Periodontal Inflammation And Systemic Diseases

Periodontal Inflammation And Systemic Diseases

Inflammation is a physiologic series of responses generated by the host in response to infection or injury.

• The initial events of inflammation are initiated by vascular reactions at the site of injury leading to extravasation of fluid and plasma proteins and recruitment of leucocytes to the site of injury.
• Inflammation is a natural beneficial response confirming the injury or infection, and serves as the first step in the initiation of the immune response.
• Ideally, the innate immune or inflammatory response is sufficient to eliminate the infection, allowing for healing and return to homeostasis.
• If the innate immune response fails, chronic inflammation ensues.
• In the case of chronic inflammation, the persistence of the response leads to host tissue self-destruction and may result in irreversible pathological changes.
• Various cell types including mast cells, platelets and leukocytes generate inflammatory mediators (chemokines and cytokines).
• Elevated levels of these molecules promote inflammation and amplify the response.
• Proteins-including cytokines and chemokines. low molecular weight lipids derived from arachidonic acid, nitric oxide and carbon monoxide, reactive oxygen species, and nucleotides are recognized as inflammatory mediators.
• Neutrophils are the most abundant white blood cells recruited to the early inflammatory periodontal lesion.

• The early response that initiates the inflammatory cascade begins with expression of cell adhesion molecules on endothelial cells and secretion of various cytokines such as lL-8 and MCP-l in response to the bacterial stimulus that recruits neutrophils to the site of invasion.
• If the first line of defense fails to clear the bacteria, the lesion matures as described histologically by Page and Schroeder, the established chronic gingivitis lesion exhibiting all the components of an immune lesion with T-cells, B-cells and antibody-secreting plasma cells. The trigger for transition from the established (stable) gingivitis lesion to the advanced or progressing periodontitis lesion remains elusive, but it is known that it is characterized by a continuous and uncontrolled response by neutrophils. Interestingly, it would appear that in the progressing immune lesion of periodontitis, there is continuous neutrophil activation leading to ‘neutrophil-mediated tissue injury’.