NON-NEOPLASTIC BONE AND JOINT LESIONS

It includes: Osteoporosis, Osteomalacia and Rickets, Hyperparathyroidism
Osteoporosis

• Metabolic disease characterized by diffuse skeletal lesions due to a decreased mass of normally mineralized bone
• Post-menopausal females
• Increased bone resorption (osteoblastic activity is normal)
• Estrogen may lead to increased secretion of IL-1, IL-6, TNF and MCSF by stromal cells which will stimulate osteoclasts 

Primary osteoporosis

• Some genetic basis
• Dependent upon levels of Ca++ and vitamin D
• Exercise

Secondary osteoporosis

• Corticosteroid excess (endogenous or exogenous)
• Hyperthyroidism
• Hypogonadism
• Multiple myeloma
• PTH-secreting tumors
• Malabsorption
• Alcoholism

Osteomalacia and Rickets
Accumulation of unmineralized bone matrix resulting from a diminished rate of mineralization
Causes:

• Dietary deficiency in vitamin D
• Defective bone mineralization
• Congenital or acquired defects in vitamin D or phosphate metabolism
• Malabsorption (most common cause in US)
• Crohn’s disease
• Celiac disease
• Cholestatic liver disease
• Biliary obstruction
• Chronic pancreatitis

Hyperparathyroidism

• Increased bone resorption secondary to increased PTH
• Classic pathologic change referred to as osteitis fibrosa cystica
• Replacement of marrow by fibrous tissue
• Numerous microfractures
• Hemosiderin-laden macrophages
• Eventually cystic degeneration and classic gross appearance referred to as “brown tumor”

Osteopetrosis (marble bone disease, Albers-Schönberg disease)

• Inherited lysosomal defect
• Most severe form (autosomal recessive) is severe and often lethal
• Death secondary to anemia, cranial nerve entrapment, hydrocephalus and infection
• Dense bones weighing 2-3 times normal
• TX with BMTx and IFN

by
Akshaya Srikanth
Pharm.D Intern
Hyderabad, India