Abstract
Glucocorticoids are one of the causes of secondary osteoporosis. The aqueous extract of Piper sarmentosum contains flavonoids that possess antioxidant effects. In this study, we determined the effects of aqueous Piper sarmentosum leaf extract on structural, dynamic and static histomorphometric changes from osteoporotic bones of rats induced with glucocorticoids. Thirty-two Sprague-Dawley rats were divided equally into four groups—Sham control group given vehicles (intramuscular (IM) olive oil and oral normal saline); AC: Adrenalectomised (Adrx) control group given IM dexamethasone (DEX) (120 μg/kg/day) and vehicle (oral normal saline); AP: Adrx group administered IM DEX (120 μg/kg/day) and aqueous Piper sarmentosum leaf extract (125 mg/kg/day) orally; and AG: Adrx group administered IM DEX (120 μg/kg/day) and oral glycyrrhizic acid (GCA) (120 mg/kg/day). Histomorphometric measurements showed that the bone volume, trabecular thickness, trabecular number, osteoid and osteoblast surfaces, double-labelled trabecular surface, mineralizing surface and bone formation rate of rats given aqueous Piper sarmentosum leaf extract were significantly increased (p < 0.05), whereas the trabecular separation and osteoclast surface were significantly reduced (p < 0.05). This study suggests that aqueous Piper sarmentosum leaf extract was able to prevent bone loss in prolonged glucocorticoid therapy. Thus, Piper sarmentosum has the potential to be used as an alternative medicine against osteoporosis and osteoporotic fractures in patients undergoing long-term glucocorticoid therapy.
Highlights
Osteoporosis is a systemic skeletal disease involving low bone mass and microarchitectural deterioration of bone tissue, leading to high bone fragility and fracture risk [1]
Dexamethasone treatment for eight weeks significantly reduced the bone volume of AC compared to Sham
bone volume/tissue volume (BV/tissue volume (TV)) was significantly higher in AP compared to AC
Summary
Osteoporosis is a systemic skeletal disease involving low bone mass and microarchitectural deterioration of bone tissue, leading to high bone fragility and fracture risk [1]. Risk factors associated with glucocorticoid-induced osteoporosis are aging, low body mass index, increased 11β-hydroxysteroid dehydrogenase (11β-HSD) enzyme expression, low bone mineral density, high doses of glucocorticoids, underlying chronic diseases such as rheumatoid arthritis, and glucocorticoid receptor genotypes. Progression of bone loss occurs even with very low doses of pharmacological glucocorticoids; depending on the dosage and duration of the therapy received [3]. These changes affect trabecular bone more than cortical bone, increasing the risk of fracture [4,5]
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