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Perio-Systemic Realtionship: Periodontal Surface Area. Does it Matter??

Focal Infection ( Defined as: A bacterial infection localized in a specific part of the body, such as the tonsils or oral cavity, that may spread to another part of the body.) has been an old theory set during the times of W.D Miller and William Hunter (Era of focal infection: in around 1900 – 1950). This theory was revisited with the advent of the periodontal medicine, relating various systemic diseases with periodontal disease. Every day data are piling up showing the different relation between systemic diseases and periodontal condition.. There are studies showing evidence that diabetes and diabetic control is influenced by presence of periodontal disease. Scientists are exploring and gathering evidence for relationship between periodontitis and other systemic diseases like cardiovascular disease, pre-term delivery, respiratory disease, osteoporosis and rheumatic arthritis to name a few.

These studies associating the systemic and periodontal disease explain it based on the hypothesis that either the bacteria pass through the periodontal pocket into the blood stream causing complications or through host response to those bacteria causing the connective tissues underlying pocket epithelium to secrete inflammatory mediators(1) . Several of the studies and literature (2 ) reported that in patients with moderate periodontitis, the surface area of pocket could be size of the palm of the hand (75cm2) or ventral surface of fore arm (≈ 200cm2) and that this amount of surface area would influence the systemic health. This formed the basis of many studies in explaining the perio-systemic relationship.

During one of my literature searches I hit upon an interesting article which refuted the above made claims of regarding the pocket surface area. In this study the dentogingival surface area was measured in healthy and diseased sites and the findings were thus:

“Among individuals with periodontitis, the mean dentogingival epithelial surface (DGES) in populations ranged from 8 cm2 to 20 cm2. The maximum DGES observed among the 5,184 individuals in the three populations with periodontitis was 44 cm2. The increases in DGES associated with periodontitis ranged somewhere between the ventral surface area of an average adult fingertip (3 cm2) to the ventral surface of one to two average adult fingers (15 cm2).” (1)

Now the question that obviously creeps up I ones mind is how you explain the perio-systemic relationship? Well the amount of surface area of pocket affecting the systemic health is just a part of the hypothesis. The host response which causes periodontitis could also be the trigger. The LPS from the perio-pathogens which turn on the cells in the local area acting as repeated systemic challenges, could also trigger systemically the host immune cells to secrete inflammatory mediators affecting systemic health. The host immune cells by feedback mechanism can initiate a hyper response in the body leading to increased enzyme and inflammatory mediators being secreted by host cells at distant sites.

For example the DQ gene and the dietary low density lipoprotein (LDL) are know to cause the monocyte to be hyper-responsive and triggering of such a monocyte by bacterial products (lipopolysaccharide,toxins and enzymes) leads to increased cytokine release. The increased cytokines which initiate the other enzymes and inflammatory mediators could then lead to connective tissue break down or systemic disease depending on site of action. (congestive heart disease, periodontitis). So in the end how much dose the surface area matter??

(This is just the authors view)

Refrences:

1. The dentogingival epithelialsurface area revisited.

Hujoel PP, White BA, GarcõÂa RI, Listgarten MA: J Periodont Res 2001; 36: 48- 55.

2. Clinical Periodontology and Implant Dentistry

Edited by: Jan Lindhe, Thorkild Karring and Niklaus Lang, Fourth Edition.

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