Rickets is a classic metabolic bone

disease of humans and animals, first

described in the first and second
centuries. With the discovery that
vitamin D could prevent rickets, the
prevalence of this disease in developed
countries plummeted; however, it still
occurs.
Pettifor JM: Rickets and vitamin D deficiency in children and adolescents.
Endocrinol Metab Clin North Am 34:537–553, 2005

The pathogenesis of rickets involves

impaired mineralization of physeal and
epiphyseal cartilage during
endochondral ossification and of newly
formed osteoid. Most cases in domestic
animals are caused by dietary deficiency
of either vitamin D or phosphorus, but
occasional inherited forms are reported.
Klein GL: Nutritional rickets and osteomalacia. In: Primer on the Metabolic Bone
Diseases and Disorders of Mineral Metabolism ed. Favus MJ, 4th ed., pp. 315–
319. Lippincott Williams & Wilkins, Philadelphia, PA, 1999.

Pathology of Rickets
The characteristics of rickets are similar
in all species. Lesions are typically most
severe in the fastest-growing bones,
including the radius, the tibia, and the
metacarpals and metatarsals. On
radiographic and postmortem
examination, widening of the physeal
growth plate is the most archetypal
change. Other abnormalities seen
radiographically may include
metaphyseal flaring, thinning of the
cortex, poor mineralization of the
skeleton, and pathological fractures. In
addition, postmortem examination may
reveal irregular thickening of the physeal
cartilage, erosion of articular cartilage
due to collapse of subchondral bone,
and spontaneous fractures. Enlargement
of costochondral junctions, the so-called
rachitic rosary, is also a classic lesion of
rickets that may be seen on radiographic
or postmortem examination. mpaired
provisional calcification of cartilage at
sites of endochondral ossification leads
to the accumulation of hypertrophic
chondrocytes, resulting in 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. One
of the early pioneers of research into
rickets, Sir Arnold Theiler, regarded the
pathognomonic change as “the presence
of osteoid tissue in quantities surpassing
normal physiological limits.”
Hemorrhage and signs of trauma may be
seen in the metaphysis and primary
spongiosa because of damage to
weakened trabeculae of poorly
mineralized bone.
Dogs
There are few reports of naturally
occurring rickets in dogs and cats, and
the disease is considered rare.
Carnivores are unlikely to suffer from
phosphorus deficiency given that
phosphorus concentrations in meat are
relatively high, and although they may
not manufacture vitamin D in their skin,
adequate levels of which are added to
commercial rations. Dogs and cats fed
predominantly meat- or offal-based
rations without vitamin D supplements
develop fibrous osteodystrophy rather
than rickets, owing to nutritional
secondary hyperparathyroidism
Thompson KG: 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, 2007.

Cats
Cats are unable to synthesise vitamin D3
(cholecalciferol) from sunlight and are,
therefore, totally dependent on
obtaining it from their diet. Under
normal conditions, vitamin D3 is
absorbed intact from the intestine in
association with dietary fat. It is
transported via chylomicrons to the
liver, in association with vitamin D
binding protein (VDBP), where it is
hydroxylated to produce 25-
hydroxycholecalciferol (25[HO]D3). This
molecule is transported to the kidney
where it undergoes a second
hydroxylation in the mitochondria of the
cells of the proximal convoluted tubules.
This enzymatic step is tightly controlled
(see below) and results in the formation
of the active metabolite, 1,25(HO)D3
(calcitriol), which acts to increase levels
of calcium and phosphate in the serum
via its actions on the intestines, kidneys
and bone.
Fraser DR. Regulation of the metabolism of vitamin D. Physiolog Review 1980; 60:
551–613.

In the intestine, calcitriol binds to

vitamin D receptors in the cytoplasm of
enterocytes, increasing calcium and
phosphate transport from gut to serum.
In the kidneys, calcitriol increases
tubular resorption of calcium and
phosphorus from the glomerular filtrate,
while in bone it maintains levels of
calcium and phosphorus sufficient to
mineralise newly formed osteoid.1–3
Calcitriol also regulates the production
of some bone proteins produced by
osteoblasts.
Schenk PA, Chew DJ, Nagode LA, Rosol TJ. Disorders of calcium: hypercalcemia
and hypocalcemia. In: DiBartola SP, ed. Fluid, electrolyte and acid-base disorders
in small animal practice, 3rd edn. St Louis; Saunders Elsevier, 2006: 122–94

Hereditary rickets in cats is secondary to

a defect in vitamin D pathway, the
vitamin D receptors, or renal tubular
reabsorption of phosphate.
Cole, R., & Hespel, A. M. (2020). Overview of the Musculoskeletal System. Feline
Diagnostic Imaging, 579-619.

Rickets unrelated to dietary deficiency

has been recorded in cats, due to inborn
errors in vitamin D3
metabolism.Historically, cases have
divided into (i) vitamin D-dependent
type 1, caused by a defect in the gene
encoding the enzyme 25-hydroxy-
vitamin D3-1-α-hydroxylase (CYP27B1)
and (ii) vitamin D-dependent type 2,
caused by a defect in the receptor gene
(VDDR11) for the active 1,25(HO)D3
metabolite. In reported type 1 cases,
levels of 25(HO)D3 are in the reference
interval (RI), but failure of the
hydroxylation step in the renal tubules
leads to low levels of 1,25(HO)D3 in
serum. In type 2 cases, levels of
25(HO)D3 are also normal, but levels of
1,25(HO)D3 are increased due to
‘receptor resistance’.
Godfrey DR, Anderson RM, Barber PJ, Hewson M. Vitamin D-
dependent rickets type II in a cat. J Small Anim Pract 2005; 46:
440–43.