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Hypotheses related to pathogenesis of dry socket (alveolar osteitis)

Etiology and Pathogenesis
Related to cascade of events after tooth extraction—
- Liberation of plasmin, which contributes to fibrinolysis and activation of kinins
- Localized infection due to lack of blood clot (absence or clot lysis soon after formation)
Other contributing factors
- Bacteria—possible role of treponemes in clot degradation;
- AO significantly more common in the context of poor oral hygiene
- Trauma—local trauma at the extraction site activating inflammatory mediators
- Smoking—two theories postulated
- Negative pressure from sucking on cigarettes postulated to mechanically dislodge blood clots
- Vasoconstriction mediated by nicotine
- Medications—oral contraceptive pill usage linked to increased occurrence of AO mediated by increased
fibrinolysis from reduced levels of plasminogen activator inhibitor
- Anatomic—AO incidence greater after mandibular tooth extractions (especially third molars); theorized
to result from greater vascularity predisposing to clot breakdown
Chow et al. Review of Current Concepts of AO. J Oral Maxillofac Surg 2020.
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