Trisha E. O`Hehir, RDH
Periodontal disease is clearly a bacterial infection that is altered by the immune response of each individual. Many years ago, it was thought that bacteria directly attacked supporting periodontal structures by actually biting off chunks of bone and connective tissue. Sophisticated research has determined that periodontal destruction, although triggered by bacterial toxins, is caused by the patient`s own immune system.
In an attempt to protect itself, the body sets in motion complex activities which destroy both bone and connective tissue. The body will contain and localize an infection and then eliminate the bacteria by eliminating the teeth and surrounding tissues harboring bacterial plaque.
Clinical aspects and the eventual outcome of periodontal disease are well documented. But the very start of the disease process has only recently received attention. Cell-level activity, which allows bacterial toxins to invade the body through the gingival sulcus, provides the answers.
The epithelial attachment provides a physical barrier to bacterial penetration. However, we know that bacterial antigens are capable of passing through the attachment. It is a two-way barrier with gingival crevicular fluid flowing out and very limited substances passing inward. Until recently, research focused on the substances which passed through the epithelial attachment and into the underlying tissues.
We see what happens, but not when it starts
The question most often asked was: Did whole bacteria pass this barrier or just their by-products? Although some bacteria have been identified within tissue samples, it is generally accepted that adult periodontal disease does not involve direct invasion of bacteria through sulcular epithelium. The question now is not what passes through the attachment, but what allows this transfer of toxins to occur. Despite what we do know about the pathogenesis of periodontal disease and the bacteria involved, we also need to know what allows bacterial antigens to pass through the epithelial attachment. When does the epithelial attachment become permeable? When does the protective epithelial barrier fail to keep out bacterial antigens? In other words, when does periodontal disease start?
A recent communication in the Journal of Periodontology addressed this issue. Dr. Perry Ratcliff, periodontist and professor emeritus of the University of California, San Francisco, presented a model of pathogenesis which uses antigen penetration through the sulcular epithelium as the actual start of disease.
As clinicians, we must rely on the clinical evidence of disease rather than on biochemical changes occurring on a cellular level. However, what we see is not the actual start of the disease, but the visible signs of disease progression. Our clinical observations depend on tissue destruction resulting from periodontal disease. At this time, we have no tool or test to measure the very start of disesase - just the results.
If we understand the mechanisms by which sulcular epithelial cells increase in permeability, we would better understand the process by which bacterial antigens are allowed to pass though the attachment. Healthy epithelial cells have a normal life span of two to four days, at which time they are replaced. Normal shedding of epithelial cells occurs from the sulcus, the oral mucosa, and the tongue.
Once shed, these epithelial cells are broken down by oral bacteria, releasing volatile sulphur compounds (VSC), specifically hydrogen sulfide and methal mercaptan. These compounds are released into the saliva where they are taken up by supragingival bacterial plaque. Wicking action then draws these agents into the sulcus by way of subgingival bacterial plaque. Thus, the VSC or permeation agents are delivered directly to the epithelial attachment, where their chemistry increases the permeability of the epithelial attachment, allowing bacterial antigens to cross the defensive barrier. This important finding adds to our understanding of the pathogenesis of periodontal disease.
The majority of our work in periodontics now involves people who have already lost attachment and bone. But earlier intervention in those cases could prevent such losses. In the past, more research attention has been placed on the connective tissue ramifications of inflammatory periodontal disease, overlooking the actual permeation of bacterial antigen through the epithelial attachment.
This concept of pathogenesis may lead to research in the area of antigen permeation which could provide clinical applications. This information would allow us to intervene at the start of the disease process, before periodontal disease had a chance to destroy connective tissue and bone.
Research on the cellular activity of the epithelial attachment will eventually lead to clinical applications. Although it is possible to measure VSC levels clinically, this technology is currently being used simply to monitor oral malodor. However, a recent report by Japanese researchers correlated elevated VSC levels with periodontal disease.
Perhaps future work will identify a critical level for permeation agents, the level at which bacterial antigen is capable of penetrating the epithelial attachment. We would then know exactly when periodontal disease begins. Although early cell-level changes are not perceived through clinical evaluation, knowledge of antigen penetration could be used to develop a diagnostic tool. In that way, cell level activity could easily be monitored by dental hygienists in clinical practice, or even patients at home.
Trisha E. O`Hehir, RDH, is a senior consulting editor of RDH. She also is editor of Perio Reports, a newsletter for dental professionals that addresses periodontics.
