Importance and Surgical Methods of Induction of Endometriosis and Osteoporosis Following Menopause in Rats: an Overview Study

Message:
Article Type:
Review Article (دارای رتبه معتبر)
Abstract:
Introduction

Endometriosis is one of the main causes of pelvic pain and subfertility, which is characterized by endometrial-like tissues outside the uterus and primarily is created in the pelvic peritoneum, ovaries, walls between the rectum and vagina and in rare cases in the diaphragm, pleura and pericardium. Some risk factors for endometriosis are obstruction in menstrual hemorrhage, an increase in the duration of endogenous estrogen, short menstrual cycles and childbirth at an early age. On the other hand, osteoporosis is a metabolic disease that is determined by bone mineral density and the destruction of the bone microstructure that increases the risk of bone fracture. About 200 million people worldwide are suffering from osteoporosis, that 34% of them are women over 50 years old. The first and most commonly used model for the induction of this disease is the ovariectomy model in rats, which gives a model of the relationship between osteoporosis and menopause.

Conclusion

Endometriosis animal models are highly contributing to the development of new non-invasive diagnostic tools and improve therapeutic methods for treatment of endometriosis in women. Although no animal models are absolutely ideal and excellent, but the presence of many similarities in the response of the human skeletal system and rats to reduce estrogen levels and therapeutic compounds caused by the ovariectomy model of the rat, a suitable model for osteoporosis research. The response of rat bones to ovariectomy depends on the type of bone (trabecular against cortical), bone sites (femur, proximal Tibia, and lumbar vertebrae) and it depends on the time elapsed after ovariectomy (the time required to reduce the amount of estrogen levels).

Language:
Persian
Published:
Journal of Shaeed Sdoughi University of Medical Sciences Yazd, Volume:30 Issue: 5, 2022
Pages:
4793 to 4812
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