Hormones Roles in Bone Metabolism -Study Notes

Hormones Roles in Bone Metabolism -Study Notes

Hormones Roles in Bone Metabolism -Study Notes

These are the 7 hormones responsible for bone and bone growth metabolism

  1. Growth hormone
  2. thyroid hormones
  3. Insulin
  4. Glucocorticoids
  5. Calcitonin
  6. Sex hormones
  7. Leptin

Growth Hormone (GH)

Action:

  • • Stimulates IGF-1 (somatomedin) from liver
  • • IGF-1 → chondrocyte proliferation in epiphyseal plate
  •  • Longitudinal bone growth
  • :

Clinical Correlation

  •  Excess pre-fusion → Gigantism
  • Excess post-fusion → Acromegaly
  • Deficiency → Dwarfism (proportionate)

Parathyroid Hormone (PTH)

  • Action:
    • • ↑ Osteoclast activity → bone resorption → ↑ serum Ca²⁺• ↑ Renal Ca²⁺ reabsorption
    •  • ↑ Vitamin D activation (1α hydroxylase)
  • Clinical Correlation:
    • • Hyperparathyroidism → Osteitis fibrosa cystica• (Brown tumours, pathological fractures, ‘pepper-pot skull’) Hormones in Bone Metabolism
    • Calcitonin Action:

Calcitonin

Action:

  • Secreted by parafollicular C-cells of thyroid

    • ↓ Osteoclast activity → ↓ bone resorption → ↓ serum Ca²⁺

Therapeutic use:

  •  Paget’s disease, oasteoporosis, hypercalcaemia

  • •Calcitonin nasal spray used in post-menopausal osteoporosis

Sex Hormones (Oestrogen / Testosterone)

Action:

  • ↑ Osteoblast activity; inhibit osteoclasts
  • Cause epiphyseal plate fusion at puberty
  • Maintain bone density throughout reproductive life

Clinical:

  • Oestrogen ↓ (post-menopause) → post-menopausal osteoporosis
  • Most common cause of osteoporosis worldwide

Thyroid Hormones (T3/T4)

Action:

  • required for normal bone development and maturation

  • Stimulate osteoblast activity and collagen synthesis

  • Permissive for GH action on the growth plate

Clinical Correlation:

  • Hypothyroidism → delayed bone maturation, cretinism, short stature
  • Hyperthyroidism → accelerated bone resorption, osteoporosis

Glucocorticoids (Cortisol)

 Action:

 • Inhibit osteoblasts → ↓ bone formation

• ↓ Intestinal Ca²⁺ absorption

 • ↑ Renal Ca²⁺ excretion → 2° hyperparathyroidism

ClinicalCorrelation

• Prolonged exogenous steroid use → glucocorticoid-induced osteoporosis

• Most common preventable cause of secondary osteoporosis

Insulin

Action:

  • Stimulates osteoblast activity and bone formation
  • Promotes collagen synthesis in bone matrix
  • Increases amino acid uptake by osteoblasts

Clinical Correlation:

  • Type 1 DM (insulin deficiency) → reduced bone density

  • Osteoporosis risk increased in poorly controlled diabetes

Leptin (from adipocytes)

Action:

  • Acts via the hypothalamus to regulate bone remodelling• Central pathway: ↑ SNS activity → ↓ osteoblasts

  • Peripheral (direct): ↑ osteoblast proliferation

Clinical Correlation:

  • • Obesity paradox: high BMI is protective against osteoporosis

  • • Leptin deficiency  (ob/ob mice) → high bone density

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