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Heat Shock Proteins and the Oral-Systemic Connection

The body has natural mechanisms to help protect itself and its processes in times of stress and duress. One of those self-protective processes involves mechanisms to protect protein functionality with increased heat, pH changes, pressure, and microbial challenge. “Stress proteins” otherwise known as Heat Shock Proteins are one such mechanism.

One of the basic evolutionary conserved mechanisms in bacterial and human cells involves the creation of Heat Shock Proteins which help protect native proteins against changes in folding and functionality when altered by a challenge. These challenges include infections, mechanical pressures (eg high blood pressure), temperature, and so forth. Stress on the organism’s cells up-regulates the creation of these proteins. But there is also a dark side to the equation.

It turns out that Porphyromonas gingivalis which contain endotoxic lipopolysaccharide particles (LPS) are homologous to human Heat Shock Proteins (hHSP60, where “60” is the weight of the protein). This means that the Pg HSP (called “GroEL) is similar in shape and molecular recognition as that of human HSP.

The body’s immune system recognizes the Pg GroEl HSP and creates an antibody to it. Because of its homologous appearance with hHSP60, the bacterial GroEL antibody also attacks the hHSP60 molecule, causing damage to the associated cell. This sets the stage for an interesting array of autoimmune considerations, as well as direct damage to tissues and cells within the body. This means that in the presence of periodontal disease and bacterial GroEL, the body’s natural immune mechanism is primed to attack similar looking human heat shock proteins and the cells related to them.

When these cells are endothelial cells, and damage is done to them, they are set up to incur inflammation damage, setting off the inflammation cascade including the creation of atherosclerosis, according to published studies on this topic.

This explanation, also referred to as “molecular mimicry”, offers an additional mechanism through which oral health is related to systemic health - and underscores the importance of detection of specific bacteria involved in periodontal disease, and their eradication through appropriate periodontal therapy. It also highlights the importance of informed co-management in an interdisciplinary manner with physicians and other health professionals.

References:

  • Lamb et al., Molecular mimicry in atherosclerosis: a role for heat shock proteins in immunization. Atherosclerosis, Volume 167, Issue 2, April 2003, Pages 177–185.
  • Jeong E et al., Predominant immunoreactivity of Porphyromonas gingivalis heat shock protein in autoimmune diseases. J Periodontal Res. 2012 Dec;47(6):811-6.
  • Ford PJ, et al., Anti-P. gingivalis response correlates with atherosclerosis. J Dent Res. 2007 Jan;86(1):35-40.