Periodontitis and Systemic Disorder-An Overview of Relation and Novel Treatment Modalities

Abstract

Periodontitis, a major oral disease, affects a vast majority of the population but has been often ignored without realizing its long-fetched effects on overall human health. A realization in recent years of its association with severe diseases such as carditis, low birth weight babies, and preeclampsia has instigated dedicated research in this area. In the arena of periodontal medicines, the studies of past decades suggest a link between human periodontal afflictions and certain systemic disorders such as cardiovascular diseases, diabetes mellitus, respiratory disorders, preterm birth, autoimmune disorders, and cancer. Although, the disease appears as a locoregional infection, the periodontal pathogens, in addition their metabolic products and systemic mediators, receive access to the bloodstream, thereby contributing to the development of systemic disorders. Mechanism-based insights into the disease pathogenesis and association are highly relevant and shall be useful in avoiding any systemic complications. This review presents an update of the mechanisms and relationships between chronic periodontal infection and systemic disorders. Attention is also given to highlighting the incidence in support of this relationship. In addition, an attempt is made to propose the various periodonto-therapeutic tools to apprise the readers about the availability of appropriate treatment for the disease at the earliest stage without allowing it to progress and cause systemic adverse effects.

Keywords: autoimmune disorders; cancer; cardiovascular diseases; diabetes mellitus; inflammation; periodonto-therapeutic; preterm birth.

Figure 1

Inflammatory cascade of periodontitis. Pathogen mediates a series of events leading to the recruitment of inflammatory cells at the infection site. This triggers the phagocytosis of bacterial cells, followed by the apoptosis of phagocytic cells and resolution of inflammation. Imbalance in this cascade leads to chronic inflammation and associated systemic complications.

Figure 2

Oral afflictions and cardiovascular disease. Oral infections mediated bacteremia generates the hyper-reactive mononuclear phagocytes, bacterial and inflammatory products, a state of hyper-coagulation and teeth loss. All this leads to vascular damage and hence results in cardiovascular complications.

Figure 3

Two-way link of periodontitis with diabetes. Bacterial endotoxins lead to an increase in interleukin (IL-1β) and the tissue necrosis factor (TNF-α) which results in hyperlipidemia. This also leads to the destruction of β cells of the pancreas and hence insulin resistance. In the reverse direction, the hyperglycemia leads to defective polymorphonuclear neutrophils’ (PMN) functions, defective host response, and collagen synthesis, which promotes RAGE (receptors of advanced glycation end-products) in PMN. All these factors ultimately aggravate the periodontal infection.

Figure 4

Hypothetical translocation of periodontal infection to fetus. Periodontopathic bacteria and their endotoxins penetrate the placenta from the gingiva via systemic circulation. This generates the inflammatory response in the placenta, resulting in the trigger of parturition [51].