Most of our patients and many of our colleagues would use the terms ‘gum disease’ or ‘gum problems’ to describe periodontitis. In light of the history of our understanding of this condition and the methods of treatment developed to address it, that makes a lot of sense.
For years, many dental professionals have been taught periodontitis is a bacterially driven gum disease. But is that really true? What if our current research had revealed it is really a bacterially-initiated, host-driven bone disease where the damage to the bone occurs through molecular and cellular mechanisms similar to rheumatoid arthritis? Big difference! Would that new understanding of periodontitis help our patients better understand our concern for their current and future periodontal health?
Redefining Periodontitis For Our Patients
‘Gum disease’ as a term for an inflammatory bone disease seems to create two issues. Most of us have heard a patient say, “My gums seem to bleed a little every once in a while, but when I brush my teeth better, it quickly goes away.” A health condition, which the patient cannot determine its degree of importance, with an apparent simple solution, is easily dismissed or trivialized.
We also hear patients say, “It is just a little gum recession – or my dentist said I have a pocket.” Doesn’t the bone have to be gone before the gum adapts? Don’t most sites of crevices deeper than 4mm develop as the supporting bone on the surface of the root deteriorates? When patients hear ‘gum recession’ is really ‘bone recession and gum adaptation,’ a new level of understanding and concern occurs for them. When patients learn a periodontal pocket develops when the bone is eroded away and leaves a gap behind, their perception of the need for care is usually elevated.
The chronic presence of a bacterial biofilm adhering to the subgingival surfaces of teeth, especially proximal surfaces, results in a response by the patient through immune/inflammatory pathways. The escalating inflammatory response in close proximity to the supporting bone leads to its progressive destruction in periodontitis susceptible individuals. The magnitude of the inflammatory response and the level of inflammation required to damage the bone is unique to each individual.
There are multiple factors influencing the extent of the bone deterioration and its location in the circumference of each tooth affected. As is common for human biofilm infections, there are no predictably effective antimicrobial or anti-inflammatory medicinal solutions. Though genetics drives many of the susceptibility factors, there are no genetic testing methods that result in favorable therapeutic outcomes.
Changing the Way We Talk About Periodontitis
Perhaps if the profession changes its language use to more accurate terms and avoids minimizing this important health issue, more productive conversations regarding periodontitis with our patients might occur. Out of those discussions, patients engaged in their own decisions, their own solutions to their periodontal health needs, could evolve. Our collaborating with those patients to support their efforts to gain and to sustain a healthy periodontium and dentition might prove to be more consistently successful.
Michael J. McDevitt, DDS, is a Contributing Writer for Spear Education [http://www.periogeorgia.com/]
References
- Schaudinn C, Gorur A, Keller D, Sedghizadeh P, Costerton JW. Periodontitis: an archetypical biofilm disease. JADA 2009; 140:978-986
- VanDyke TE. The management of inflammation in periodontal Disease. J Periodontontol 2008; 79:1601-1608.
- McDevitt MJ, Wang H, Knobelman C, Newman MG, di Giovine FS, Timms J, Duff GW, Kornman KS. Interleukin-1 genetic association with periodontitis in clinical practice. J Periodontol 2000; 77:156-163