Desordens hiperostóticas em American Bully / Hiperostotic disorders in american bully

O complexo de desordens hiperostóticas é uma condição rara e autolimitante, que tem as mesmas características histopatológicas, que cursa com proliferação óssea de caráter não neoplásico. Acomete cães jovens de raças distintas, com variabilidade quanto ao tipo de proliferação óssea e quanto aos ossos acometidos. O complexo é composto pela osteopatia craniomandibular, hiperostose da calota craniana e osteodistrofia hipertrófica. Podendo estar presente nos ossos da calota craniana, mandíbulas, coluna cervical e esqueleto apendicular. O presente relato, descreveu o quadro de uma cadela, da raça American Bully, não castrada, três meses de idade, que foi atendida com queixa de aumento de volume doloroso das mandíbulas, hiporexia e sialorreia há 15 dias, apresentando ao exame físico, amplitude de movimento diminuída e sensibilidade dolorosa da articulação temporomandibular, espessamento firme bilateral do crânio em região de fossa temporal, espessamento palpável de consistência firme das mandíbulas e crepitação respiratória. Após avaliação clínica e realização de exames complementares, chegou-se ao diagnóstico presuntivo, de complexo de desordens hiperostóticas. Foi instituído como conduta terapêutica o suporte analgésico, sendo eficaz para a manutenção das necessidades fisiológicas até a paciente alcançar a fase adulta. O prognóstico para esta paciente foi considerado bom, uma vez que não havia indícios de anquilose da articulação temporomandibular e/ou manifestações neurológicas.

The complex of hyperostotic disorders is a rare and self-limiting condition, which has the same histophatological characteristics, which courses with non-neoplastic bone proliferations. It affects young dogs of different breeds, with variability the bones affected. The complex is composed of craniomandibular osteopathy, calvarial hyperostotic syndrome and hypertrophic osteodystrophy. It may be present in the bones of the skullcap, jaws, cervical spine and appendicular skeleton. The present report describes the condition of a female dog, American Bully breed, entire, three months old, with a complaint of painful swelling of the jaws, hyporexia and drooling for 15 days, presenting on physical examination, reduced amplitude and pain of the temporomandibular joint, bilateral firm thickening of the skull in the temporal fossa region, palpable firm-consistent thickening of the mandibles and respiratory crackle. After clinical evaluation and complementary tests, a presumptive diagnosis of hyperostotic disorders complex was reached. It was instituted pain management as a treatment, being effective for the maintenance of physiological needs until the patient reaches the adulthood. The prognosis for this patient was considered good, since there was no evidence of temporomandibular joint ankylosis and/or neurological manifestations.

A case of drug-resistant staphylococcal para-aural abscess treated with photodynamic therapy in a West Highland White Terrier presenting with chronic otitis and craniomandibular osteopathy.

A 10-year-old canine with chronic unilateral otitis and a history of unsuccessful systemic and topical antibiotic treatments was referred. A computer tomography scan (CT scan) revealed unilateral chronic otitis with calcification of the ear canal, abscessation and fistula. On bacterial culture a Staphylococcus pseudintermedius sensitive to pradofloxacin was isolated. Systemic treatment with pradofloxacin, 3 mg/kg per os once daily, improved the infection and the dog had total ear canal ablation and bulla osteotomy performed. After one month, despite antibiotic treatment new fistulas developed in the same area. Bacterial culture revealed an drug-resistant S. pseudintermedius sensitive only to rifampicin. Under general anesthesia, the area was cleaned with 0.5% saline solution and 1 mL of indocyanine green (Emundo®, A.R.C.) was injected into the fistulas. A treatment with diode laser (A.R.C. Laser 810 nm, GmbH, Nurnberg, Germany) of four cycles 500 mw for 30 s, with a dosage of 50 J/cm2 in the effected area was performed. No antibiotic was administered and one week later, 50% of the fistulas were closed with a significant improvement of the patient's clinical condition. Cytology and bacterial culture were negative 72 h after the treatment. Total recovery occurred after two weeks. Photodynamic Therapy(PDT) is a promising antibacterial technique in case of localized refractory bacterial infections.

Whole Genome Sequencing Indicates Heterogeneity of Hyperostotic Disorders in Dogs.

Craniomandibular osteopathy (CMO) and calvarial hyperostotic syndrome (CHS) are proliferative, non-neoplastic disorders affecting the skull bones in young dogs. Different forms of these hyperostotic disorders have been described in many dog breeds. However, an incompletely dominant causative variant for CMO affecting splicing of SLC37A2 has been reported so far only in three Terrier breeds. The purpose of this study was to identify further possible causative genetic variants associated with CHS in an American Staffordshire Terrier, as well as CMO in seven affected dogs of different breeds. We investigated their whole-genome sequences (WGS) and filtered variants using 584 unrelated genomes, which revealed no variants shared across all affected dogs. However, filtering for private variants of each case separately yielded plausible dominantly inherited candidate variants in three of the eight cases. In an Australian Terrier, a heterozygous missense variant in the COL1A1 gene (c.1786G>A; p.(Val596Ile)) was discovered. A pathogenic missense variant in COL1A1 was previously reported in humans with infantile cortical hyperostosis, or Caffey disease, resembling canine CMO. Furthermore, in a Basset Hound, a heterozygous most likely pathogenic splice site variant was found in SLC37A2 (c.1446+1G>A), predicted to lead to exon skipping as shown before in SLC37A2-associated canine CMO of Terriers. Lastly, in a Weimaraner, a heterozygous frameshift variant in SLC35D1 (c.1021_1024delTCAG; p.(Ser341ArgfsTer22)) might cause CMO due to the critical role of SLC35D1 in chondrogenesis and skeletal development. Our study indicates allelic and locus heterogeneity for canine CMO and illustrates the current possibilities and limitations of WGS-based precision medicine in dogs.

Complex segregation analysis of craniomandibular osteopathy in Deutsch Drahthaar dogs.

This study investigated familial relationships among Deutsch Drahthaar dogs with craniomandibular osteopathy and examined the most likely mode of inheritance. Sixteen Deutsch Drahthaar dogs with craniomandibular osteopathy were diagnosed using clinical findings, radiography or computed tomography. All 16 dogs with craniomandibular osteopathy had one common ancestor. Complex segregation analyses rejected models explaining the segregation of craniomandibular osteopathy through random environmental variation, monogenic inheritance or an additive sex effect. Polygenic and mixed major gene models sufficiently explained the segregation of craniomandibular osteopathy in the pedigree analysis and offered the most likely hypotheses. The SLC37A2:c.1332C>T variant was not found in a sample of Deutsch Drahthaar dogs with craniomandibular osteopathy, nor in healthy controls. Craniomandibular osteopathy is an inherited condition in Deutsch Drahthaar dogs and the inheritance seems to be more complex than a simple Mendelian model.

IMAGING DIAGNOSIS-MAGNETIC RESONANCE IMAGING FEATURES OF CRANIOMANDIBULAR OSTEOPATHY IN AN AIREDALE TERRIER.

An Airedale Terrier was presented for evaluation of depression and reluctance to be touched on the head. Magnetic resonance (MR) imaging of the head was performed. The images revealed bone lesions affecting the calvarium at the level of the coronal suture and left mandibular ramus, with focal cortical destruction, expansion, and reactive new bone formation. Skull lesions were hypointense on T1-weighted sequences, hyperintense on T2-weighted sequences, and showed an intense and homogeneous enhancement after gadolinium administration. Reactive new bone formation and periosteal proliferation were confirmed histopathologically. The clinical signs, imaging findings, and histopathological examination were consistent with craniomandibular osteopathy.