Host Immune Response to Plaque Biofilm

Host Immune Response to Plaque Biofilm

• Periodontal disease is a bacterial infection that triggers an inflammatory response in periodontal tissues.
• Bacteria are essential for the disease, but the body's response to the bacteria, in plaque biofilm, is the primary cause of tissue destruction.
• Host response refers to the body's response to bacteria.
• The immune system attempts to eliminate pathogens and limit infection spread, not specifically preserve the tooth or its tissues.
• Virulence factors enable biofilm bacteria to colonize and damage periodontal tissues. These factors can be structural characteristics or substances produced by the bacteria.
  • Lipopolysaccharide (LPS) is a component of mature plaque biofilm. Gram-negative bacteria with LPS are virulent.
  • Certain bacteria can invade host tissues, avoiding host defenses.
  • Certain bacterial enzymes degrade host proteins, contributing to periodontal damage.
• Factors affecting host response include:
  • Genetics: Genetic factors can increase susceptibility to periodontal disease.
  • Environmental: Tobacco smoking negatively impacts the immune system and inflammatory responses.
  • Acquired: Conditions like diabetes mellitus can affect the host response due to irregular blood sugar.

Inflammation: A Protective Host Response

• Acute inflammation is the body's first line of defense against invasion, eliminating harmful agents, replacing damaged cells, and initiating tissue repair.
• Inflammation resolution (catabasis) is a regulated process that re-establishes normal tissue health following removal of a microbial challenge.
• Inflammation can be favorable or detrimental, depending on its resolution process; uncontrolled or unresolved inflammation is damaging.
• Pro-inflammatory mediators (like prostaglandins, thromboxanes, prostacyclins, and leukotrienes) are associated with periodontitis. These mediators contribute to the destructive process by attracting neutrophils (PMNs).
• Inflammation-resolving mediators help dampen the acute response and stimulate tissue repair.
• Unresolved chronic inflammation can damage host tissues if the host response cannot contain the infection quickly.

Inflammatory Biochemical Mediators

• Cytokines, prostaglandins, and matrix metalloproteinases (MMPs) are important biochemical mediators in periodontitis.
• Cytokines are proteins that regulate cell behavior; their production is stimulated during an infection/tissue injury. Some play tissue-protective roles whereas others have potential to harm.
• Prostaglandins increase blood vessel permeability, allowing immune cells influx, and trigger osteoclast activity, destroying bone.
• MMPs (a class of proteases) break down the connective tissue matrix and promote tissue destruction.
• Imbalances or excessive production of these mediators frequently contribute to damage in periodontitis.

Histological Stages of Periodontal Disease

• Histological stages of periodontal disease (initial, early, established, advanced) depict progressive tissue changes in response to plaque.
• Initial lesion: Characterized by bacterial accumulation near the gingival margin, resulting in inflammatory responses by the host (increased vascular dilation and PMN migration)
• Early lesion: Increased inflammation is evident; cytokines, prostaglandins, and MMPs are produced. Sulcular epithelial ridges also appear during this phase.
• Established lesion: Plasma cells are prevalent, tissue changes are more pronounced, and collagen loss is notable.
• Advanced lesion (periodontitis): Characterized by periodontal pocket formation, alveolar bone destruction, and tooth mobility. Significant tissue damage during this stage is considered irreversible.

Current Theory of Pathogenesis

• The interplay between microbial challenges and the host response is a multilayered process affecting periodontal disease progression.
• Risk factors like genetic predisposition, environmental factors (like smoking), and acquired factors (like diabetes) affect the host response and tissue metabolism; making an individual susceptible to developing periodontitis.
• Bacteria produce virulence factors for initiation of periodontal disease while host immune cells release and produce inflammatory mediators to try to fight the bacteria.
• If microbial infection and host inflammatory response are not controlled, damage to connective tissue/alveolar bone occurs leading to periodontitis.