Introduction
In the last few decades, dentists have relied upon the research and evidence-based presentation and prevalence of periodontal diseases to plan treatment strategies effectively to combat this common oral disease. When the dental surgeon or the patients themselves possess an accurate understanding of the underlying immunologic mechanisms that are set into motion by virtue of numerous inflammatory mediators, host immunity, and the inflammatory cascade of events that trigger the disease process, it becomes easier to plan the treatment of periodontal disease.
Periodontal disease is also known as a polymicrobial infection that affects the periodontal apparatus, the periodontal ligament, and the alveolar bone. Host response and immunity are among the most important aspects that help identify key pathogenesis aspects in developing periodontal diseases. The pathogenic bacteria of the oral cavity are characterized by their ability to;
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Colonize the host tissues.
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Evade host defense mechanisms and create an oral immune defense breach.
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Subsequent damage to the host tissues (periodontal ligament and alveolar bone).
Research shows that the mechanisms for these required steps in bacterial pathogenesis are responsible for the increased incidence of many of the commonly detected periodontal pathogens in individuals suffering from chronic periodontal disease. Interference with host defenses periodontal pathogens not only use multiple routes to interfere with host defense mechanisms but also have the capacity to prolong their presence within the gingival sulcular epithelium and the periodontal pocket.
What Are the Different Types of Host Response?
In periodontal disease, the first breach occurs through bacterial colonization of the subgingival area that consequently results in two types of host response:
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Innate host response.
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Acquired host immune response.
But even though such host response is present, the bacterial infiltration and degree of pathogenesis may cause severe outcomes in patients with poor oral hygiene and untreated local or systemic diseased individuals, immunocompromised patients, etc. The result of this infiltration is the next phase of initiation and progression of periodontitis. Alternatively, periodontal disease can also alter the immune response in individuals with defects in either their innate or acquired immunity that would limit the ability of bodily tissues and cells to mount an adequate response. Evidential documentation in dentistry has shown that the host response is, in fact, a significant determinant of the disease susceptibility of an individual.
What Is Innate Immunity?
Innate immunity plays a pivotal role in response to microbial or bacterial pathogenic colonization, which is a major phenomenon in periodontal diseases. Also, as a part of the innate response, secretory IgA, many essential enzymes, and antimicrobial factors are involved in neutralizing salivary microbial components. The factors attributed to host immunity response are lysozymes, lactoferrins, peroxidases, antimicrobial peptides, statins, defensins, cathelicidins, etc.
The enzymatic immune complex minimizes the detrimental impact of the biofilm complex by functioning synergistically. Research indicates that the neutrophil response in the host tissues is the first example of innate cellular response and probably plays a significant role in limiting the biofilm accumulation in the subgingival crevices.
What Is Acquired or Adaptive Immunity?
The adaptive or acquired immunity is directly correlated to periodontal diseases that are proven or indicated mainly by an elevation in the cell-mediated response, that is, either CD4+ or CD8+ cellular response or by the humoral response that is mediated by antibodies. The humoral or cell-mediated mechanisms have been shown to occur in periodontal disease, just as in the case of any other systemic infection of the body. The response is aggravated or mounted even more with increasing severity of periodontitis infection. Also, systemic and local antibody formations in acquired immunity demonstrate that following mechanical or chemical control through periodontal therapies by the dental surgeon or the periodontist, the host tissues regain immunity to a considerable extent post-treatment. The antibody formation is different or rather specific for various periodontal organisms; that is, for example, the immune mechanism or reactions differ based on the organism involved like:
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Aggregatibacter actinomycetemcomitans.
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Prevotella intermedia.
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Fusobacterium nucleatum.
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Capnocytophaga gingivalis.
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Capnocytophaga ochracea.
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Capnocytophaga sputigena.
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Eikenella corrodens.
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Campylobacter rectus.
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Oral spirochetes, etc.
These specific organisms are related to certain virulence factors, such as leukotoxins released, for example, by actinomycetemcomitans and the capsule of Porphyromonas gingivalis.
What Are Inflammatory Disease Mediators?
Although these bacterial pathogens are capable of causing direct destruction of the periodontal tissues, most of the pathology is directed in the oral cavity in the periodontal apparatus as an indirect process causing host cell activation through the production of tissue-degradative substances that are mentioned below.
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Cytokines: IL-1, IL-6, and IL-8 are considered essential factors in the destructive process. IL-1 promotes bone resorption and prostaglandin E2 (PGE2) stimulation by monocytes and fibroblast cells. The release of matrix metalloproteinases (MMPs) by the cytokines is also crucial for degrading the extracellular matrix. IL-6 is responsible for osteoclast formation that resorbed the alveolar bone, while IL-8 acts as a chemoattractant for neutrophils that stimulates MMP. These cytokine mediators are often discovered in elevated levels in inflamed gingival tissue.
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Tissue-Destructive Host-Derived Factors: The examples include tumor necrosis factor alpha and PGE2. These factors cause MMP production, inducing bone resorption. The combined actions of inflammatory molecules in these host-derived factors can cause significant tissue destruction.
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Human Gingival Fibroblasts: These cells demonstrate a variety of pathologic responses such as cell detachment and proliferation and eventually cause apoptosis or programmed cell death. Surface proteases, membrane lipids, and lipoproteins may further aggravate the induction of inflammatory mechanisms in the periodontal tissues that contribute to tissue damage.
Conclusion
Host immunity and adaptation play a major role in periodontal disease development and aggravation. For people suffering from periodontal disease, the major research-based hypothesis holds true that the innate and acquired immune responses are protective in minimal periodontal destruction or arresting the disease process. Also, in individuals in whom either the innate or acquired response is altered or impacted, the result is likely to be an aggressive or progressive disease that needs regular follow-up and elaborate management strategies by the dental surgeon.
