Introduction

• Osteoporosis is a skeletal/metabolic disease characterized by bone mass loss and micro-architectural deterioration of the whole skeletal system, which augments skeletal fragility and fracture prevalence.
• Cause: ovariectomy/ovariohysterectomy, glucocorticoid use, lack of UV light exposure, calcium-deficient diet, secondary hyperparathyroidism.
• Signs: dental disease, fractures.
• Diagnosis: radiology, low blood calcium levels, increase blood PTH (parathormone) levels.
• Treatment: anabolic drugs, calcium supplements, exposure to UV light.
• Prognosis: worsens as severity increases.

Pathogenesis

Etiology

• Osteoporosis affects more than 200 million people, and rabbits have been used as a model animal for the investigation of this disease.
• Glucocorticoids Therapeutics: glucocorticoids induce a loss in cortical and trabecular bone, increase osteoclastic resorption, and decrease new bone formation:
  • Glucocorticoids can produce signs of osteoporosis after just 4 weeks of use.
  • The higher the dose, the more likely to develop osteoporosis.
  • The effects of glucocorticoids are cumulative.
• Ovariectomy/ovariohysterectomy Ovariohysterectomy causes osteoporosis due to associated estrogen deficiency:
  • Estrogen deficiency increases osteoclastogenesis and reduces intestinal and renal calcium absorption.
  • By 13 weeks after surgery a 10% bone mass loss is seen in lumbar vertebrae.
  • At 17 weeks after surgery the reduction of bone mineral density is 20% in the proximal tibia and 10% in the femur.
  • The negative effects of surgery on bones increase with time.
• The prolonged use of GnRH agonists, eg deslorelin, suppresses estrogen production and can have similar effects on bone density.
• Low calcium diets Nutrition: dietary requirements and lack of UV-light exposure are also involved in osteoporosis and other metabolic bone diseases. 
• Other drugs can also contribute to osteoporosis, such as heparin.
• The effects of all these different causes may be combined and may be cumulative. The combination of ovariectomy/ovariohysterectomy and glucocorticoid use (particularly at moderate and high doses) is commonly used in research to generate models of osteoporosis in rabbits.

Predisposing factors

General

• Captivity.
• Osteoporosis and other metabolic bone diseases are rarely seen in wild rabbits.

Specific

• Glucocorticoid use.
• Ovarian removal/suppression in females, eg ovariectomy, use of deslorelin.
• Lack of access to UV-light exposure.
• Low calcium diets.

Pathophysiology

• Osteoporosis produces a demineralization of the jaw, particularly affecting the perialveolar area. This enhances tooth movement and the development of malocclusion Dental malocclusion/overgrowth. Malocclusion leads to lack of dental wear and elongation of dental roots, which facilitates the development of perialveolar abscesses:
  • Elongated roots and abscesses easily perforate osteoporotic jaw and skull bones.
  • Demineralization occurs earlier in the jaw than in other bones. 
• Loss of bone density in other bones predisposes rabbits to fractures, such as lumbar fractures Spinal injury .
• Osteoporosis prevents proper healing of fractured bones.

Timecourse

• Osteoporosis is a progressive disease when causes are not addressed. The cumulative effects of some actions (eg lack of estrogens due to ovariectomy, long-term treatment with glucocorticoids) and the combination of some causes (eg lack of UV-light access in ovariectomized females) may increase prevalence and severity of the disease as the animal ages.
• Bone changes compatible with osteoporosis can be evident at 4-6 months of ovariectomy, as a result of a reduction of estrogens after surgery and the chronic effects of this estrogen deficiency in calcium and bone metabolism.

Epidemiology

• Increase prevalence and severity as rabbits age.

Diagnosis

Treatment

Prevention

Outcomes