Rickets and osteomalacia are increasing in prevalence in people because of cultural practices, breast-feeding, decreased sun exposure, and increased sunscreen usage. Several hereditary forms of rickets owing to either renal phosphate wasting or defects in vitamin D metabolism are also reported in people. Rickets is well recognized in domestic animals, but published reports are not always supported by microscopic findings, and diagnoses based on clinical signs and radiology are unreliable. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported in pigs, sheep, cats, and dogs. There is variation between species in susceptibility to dietary vitamin D and phosphorus deficiency and in the ability to manufacture vitamin D in their skin. A number of mouse models have been discovered or created to study human skeletal diseases and skeletal homeostasis. With the discovery that vitamin D is involved in not only calcium and phosphorus homeostasis but also in the immune system and cancer, there is great potential for new and existing animal models to generate valuable information about vitamin D and its many functions. This review presents an overview of vitamin D metabolism and rickets in domestic and laboratory animals and makes comparisons where appropriate with the disease in humans.

Felis catus papillomavirus type 2 (FcaPV-2) causes premalignant skin lesions in cats and has also been found in a proportion of cutaneous squamous cell carcinomas (SCCs), a common and potentially fatal cancer of cats. While this could suggest a role of the virus in cancer development, FcaPV-2 has also been detected in skin swabs of normal cats making it difficult to discern whether the PV is causing the cancer or merely an 'innocent bystander'. To distinguish between these two possibilities, real-time PCR was used to determine the viral copy number and the transcriptional activity of FcaPV-2 infections present in 70 formalin fixed paraffin embedded skin lesions including 10 PV-induced premalignant lesions and 60 SCCs. FcaPV-2 gene expression was found in 21 of 60 (35%) SCCs, all 10 premalignant lesions, and none of 10 normal skin samples. The results showed two distinct subsets of SCCs. The majority of the SCCs had low copy numbers of FcaPV-2 DNA (mean of 17 copies per copy of reference gene DNA) and no FcaPV-2 gene expression, suggesting the virus was an incidental finding. In contrast, 20 SCCs had detectable FcaPV-2 E6/E7 gene expression and very high copy numbers of FcaPV-2 DNA, with a mean of 32930 copies per copy of reference gene DNA. The relative quantity of E6/E7 gene expression and the viral copy number in this group was similar to that found in the PV-induced premalignant lesions suggesting that FcaPV-2 may play a role in the development of a subset of feline cutaneous SCCs.

Within the lay literature, and social media in particular, there is often debate about the age at which a horse should be started and introduced to racing or sport. To optimize the welfare and longevity of horses in racing and sport, it is important to match exercise with musculoskeletal development and the ability of the musculoskeletal system to respond to loading. The justification for not exercising horses at a certain age is often in contrast to the scientific literature and framed, with incorrect generalizations, with human growth. This review provides a relative comparison of the growth and development of the horse to the descriptors used to define growth and development in humans. Measures of physeal closure and somatic growth demonstrate that the horse completes the equivalent of rapid infant growth by weaning (4–6 months old). At approximately 11 months old, the horse completes the equivalent of the childhood phase of growth and enters puberty. At 2 years old, the horse has achieved most measures of maturity used within the human literature, including the plateauing of vertical height, closure of growth plates, and adult ratios of back length:wither height and limb length:wither height. These data support the hypothesis that the horse evolved to be a precocious cursorial grazer and is capable of athletic activity, and use in sport, relatively early in life.

Inherited rickets of Corriedale sheep is characterized by decreased growth rate, thoracic lordosis and angular limb deformities. Previous outcross and backcross studies implicate inheritance as a simple autosomal recessive disorder. A genome wide association study was conducted using the Illumina OvineSNP50 BeadChip on 20 related sheep comprising 17 affected and 3 carriers. A homozygous region of 125 consecutive single-nucleotide polymorphism (SNP) loci was identified in all affected sheep, covering a region of 6 Mb on ovine chromosome 6. Among 35 candidate genes in this region, the dentin matrix protein 1 gene (DMP1) was sequenced to reveal a nonsense mutation 250C/T on exon 6. This mutation introduced a stop codon (R145X) and could truncate C-terminal amino acids. Genotyping by PCR-RFLP for this mutation showed all 17 affected sheep were “T T” genotypes; the 3 carriers were “C T”; 24 phenotypically normal related sheep were either “C T” or “C C”; and 46 unrelated normal control sheep from other breeds were all “C C”. The other SNPs in DMP1 were not concordant with the disease and can all be ruled out as candidates. Previous research has shown that mutations in the DMP1 gene are responsible for autosomal recessive hypophosphatemic rickets in humans. Dmp1_knockout mice exhibit rickets phenotypes. We believe the R145X mutation to be responsible for the inherited rickets found in Corriedale sheep. A simple diagnostic test can be designed to identify carriers with the defective “T” allele. Affected sheep could be used as animal models for this form of human rickets, and for further investigation of the role of DMP1 in phosphate homeostasis.