Rickets

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Varus deformity in an adult dog from vitamin D-dependent juvenile rickets[1]

Rickets is a term traditionally synonymous with osteomalacia and was originally reported as a vitamin D and/or phosphorus deficiency[2].

However, there has since emerged two recognized forms of canine rickets:

  • Type I Vitamin D-dependent rickets - resulting in vitamin D-responsive secondary nutritional hyperparathyroidism[3]
  • type II Vitamin D-resistant rickets - resulting in vitamin D-non-responsive secondary nutritional hyperparathyroidism[4]

Most cases of rickets in dogs are type I, caused by dietary deficiency of either vitamin D or phosphorus or excess calcium[5], particularly large-breed dogs. However, congenital diseases such as biliary tract atresia[6] or familial rickets[7] have also been reported, which result in interference with vitamin D production.

The pathogenesis of rickets involves impaired mineralization of physeal and epiphyseal cartilage during endochondral ossification and of newly formed osteoid.

Only a few foods, including cod liver oil and fatty fish such as salmon and sardines, naturally contain high concentrations of vitamin D[8]. Vitamin D is also present in certain plants owing to conversion of ergosterol to vitamin D by ultraviolet light, and dogs can also generated vitamin D from sunlight. The formation efficiency of vitamin D in the skin is influenced by skin pigmentation and ultraviolet light intensity[9].

In their natural state, dogs would have satisfied their vitamin D requirements from ingesting the fat, liver, and blood of their quarry, but pet dogs and cats now rely on dietary supplements.

It has since been recognized as also having a genetic component, with familial rickets recognized in dogs due to vitamin D insensitivity by intestinal epithelial cells.

Clinically affected dogs present with joint pain, lameness, limb deformities such as lateral bowing of the antebrachii and focal hard swellings proximal to the tarsi and carpi, spontaneous fractures and 'rubber jaw' syndrome due to mandibular an maxillary bone malformations.

A tentative diagnosis is based on clinical history of lethargy, decreased long bone growth, angular limb deformity, together with a dietary regimen deficient in nutrients.

Blood tests frequently display marked hypocalcemia, hypophosphatemia and subnormal levels of vitamin D[10].

Radiographs are usually characteristic of osteopenia and assist in a definitive diagnosis. There is usually club-like thickening of metaphyses and compression of epiphyses, as well as deformities of long bones such as the proximal humerus, distal radius, ulna and ribs, with enlargement of costochondral junctions ('rachitic rosary').

A definitive diagnosis requires histological analysis of bone biopsies, with affected bone displaying signs of thickened and irregular growth plates with islands and tongues of chondrocytes extending into the metaphyses. Similar changes occur beneath articular epiphyseal cartilage complexes in the expanding epiphyses of young animals. Other microscopic changes may include thick osteoid seams lining trabeculae and disorganization or absence of the primary spongiosa[11].

A differential diagnosis would include hypertrophic osteodystrophy, osteogenesis imperfecta, hyperparathyroidism[12] (usually older dogs), panosteitis, dwarfism and polyostotic lymphoma.

Most cases respond to dietary supplementation within three months with nutritional management, using additives of calcium, phosphorus and cholecalciferol, but major bone deformities usually persist into adulthood[13].

References

  1. ARF Newsletter
  2. Chesney RW (2012) Early animal models of rickets and proof of a nutritional deficiency hypothesis. J Pediatr Gastroenterol Nutr 54(3):322-327
  3. Taylor MB et al (2009) Diffuse osteopenia and myelopathy in a puppy fed a diet composed of an organic premix and raw ground beef. J Am Vet Med Assoc 234(8):1041-1048
  4. LeVine DN et al (2009) Hereditary 1,25-dihydroxyvitamin D-resistant rickets in a Pomeranian dog caused by a novel mutation in the vitamin D receptor gene. J Vet Intern Med 23(6):1278-1283
  5. Schoenmakers I et al (2000) Effects of diets with different calcium and phosphorus contents on the skeletal development and blood chemistry of growing great danes. Vet Rec 147(23):652-660
  6. Schulze C et al (2000) Extrahepatic biliary atresia in a border collie. J Small Anim Pract 41(1):27-30
  7. Dittmer KE & Thompson KG (2011) Vitamin D metabolism and rickets in domestic animals: a review. Vet Pathol 48(2):389-407
  8. Dusso AS et al (2005) Vitamin D. Am J Physiol Renal Physiol 289:F8–F28
  9. Holick MF (1981) The cutaneous photosynthesis of previtamin D3: a unique photoendocrine system. J Invest Dermatol 77:51–58
  10. Malik R et al (1997) Rickets in a litter of racing greyhounds. J Small Anim Pract 38(3):109-114
  11. Thompson KG (2007) Bones and joints. In: Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals, ed. Maxie MG, 5th ed., pp:1–184. Elsevier Saunders, Philadelphia, PA
  12. Carmichael DT et al (1995) Renal dysplasia with secondary hyperparathyroidism and loose teeth in a young dog. J Vet Dent 12(4):143-146
  13. McMillan CJ et al (2006) Dietary-related skeletal changes in a Shetland sheepdog puppy. J Am Anim Hosp Assoc 42(1):57-64