Osteoclast-specific Plastin 3 knockout in mice fail to develop osteoporosis despite dramatic increased osteoclast resorption activity.

loss-of-function mutations in humans and mice cause X-linked primary osteoporosis. However, it remains largely unknown how mutations cause osteoporosis and which function PLS3 plays in bone homeostasis. A recent study showed that ubiquitous KO in mice results in osteoporosis.

Plastin 3 influences bone homeostasis through regulation of osteoclast activity.

Over 200 million people suffer from osteoporosis worldwide, one third of which will develop osteoporotic bone fractures. Unfortunately, no effective cure exists. Mutations in plastin 3 (PLS3), an F-actin binding and bundling protein, cause X-linked primary osteoporosis in men and predisposition to osteoporosis in postmenopausal women.