1.Prof. M.C.Bansal MBBS,MS,MICOG,FICOG Professor OBGY Ex-Principal & ControllerJhalawar Medical College & Hospital Mahatma Gandhi Medical College, Jaipur.

2. Introduction Fibroids(Myoma, Leiomyoma,Fibromyoma) 5-20% women in their reporductive age are reported tohave fiboroids. Most common Monoclonal Benign tumors of uterusarising in the smooth muscle cells of myometrium. Contain large aggregation of extracellular matrixconsisting of collagen, elastin, fibronectin andproteoglycan. Each fibroid is derived from smooth muscle cells rests,either from vessel wall or uterine musculature 3. Incidence Most common----77% specimen of hysterectomy werehaving Fibroids invariable number ,size (micro-macro)and site. Sonographic survey in35-49yrs aged Africo- Americanwomen reported Fibroids in 60% while about 80%among the women > 50 yrs. of age. White women have lower prevalence---40%at age 35and almost 70% by age 50. 4. etiology Precise cause of Fibroids is not known. Advances have been made in understanding the molecular biology of these benign tumors and there dependence on genetic, hormonal and growth factors . (A) Genetic Fibroids are monoclonal and about 40% have chromosomal abnormalities that include-(a) translocations between chromosomes 12 and14.(b) deletions of chromosome 7(c) Trisomy of chromosome 12 in large tumors. 60% may have yet undetected mutations 5. Etiology Genetic more than 100 genes were found to be up- down regulated in fibroid cells. Many of them appear to regulate cell growth, proliferation, differentiation and mitogenesis. Genetic differences between fibroid and Leiomyosarcomas indicate that Leiomyosarcomas do not result due to malignant changes in fibroids . 6. Etiology (B) Hormones - Both increase in number and responsiveness of receptors for estrogen and progesterone appear to promote fibroid growth, as these are rarely found before puberty, develop and increase during reproductive period of life and so also during pregnancy, regress after menopause/ bilateral oophorectomy. Found more with hyper estrogenic states like obesity, increases after ERT therapy in menopausal women, endometriosis, Cancer endometrium, an ovulatory infertility and early menarche. Decreased incidence are found in athletes with low body mass, increased parity. estrogen induces increased expression of progesterone receptors thus promoting oncogenic effect of progesterone. 7. Etiology Hormones Progesterone is most important in pathogenesis of fibroids, which have more concentration of receptors A & B as compared to normal myometrium. Highest mitotic counts are found in fibroid cells when progesterone concentration is also high. GnRH agonist decrease the size of fibroid. Concurrent Progesterone and GnRH therapy prevent regression in size of fibroid. Anti progesterone RU486 reduces the growth of fibroids. Estrogen dependent- never develop before puberty, regress after menopause, newer tumor seldom develop after menopause, 8. Etiology(C) Growth Factor Growth factors, proteins polypeptides produced locally bysmooth muscle cells and fibroblasts appear to promote growth offibroids primarily by increasing extracellular matrix. Many growth factors are participating in proliferation andgrowth of cells of fibroid Tumor Growth Factor-Beta, Basic-Fibroblast Growth Factor,increased DNA synthesis, EpidermalGrowth factor, Platelet Derived Growth Factor, Insulin likegrowth factor, PRL,Vascular endothelial factor etc 9. Locations Uterine Body-Intramural or intrstitial75%,submucous15% (sesile /Pedunculated, subserous 10%(pedunculatd torsion/ parasitic). Cervical.50% intramural6subserosal