Pathobiology of myomatosis uteri: the underlying knowledge to support our clinical practice

Uterine myomatosis, a benign condition, is the most common indication for hysterectomies worldwide, affecting the reproductive goals and quality of health of women. However, gynecologists have been provided with interesting insights on its pathobiology, which are the basis for uterine-preserving therapies. The aim of this paper is to discuss the latest evidence on these mechanisms and its importance in the clinical practice.

A comprehensive literature search was made in Pubmed, Medline, the Cochrane Library, Orbis plus and Google Scholar for articles related to the epidemiological, biological, and genetic bases.

There is extensive evidence that genetic, epigenetic, hormonal, environmental, proinflamatory, angiogenetic, and growing factors are involved in the biology of myomatosis. Such factors are capable of activating and promoting inhibitory signaling pathways leading to initiation, development, and regression of myomata through changes in myometrial cells and myomata fibers, such as cellular proliferation, differentiation, apoptosis, angiogenesis, and changes in the surrounding environment.

A good understanding of the pathobiologic mechanisms of myomatosis gives reasons to physicians to elect conservative or combined therapies, and allow affected women to receive an individualized management, according to age, reproduction desire, and clinical condition.