lavradeiro breed was maintained on a pasture with B. humidicola and presented bilaterally enlarged facial bones, a high respiratory rate, noises during inspiration-expiration and dyspnea. Based on its history, age and clinical
 signs, the diagnosis was fibrous osteodystrophy associated with B. humidicola ingestion. Treatment was based on the administration of calcium gluconate, vitamins A, D and E, and clenbuterol. All other horses were transferred to a field with native forage and were supplemented with calcium carbonate. In Roraima state,
 the use of tropical forages in equine feeding is very common and represents a risk factor for the occurrence of fibrous osteodystrophy due to the continuous ingestion of oxalates. In horses, the diagnosis is achieved by clinical exam and treatment aims to correct the imbalance in Ca:P ratio, associated with support therapy.

Clinical case report on nutritional dystrophy in goats at S. A. Quadary Veterinary Teaching Hospital, CVASU, Chittagong

Background: Nutritional fibrous osteodystrophy may be developed due to dietary deficiency of calcium or dietary excess of phosphorus. Fibrous osteodystrophy (FOD) provokes hyperostotic distortion of cancellous bones, conjunctive tissue proliferation, and poor mineralization of bone. The objectives of this study were to report the clinical characteristics and therapeutic management of FOD in goats. Materials and methods: Four out of 8 Jamnapari goats developed fibrous osteodystrophy in a small scale intensive household farm in Chittagong. The age range of the affected goats was 4-5 months. The feeding history of goats was primarily wheat bran, gram and pea husk. Blood sample from all affected and non-affected animals and feed sample from household farm were collected for laboratory analysis. Fibrous Osteo-dystrophy was primarily diagnosed by observing clinical signs of mandibular and maxillary enlargement, pain on pressure at the enlarged bone, protruded tongue and dyspnea which was then confirmed by high level of phosphorus in serum evaluation. Results: The calcium and phosphorus contents in the sampled gram, pea husk and bran were 0.5%, 0.3% and 0.5%, and 0.71%, 0.49% and 0.61%, respectively. Most of the affected animals had increased serum levels of phosphorus, glucose and alkaline phosphatase and decreased level of calcium. Based on the clinical findings and the laboratory report, the cases were diagnosed as fibrous osteodystrophy due to nutritional imbalance in diet. The owner was advised strictly to stop providing any bran to animals (affected and healthy). Affected animals were additionally treated with calcium preparation vitamin ADE, ketoprofen, protein, and penicillin-streptomycin combination. Conclusion: Treatment of fibrous osteodystrophy required a long time recovery along with balanced ration. A combined therapy of calcium and vitamin D and protein preparation is effective for treatment along with adequate green grass and balanced rations.

Paradise lost: Evidence for a devastating metabolic bone disease in an insular Pleistocene deer

PurposeThis communication reports skeletal pathology in a Pleistocene endemic deer from the Mavromouri caves of Crete. Materials287 bones and bone fragments from Mavromouri caves are compared to 2986 bones from Liko Cave. MethodsBones were evaluated macroscopically, and measurements were made of morphometric characteristics of limb long bones. Representative bone specimens were examined radiographically and histologically. ResultsMacroscopic hallmarks were loss of bone mass and increased porosity. The long bones were brittle, some of them having thin cortices, and others reduction of medullary cavities that contain dense Haversian tissue. The flat bones were spongy and fragile. Erosions of the metaphyses and articular surfaces were noted. Histological findings included: sub-periosteal resorption; loss of lamellar bone; enlargement of vascular canals; and remodeling of cortical bone. Two types of fibrous osteodystrophy were recognized in skeletal remains, subostotic and hyperostotic. ConclusionsThe deer of Mavromouri caves were affected by severe metabolic bone disease, likely nutritional secondary hyperparathyroidism. We hypothesize a multifactorial cause, including overgrazing, flora senescence, soil mineral deficiencies, and a prolonged period of climate extremes, degrading the Cretan deer habitat. ValueThis is the first evidence of a metabolic bone disease causing this level of destructive pathology in an insular fossil deer. LimitationsThe lack of absolute chronometric dates for the site limits potential linking with the prevailing environmental conditions. Suggestions for further researchInvestigation of similar skeletal pathologies at other islands or isolated habitats is advised.

Nutritional fibrous osteodystrophy with chondroid metaplasia in a Nile monitor, Varanus niloticus

Carnivorous reptiles are not usually thought of as being prone to metabolic bone disorders. A constant diet lacking in calcium or bone and/or high in phosphorus or low in vitamin...

Metabolic bone diseases in a wild crab-eating hawk and a caboclo hawk in Paraiba

The amount of research on metabolic bone diseases in commercial birds is considerable, however, there is a large gap in the knowledge of these diseases in wild birds. Aspects related to diet are the main factors that cause these diseases, such as: vitamin D deficiency, insufficient calcium intake, or imbalance of calcium and phosphorus in the diet, and problems in the absorption and metabolism of these compounds. This study reports two cases of bone diseases in birds of the order Accipitriformes, which are wild in the state of Paraiba, a crab-eating hawk with rickets, and a caboclo hawk with fibrous osteodystrophy. The diagnosis in both cases was based on macroscopic and microscopic findings. These reports are subsidies for the bird clinic of the order Accipitriformes and for the maintenance of these birds in nurseries and zoos. This study demonstrates the need for further studies to assess whether such cases can be used as indicators of environmental imbalance.

Evaluation of promising biochemical markers of nutritional osteodystrophy in goats

Fibrous osteodystrophy (FO), a metabolic bone disorder, has been reported in different animal species with variable susceptibility. Albeit, it is commonly reported in horses, the clinical disease is also recorded globally in goats. Diagnosis of fibrous osteodystrophy is mainly based on various clinical examination methods including biochemical alterations which can be adopted as routine diagnostic method. Therefore, the present study was aimed to investigate calcium: phosphorus (Ca:P) ratio and alkaline phosphatase (ALP) activity as biochemical diagnostic markers in goats diagnosed for fibrous osteodystrophy by clinical and radiological examinations. Blood samples were obtained from 11 goats diagnosed to have clinical fibrous osteodystrophy and 10 healthy goats, and used for harvesting serum. Goats with fibrous osteodystrophy revealed markedly elevated serum phosphorus level and ALP activity, and lowered calcium level in comparison to healthy goats. Remarkably lower serum Ca:P ratio was also observed in diseased goats. Radiological examination of skull of diseased goats revealed radio-lucent areas on the mandible as well as the upper jaw. In conclusion, marked reduction in Ca:P ratio and elevation in ALP activity could be promising biochemical diagnostic marker of fibrous osteodystrophy in goats.

Causes of death of domestic cats in a veterinary hospital of Uberlândia, Minas Gerais state: a retrospective study

Os gatos apresentam papel relevante como animal de estimação na sociedade atual. Neste sentido, o conhecimento das principais enfermidades e causas de morte desses animais é fundamental para prevenção de várias patologias. No entanto, quanto ao gato doméstico, essas pesquisas ainda são escassas na medicina veterinária. Assim, este trabalho realizou um estudo retrospectivo das causas de morte de gatos registradas das necropsias efetuadas pelo Laboratório de Patologia Animal da Universidade Federal de Uberlândia, em um período de 36 anos, no qual 350 gatos foram necropsiados. As doenças do sistema digestivo foram as mais frequentes (48 gatos – 13,71%) e destas, a lipidose hepática foi a etiologia de maior ocorrência (18,75%). O sistema respiratório foi o segundo mais afetado (10,86%), sendo pneumonia aguda, edema pulmonar e hérnia diafragmática as principais doenças deste sistema responsáveis pela morte de gatos. Outras causas de óbito importantes foram raiva, carcinoma de células escamosas, osteodistrofia fibrosa, fraturas e traumatismos, choque hipovolêmico e síndrome urológica felina. Este tipo de análise pode fornecer informações básicas sobre as enfermidades que mais acometem os felinos de uma determinada região, contribuindo para que os profissionais médicos veterinários passem a adotar as respectivas ações de prevenção e controle.