Download - Periodontal Disease and Preterm Birth Gazabpreet Bhandal 1 st year Resident, Dept. of Periodontics
Outline
• Pathogenesis of Periodontitis
• Pathogenesis of Preterm Birth
• Inter-relationship between Periodontitis and Preterm Birth
• Conclusion
Periodontal DiseaseAn infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment and bone loss and is characterized by pocket formation and/or recession of the gingiva.
RISK FACTORS:
1. Bacterial factors
2. Smoking
3. Age
4. Host Response Related
- Systemic ( eg: Diabetes, Pregnancy )
- Stress
- Genetics
* Periodontal diseases are “a specific mixed infections which cause periodontal destruction in the appropriately susceptible host” (Offenbacher 1996)
Pathophysiology of the Periodontal Disease
Periodontal
Disease
Direct effects of bacteria:Inc. edema
Inc. GCFProteases, Collagenases,
Fibrinolysin, phospholipase A
H2S, NH3
Genetic Risk Factors:Host Immuno-inflammatory
responseConnective tissue
and bone metabolism
Environmental and Acquired Risk factors
Indirect Effects of bacteria:
PMNsLymphocytesMonocytesFibroblasts
LPS Pro-inflammatory
cytokines: (IL-1,IL-6,IL-8,TNF-α, PGE-2, MMPs)
Organic Molecule Function
Collagenase Breaks peptide bonds in collagen.Virulence factor
Fibrinolysin Inactivates fibrin molecules occurring in undesirable exudates
Phospholipase A Involved in breakdown of phospholipids to Fatty Acids
MMPs Zn dependent endopeptidases responsible for degradation of extracellular matrix
TNF-alpha Adipokine ; Produced chiefly by activated macrophages.
LPS Endotoxin; binds to CD14/TLR4/MD2 receptor complex stimulates pro-inflammatory cytokines and NO.
Low Birth Weight Preterm Birth
• According to WHO, preterm birth is defined as delivery before 37 completed weeks of gestation.
• Low Birth Weight is defined as weight less than 2,300gms
Chorioamnionitis
• Chorioamnionitis or intraamniotic infection is an acute inflammation of the membranes and chorion of the placenta, typically due to ascending microbial infection in the setting of membrane rupture.
• Overall, 1-4% of all births in the US are complicated by chorioamnionitis.
Ascending InfectionMicroorganisms residing in the
external genitalia gain access to the
amniotic sac
Debilitatio
n and
rupture of the
sac
Spread of the
infectious
agent into the
amniotic fluidAspiration/
swallowing of the micro-
organisms
Immune response
triggered on the amniotic
sac by infection
Induction of labor
Role of pro-inflammatory cytokines in preterm birth
Infected sites (eg: Periodontium) or Placenta
Pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha)
Stimulation of PGE2 synthesis by human placenta and chorioamnion
Induction of Abortion or labor
• Examination of effect of P.gingivalis on pregnant hamsters revealed elevation of PGE2 and TNF-alpha levels (Collins 1994)
Offenbacher (1996), Jeffcoat (2001), Jarjoura (2005) : Proposed that periodontal disease is a risk factor for PLBW.Scaling and Root Planing in pregnant females reduced the incidence of preterm birth (Jeffcoat 2001)
Negative evidences:
• Davenport et al(2002), Noack et al(2004), Veltore et al (2008), Rajapakse et al(2005): No evidence for association between periodontal disease and preterm low birth weight.
• Hoolbrook et al(2004), Moore et al(2005) : Reported no association between the severity of the periodontal disease and pregnancy outcome.
• Buduneti et al(2005): No difference in dental and periodontal parameters between cases and controls.
Sources of Bias:
1. Variation in the definition of the periodontal disease.
2. Variation in the definition of the Adverse Pregnancy Outcomes (APOs)
3. Confounding factors (eg: socio-economic status and smoking)
Conclusion
• There are numerous studies that support a positive association between periodontal disease and preterm birth but unfortunately trials of antibiotic treatment have not shown any significant decrease in the rate of preterm birth.
• The effectiveness of antimicrobial therapy in eradicating these infections suggests that its failure to prevent preterm births is evidence that the infections alone are not causal.
• Longitudinal studies are warranted to establish a stronger and causal relationship between the two.