How does biofilm lead to development of periodontal diseases – introduction

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14 Terms

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Periodontal Diseases

Bacterially-induced, immune-mediated inflammatory diseases of the tissues supporting the teeth.

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-Healthy sites: Well defined, precisely orchestrated, effective immune response.

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-Diseased sites: Exacerbated, uncontrolled, detrimental immune response

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Periodontitis – Risk Factors (multi-factorial aetiology)

  • Dental plaque- primary aetiological factor

  • Local factors - promote accumulation of dental plaque (calculus, restorations with overhanging margins),

  • Systemic factors – modify the host-bacteria interaction (Diabetes mellitus, puberty, pregnancy, immunodeficiency

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systemic factors can be further classified into…

modifiable and non modifiable

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systemic - Non-modifiable (background) factors 4 

  1. Age

  2. Race

  3. Gene polymorphism

  4. Hyper-responsive phenotype

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systemic - modifiable - Environmental, acquired factors: 3 

  1. Smoking

  2. Systemic diseases, medications

  3. Psychosocial factors

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Prerequisites for Periodontal Disease Initiation and Progression 3 

  1. Virulent periodontal pathobionts (adhesins, co-aggregation, invasion, factors that cause tissue damage),

  2. Local environment,

  3. Host susceptibility (gene polymorphism, PMN defects, smoking, diabetes, immunosuppression)

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Periodontal Tissues Destruction -split

  • Direct action of the microorganisms (20%)

  • De-regulated inflammatory (immune) response to dental plaque m.o. (disruption of protective innate immunity or unresolved inflammation) 80%

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Bacterial Virulence Factors

Early colonisers are mainly using glycolysis, late colonisers use proteolysis - they use a different set of enzymes 

They can produce collagenases - destroy periodontal tissues. Toxins to osteoblasts.

Direct tissue damage or poorly controlled immune response damage - which causes tissue damage 

Specific pathobionts as late colonisers - antigens - triggers host inflammatory response - leads to tissue damage - clinical expression

Many cells can sense antigens - can produce cytokines. The duration of the inflammation depends on the ratio of cytokines - prevalence of the pro-inflammatory cytokines - reach the peak of the inflammation 


<p><span style="background-color: transparent;"><span>Early colonisers are mainly</span><strong><span> using glycolysis, </span></strong><span>late colonisers use </span><strong><span>proteolysis</span></strong><span> - they </span><strong><em><span>use a different set of enzymes&nbsp;</span></em></strong></span></p><p><span style="background-color: transparent;"><span>They can produce </span><strong><span>collagenases -</span></strong><span> destroy periodontal tissues. Toxins to osteoblasts.</span></span></p><p><span style="background-color: transparent;"><span>Direct tissue damage or poorly controlled immune response damage - which causes tissue damage&nbsp;</span></span></p><p><span style="background-color: transparent;"><span>Specific pathobionts as </span><strong><span>late colonisers - antigens</span></strong><span> - triggers host inflammatory response - leads to tissue damage - </span><strong><span>clinical expression</span></strong></span></p><p><span style="background-color: transparent;"><span>Many cells can sense antigens - can produce cytokines. The duration of the inflammation depends on the ratio of cytokines - prevalence of the pro-inflammatory cytokines - reach the peak of the inflammation&nbsp;</span></span></p><p><br></p>
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<p>Direct and Indirect Tissue Damage</p>

Direct and Indirect Tissue Damage

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Tissue damage can occur for either combo

<p><span style="background-color: transparent;"><span>Tissue damage can occur for either combo</span></span></p>
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interleukin 1, 6 , 8 , 10

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