Aggressive Periodontitis (Part 1) - Etiology and Pathogenesis
TLDRPeriodontitis, inflammation of periodontal tissues around teeth, is caused by microorganisms leading to tissue and bone destruction. Chronic periodontitis affects adults and children, influenced by various factors, while aggressive periodontitis (AP) rapidly destroys periodontium in healthier individuals, often genetically predisposed. AP is categorized into localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP). The bacterium Aggregatibacter actinomycetemcomitans is considered the primary pathogen due to its high presence in LAP patients and its ability to evade the immune system, destroy connective tissue, and inhibit neutrophil function, contributing to the disease's progression.
Takeaways
- π¦· Periodontitis is an inflammation of the periodontal tissues surrounding teeth, caused by specific micro-organisms.
- π Chronic periodontitis is the most common form, affecting adults and sometimes children, and is associated with plaque and calculus accumulation.
- π₯ Aggressive periodontitis (AP) differs from chronic form, primarily affecting adolescents and young adults, with rapid destruction and little plaque or calculus accumulation.
- π AP is classified into localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP), with LAP affecting incisors and first molars, and GAP causing widespread destruction.
- 𧬠The pathogenesis of AP is mainly attributed to microbiological factors and genetic predispositions to certain immunologic abnormalities.
- π Aggregatibacter actinomycetemcomitans is considered the primary pathogen in AP, with 97% of LAP patients harboring high numbers of this microorganism.
- π‘οΈ Leukotoxin, a protein toxin produced by A. actinomycetemcomitans, helps it thrive and can potentially kill neutrophils, the first line of defense in inflammation.
- π« A. actinomycetemcomitans releases factors that inhibit neutrophil response and evade the host immune system, contributing to the disease progression.
- π’ The host inflammatory response, elicited by the bacteria, causes tissue damage while trying to protect the host, with hyper-responsive monocytes and macrophages contributing to rapid bone resorption.
- 𧬠Genetic predispositions in individuals with LAP include defective neutrophil chemotaxis and inefficient antibody binding to bacterial antigens, which can amplify the disease response.
Q & A
What is periodontitis?
-Periodontitis is the inflammation of the supporting periodontal tissues that surround the tooth, caused by specific groups of micro-organisms, leading to progressive destruction of the periodontal fibers and the alveolar bone.
What are the two main types of periodontitis?
-The two main types of periodontitis are chronic periodontitis and aggressive periodontitis (AP).
Who is most commonly affected by chronic periodontitis?
-Chronic periodontitis most commonly affects adults, and sometimes children and adolescents.
How does aggressive periodontitis differ from chronic periodontitis?
-Aggressive periodontitis primarily occurs in adolescents and young adults, causes rapid destruction of the periodontium with minimal or no plaque and calculus accumulation, and affects healthy individuals with no systemic disease, often having a genetic predisposition.
What are the two classifications of aggressive periodontitis?
-Aggressive periodontitis is further classified as localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP).
What is the primary pathogen believed to cause aggressive periodontitis?
-Aggregatibacter actinomycetemcomitans is thought to be the primary pathogen involved in aggressive periodontitis.
Why is A. actinomycetemcomitans considered the primary pathogen in aggressive periodontitis?
-A. actinomycetemcomitans is considered the primary pathogen because almost 97% of patients with this disease harbor a very high number of this microorganism, and it has been found that reducing its load during treatment correlates positively with the clinical success of the treatment.
How does A. actinomycetemcomitans contribute to the disease progression?
-A. actinomycetemcomitans can translocate through the junctional epithelium into the connective tissue and produce a protein toxin called leukotoxin, which can kill neutrophils or suppress lymphocytic activity, inhibiting the host's immune response and causing rapid destruction of connective tissue and bone.
What role does the host inflammatory response play in aggressive periodontitis?
-The host inflammatory response, elicited by the bacteria, causes damage to the host tissues while trying to protect them. Patients with aggressive periodontitis may have hyper-responsive monocytes and macrophages, releasing bone resorbing proteins like Interleukin-1 and Prostaglandin-E2 in excess, thus contributing to rapid bone resorption.
What genetic predispositions are associated with aggressive periodontitis?
-Individuals with aggressive periodontitis are known to have genetic predispositions to immunologic abnormalities, such as defective neutrophil chemotaxis and inefficient antibody binding to bacterial antigens, which can amplify the disease response.
How does the genetic predisposition affect LAP patients?
-LAP tends to occur among family members, and the neutrophil defect has a genetic predisposition. Additionally, LAP patients may have antibodies that cannot efficiently bind to bacterial antigens, leading to a robust and increased antibody response to counteract the inefficient binding.
Outlines
π¦· Understanding Periodontitis and Its Forms
This paragraph discusses periodontitis, an inflammation of the tissues surrounding teeth, caused by micro-organisms leading to destruction of periodontal fibers and alveolar bone. Chronic periodontitis is the most prevalent, affecting adults and sometimes children, and is linked to plaque and calculus accumulation. In contrast, aggressive periodontitis (AP) primarily affects adolescents and young adults, causing rapid destruction with minimal plaque or calculus. AP is further divided into localized aggressive periodontitis (LAP), affecting incisors and first molars, and generalized aggressive periodontitis (GAP), with widespread destruction. The pathogenesis of AP is mainly attributed to microbiological factors and genetic predispositions, with Aggregatibacter actinomycetemcomitans being the primary pathogen. The paragraph delves into why A. actinomycetemcomitans is considered the main culprit, its prevalence in LAP patients, and the mechanisms by which it causes disease, including its ability to invade connective tissue and produce leukotoxin, which disrupts the immune response and contributes to rapid bone resorption. Additionally, the host's inflammatory response, hyper-responsive monocytes, and macrophages exacerbate the condition.
π©Έ Genetic and Immune Factors in LAP
This paragraph focuses on the genetic and immune factors associated with localized aggressive periodontitis (LAP). It highlights that 70-75% of LAP patients have defective neutrophil chemotaxis, and there is a tendency for LAP to occur among family members, indicating a genetic predisposition. The paragraph also discusses another defect in LAP patients where antibodies are less efficient at binding to bacterial antigens, which impairs the complement-mediated removal of these micro-organisms. As a result, LAP patients often exhibit a robust and increased antibody response to compensate for this inefficiency.
Mindmap
Keywords
π‘Periodontitis
π‘Plaque
π‘Calculus
π‘Aggressive Periodontitis (AP)
π‘Localized Aggressive Periodontitis (LAP)
π‘Generalized Aggressive Periodontitis (GAP)
π‘Porphyromonas gingivalis
π‘Leukotoxin
π‘Neutrophils
π‘Genetic Predisposition
π‘Immune Response
Highlights
Periodontitis is the inflammation of the supporting periodontal tissues surrounding the tooth.
It is caused by specific groups of micro-organisms, leading to progressive destruction of periodontal fibers and alveolar bone.
Chronic periodontitis is the most common form, affecting adults and sometimes children and adolescents.
Disease progression depends on local, systemic, and environmental factors, as well as plaque and calculus accumulation.
Aggressive periodontitis (AP) primarily occurs in adolescents and young adults, causing rapid destruction with minimal plaque or calculus.
AP occurs in healthy individuals with no systemic disease and has a genetic predisposition.
AP is classified into localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP).
LAP is characterized by localized destruction around the incisors and first molars, whereas GAP involves more widespread damage.
The pathogenesis of AP is mainly attributed to microbiological factors and genetic predispositions to immunologic abnormalities.
Aggregatibactor actinomycetemcomitans is considered the primary pathogen involved in AP.
Almost 97% of LAP patients harbor a high number of A. actinomycetemcomitans, compared to 21% of chronic periodontitis patients.
LAP patients show elevated levels of A. actinomycetemcomitans at sites of destruction and elevated serum antibody levels against it.
Reducing the load of A. actinomycetemcomitans during treatment positively correlates with the clinical success of the treatment.
A. actinomycetemcomitans can translocate through the junctional epithelium, invading the connective tissue.
Leukotoxin, a protein toxin produced by A. actinomycetemcomitans, can kill neutrophils or suppress lymphocytic activity.
The bacteria release chemotactic inhibitory factors, impairing neutrophils' ability to respond to chemotactic factors and migrate to diseased sites.
A. actinomycetemcomitans evades the host immune response and produces collagenases and bone resorbing factors, causing rapid tissue and bone damage.
The host inflammatory response, elicited by the bacteria, can cause damage to host tissues and contribute to rapid bone resorption.
Patients with LAP have genetic predispositions to immunologic abnormalities, such as defective neutrophil chemotaxis.
LAP tends to occur among family members, indicating a genetic predisposition to the neutrophil defect.
In LAP patients, antibodies cannot efficiently bind to bacterial antigens, leading to an increased antibody response to counter this inefficiency.
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