Osteodystrophies are diseases in which there is either a failure of normal development or abnormal metabolism in bone which is already mature. The principal causes of
Terminology
CT Computed tomography HOD Hypertrophic osteodystrophy MO Metaphyseal osteopathy MRI Magnetic resonance imaging PFFD Proximal femoral focal deficiency PTH Parathyroid hormone
SCFE Slipped capital femoral epiphysis
Site Dog Cat Approximate age at which
ossification centre appears Approximate age at which
physeal closure occurs Approximate age at which
ossification centre appears Approximate age at which physeal closure occurs Scapula
• Supraglenoid tubercle 6–7 weeks 4–7 months 7–9 weeks 3.5–4 months
Humerus
• Proximal
• Lateral and medial parts of condyle
• Medial epicondyle
• Condyle to shaft
1–2 weeks 2–3 weeks 6–8 weeks
10–15 months 6–10 weeks 6–8 months 6–8 months
1–2 weeks 2–4 weeks 6–8 weeks
18–24 months 3.5 months 3.5–4 months Radius
• Proximal
• Distal 3–5 weeks
2–4 weeks 7–10 months
10–12 months 2–4 weeks
2–4 weeks 5–7 months
14–22 months Ulna• Olecranon tubercle
• Anconeal process
• Distal
6–8 weeks 6–8 weeks 5–6 weeks
7–10 months
<5 months 9–12 months
4–5 weeks 3–4 weeks
9–13 months 14–25 months Carpus
• Radial carpal (three centres)
• Other carpal bones
• Accessory carpal – proximal
• Accessory carpal – distal
• Sesamoid in abductor pollicis longus
3–6 weeks 2 weeks 2 weeks 6–7 weeks 4 months
3–8 weeks 3–8 weeks 3–8 weeks 3–8 weeks
Metacarpal/tarsal
• Proximal (digit I)
• Distal (digits II–V) 5–7 weeks
3–4 weeks 6–7 months
6–7 months 3 weeks 4.5–5 months
4.5–5 months First phalanx
• Proximal
• Distal 5–7 weeks
4–6 weeks 6–7 months 3–4 weeks
3–4 weeks 4–5 months
Second phalanx
• Proximal 4–6 weeks 6–7 months 4 weeks 4–5 months
Femur
• Proximal
• Greater trochanter
• Lesser trochanter
• Distal
1–2 weeks 7–9 weeks 7–9 weeks 3–4 weeks
8–11 months 9–12 months 9–12 months 9–12 months
2 weeks 5–6 weeks 6–7 weeks 1–2 weeks
7–11 months 13–19 months
Stifle sesamoid bones
• Patella
• Fabellae
• Popliteal sesamoid
6–9 weeks 3 months 3–4 months
8–9 weeks 10 weeks Tibia
• Tibial tuberosity
• Proximal
• Distal
• Medial malleolus
7–8 weeks 2–4 weeks 2–4 weeks 3 months
10–12 months 9–10 months 12–15 months 3–5 months
6–7 weeks 2 weeks 2 weeks
9–10 months 12–19 months 10–12 months Fibula
• Proximal
• Distal 8–10 weeks
4–7 weeks 10–12 months
12–13 months 6–7 weeks
3–4 weeks 13–18 months
10–14 months Tarsus
• Calcaneal tuberosity
• Central tarsal bone
• 1st and 2nd tarsal bones
• 3rd tarsal bone
• 4th tarsal bone
6 weeks 3 weeks 4 weeks 3 weeks 2 weeks
6–7 months 4 weeks
4–7 weeks 4–7 weeks 4–7 weeks 4–7 weeks Radiographic appearance of centres of ossification and physeal closure times in the dog and cat.
(Data adapted from Thrall DE and Robertson ID (2011) Introduction. In: Atlas of Normal Radiographic Anatomy and Anatomic Variants in the Dog and Cat, pp. 8–16. Elsevier, St Louis)
8.1
many juvenile osteodystrophies are deficiencies or imbal-ances of dietary calcium, phosphorus and vitamin D, as well as dysregulation of parathyroid hormone (PTH) activity, and hence an understanding of basic bone metabolism is essential.
The primary source of calcium and phosphorus is the diet. These elements are absorbed in amounts dependent on the source of the minerals, intestinal pH and dietary levels of vitamin D, calcium, phosphorus, iron and fat. If vitamin D or its activity is decreased, calcium and
phosphorus absorption is reduced. Vitamin D is obtained either through the diet or by production when the skin is exposed to sunlight (ultraviolet radiation); dietary uptake is the primary source of Vitamin D in dogs and cats (Figure 8.2). Before vitamin D can be used, it must be processed into its metabolically active form in two consecutive enzyme-dependent hydroxylation steps in the liver and kidney. Dietary vitamin D is absorbed by the intestines and transported to the liver where it is hydroxylated into calci diol (25-hydroxycholecalciferol) by means of the
Vitamin D metabolism and hormonal responses to low serum calcium. Inhibitory mechanisms are not illustrated.
8.2
Cholecalciferol (Vitamin D3)
Calcidiol
(25-Hydroxycholecalciferol)
Calcitriol
(1,25-Dihydroxycholecalciferol) Calcitriol
(1,25-Dihydroxycholecalciferol)
Liver
Small intestine
Small intestine Pre-vitamin DSkin
Parathyroid glands Low serum calcium stimulates parathyroid hormone (PTH) release
Increased serum calcium
Kidneys
PTH
Increases calcitriol formation which decreases renal excretion of calcium
Decreases renal excretion of calcium
Decreases renal excretion of calcium
Increases absorption of dietary calcium Increases osteoclastic activity
leading to bone resorption
PTH Bone
Enzyme: Vitamin D-25 Hydroxylase
Enzyme: 25-Hydroxycholecalciferol α-hydroxylase
enzyme vitamin D-25 hydroxylase. A second hydroxylation takes place in the kidneys by means of the enzyme 25-hydroxycholecalciferol α-hydroxylase, and calcitriol (1,25-dihydro xycholecalciferol) is formed. Calcitriol is necessary for osteoid and cartilage mineralization and acts on the intestinal tract to increase absorption of dietary calcium. Through a negative feedback loop, it also con - tri butes to the regulation of PTH secretion.
Secretion of PTH occurs in response to a low circu-lating calcium concentration. The target organs of PTH are the kidneys, bones and intestines. In the kidneys (see Figure 8.2), PTH increases the activity of 25-hydroxycholecal - ciferol α-hydroxylase, which increases calcitriol formation.
Calcitriol promotes renal tubular absorption of calcium while enhancing the renal excretion of phosphorus. In the intestine, PTH promotes absorption of calcium. PTH also facilitates mobilization of calcium and phosphorus from bone by allowing utilization of calcium from the osteoid matrix. Calcitonin is a hormone secreted by the thyroid glands which acts to inhibit bone resorption stimulated by PTH. Increased serum calcium concentrations stimulate calcitonin secretion; this has the opposite effect to PTH on bone and inhibits osteoclastic activity and stimulates endochondral ossification.
Alternative imaging techniques
Radiography is the most useful method for routine, non-invasive evaluation of skeletal lesions and is usually all that is required when imaging juvenile long bones. Other imag-ing techniques (see Chapters 2 to 5) which are sometimes used are:
• CT: high-resolution CT provides excellent cross-sectional images with three-dimensional (3D) reconstructions that are particularly useful to characterize dysostoses and for surgical planning of corrective or limb-sparing procedures for angular limb deformities, congenital anomalies or severe fractures
• Single-phase bone scintigraphy: useful in the diagnostic work-up of occult lameness where clinical and radiographic signs are equivocal or absent, or in overt lameness where the radiographic changes do not correspond to the clinical severity of the patient’s condition. Scintigraphic images from juvenile animals need to be interpreted with caution because normal physeal activity leads to increased radioisotope uptake at the physes
• MRI: used in particular to assess soft tissue structures around bone
• Ultrasonography: can be used to assess soft tissue swellings and draining sinus tracts overlying bones.
Abdominal ultrasonography may be indicated to assess the kidneys when skeletal changes suggestive of renal secondary hyperparathyroidism are observed in juvenile animals.