Osteoporosis is characterized by low bone mineral density and deterioration in the microarchitecture of bone that increases its fracture vulnerability. The mainstay of therapy for osteoporosis is anti-resorptive in mechanism. Parathyroid hormone (PTH) is the most recently approved anabolic agent for osteoporosis. The mechanism of PTHs skeleton anabolic action is composite involving pathways linked to common signalling peptides that affect gene osteoblast transcription. A number of animal studies and clinical trials have demonstrated that intermittent PTH administration induces anabolic effects on both cancellous and cortical bone, enhances bone mass and increases mechanical bone strength, increasing spine and hip bone mineral density and reducing fragility fractures. Preclinical studies investigating the effect of PTH on fracture healing show an increase in bone density and strength indicating an enhancement of this biological cascade. Preclinical and clinical safety assessments have revealed little evidence of toxic effects and there have been few reports of adverse events related to their use. An increase in osteosarcoma in rats probably is not prognostic of an equivalent possibility in humans. In summary, parathyroid hormone is a major advance in the treatment of osteoporosis. Additional studies addressing long-term clinical safety are needed. However the current evidence is very promising.
Keywords: Bone regeneration, biological response modifier, PTH, safety
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