The mechanics of labour traditionally concern the 3Ps, powers, passages and passengers. Studies on OASIS prevention seem concentrated on minimizing trauma to the passages. A recent study examined the powers (uterine contraction strength). It concluded that passive management of labour was more likely to cause weaker contractions, head deflexion and a larger presenting part, which was more likely to tear the anal sphincter. Comparing third and fourth degree tears (8.17%) from 100,000 primiparous women against an independent control group with the O'Driscoll active management regime (2.5% tear rate), the authors concluded that a deflexed foetal head (11.2 cm diameter) was more likely to overstretch the vagina, ligaments and external anal sphincter muscles than a flexed head (9.4 cm).The study [1] raised further questions: why do only some women undergoing passive management primiparous deliveries suffer OASIS, while most, even with a deflexed head, do not? Do the same mechanics of OASIS carry over to pelvic organ prolapse (POP) and symptom causation?To answer these questions, we examined the biomechanics of labour/delivery from a dynamic tissue injury perspective. It is evident that a foetal head at full dilatation (10 cm) will put considerable stress on the cardinal/uterosacral ligaments. What prevents these ligaments from rupturing in the vast majority of cases is that the change in collagen and glycosaminaoglycans effectively "plasticizes" the ligaments so they stretch rather than rupture. This is necessary, as the inlet and outlet diameters through which the head must pass are no more than 12-13 cm. Collagen fibrils depolymerize to lose up to 93% of their strength [2]. Pregnancy-associated softening of the uterine cervix occurs 48 h before labour. The biomechanical changes are extremely complex and not well understood. They can be explained at least partly by qualitative changes in the collagen and proteoglycans, for example an increase in dermatan sulphate. These reactions seem to be mediated by sex steroids by eicosanoids such as prostaglandin E2 and F2a and perhaps by relaxin, leukotrines and cytokines [3]. Fibroblasts, inflammatory cells such as polymorphonuclear leukocytes, eosinophils and macrophages are also of great importance, as is collagenase [3].However, not all connective tissue is protected from rupture by softening. At the pelvic inlet, dilatation of the cervix to 10 cm may overstretch the anterior attachments of the cardinal ligaments and pubocervical vaginal fascia to the cervical ring to actually tear them, causing a transverse defect (high cystocele). Approaching the outlet, damage to the pubourethral ligaments may cause stress urinary incontinence; the ATFP may become overstretched to dislocate from the pubic bone or, more likely, its attachment to the ischial spine; collagenous attachments of levators to the symphysis may cause overstretching. As the head descends to pass the pelvic outlet, the perineum must expand for the head to emerge.Why does the anal sphincter rupture? Whereas ligament...