Answer: C) Inflammatory cytokines and bacterial dissemination
Your selected answer is correct.
Explanation:
Periodontal disease is a chronic bacterial infection of the supporting structures of the teeth. The proposed mechanisms linking it to adverse pregnancy outcomes (preterm birth, low birth weight) involve two main pathways:
  1. Hematogenous bacterial dissemination - Oral pathogens (e.g., Fusobacterium nucleatum, Porphyromonas gingivalis) can enter the bloodstream (bacteremia) and reach the placenta/fetal membranes, triggering local infection and inflammation.
  2. Inflammatory cytokine pathway - Periodontal infection drives systemic elevation of pro-inflammatory mediators, including:
    • PGE2 (prostaglandin E2) - a key trigger of uterine contractions
    • IL-1β, IL-6, TNF-α - cytokines that can stimulate cervical ripening and membrane rupture
    • Matrix metalloproteinases (MMPs) - degrade fetal membrane collagen
These inflammatory mediators mimic the normal cascade that initiates labor, but trigger it prematurely.
Why the other options are wrong:
  • A) Nutrient deficiency - Not a mechanism of periodontal disease; it's a risk factor for poor pregnancy outcomes independently.
  • B) Hormonal imbalance - Hormonal changes in pregnancy actually worsen periodontal disease (not the other way around in this context).
  • D) Smoking - A confounding risk factor shared by both conditions, not the mechanistic link.
This is well-supported by evidence, including studies showing F. nucleatum isolated from placental tissue and amniotic fluid in preterm deliveries.
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