Etidronic acid (HEDP) is a diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.

Etidronate inhibits directly osteoclastic bone-resorbing activity by pit assay. Etidronate also directly induces apoptosis and disrupts actin rings in osteoclasts. [1]

Etidronate, when administered s.c. repeatedly at 10 or 40 mg/kg/day, gradually suppresses the adjuvant-induced allodynia In the rats with adjuvant arthritis, as assessed by 10-g von Frey hair. Etidronate (10-40 mg/kg/day) suppresses the adjuvant-induced mechanical allodynia in rat hindpaw. Etidronate (5–10 mg/kg/day) dose-dependently prevents the decrease in bone mineral density (BMD) in the proximal tibia of the arthritic rats. [2] Etidronate inhibits the histidine decarboxylase induction, but not the other inflammatory reactions induced by alendronate. Etidronate (unlike clodronate) also inhibits alendronate-induced BP-line formation in mice (even at 40 mmol/kg). Etidronate (160 mmol/kg) also inhibits the physicochemical changes in the tibia induced by six, weekly injections of alendronate. [3] Etidronate (10 mg/kg) combined with Calcitriol after subtotal nephrectomy (SNx) significantly inhibits thoracic and abdominal aortic calcification 3 weeks after the operation in rats. [4] Etidronate (5 mg/kg or 10 mg/kg) significantly reduces the thoracic and abdominal aortic calcification induced by calcitriol in the renal failure rat. Etidronate (5 mg/kg or 10 mg/kg) also reduces the dysfunction in aortic contraction. Etidronate (5 mg/kg) reverses the reduction in the aortic expression of matrix Gla protein mRNA observed in nephrectomized rats. [5]