Gingivitis should be the end of the line
The progression of periodontal disease from health to gingivitis to full-blown periodontitis is complex and only partially understood. Richard Nagelberg, DDS, looks into the bridge between gingivitis and gum disease, and how clinicians can prevent the latter.
Richard H. Nagelberg, DDS
The complexity of the interactions between periodontal pathogens, the inflammatory response, hard and soft periodontal tissue degradation, and the remote effects of periodontal pathogens, most notably on the arterial vasculature, cannot be overstated. The processes are massively complex and only partially understood.
The progression of periodontal disease from health to gingivitis to full-blown periodontitis is similarly complex and also only partially understood. We now know that gingivitis must necessarily precede periodontitis and this is not a random event; it must be so. The reason it works this way has to do with the hereditary events associated with both gingivitis and periodontitis. A patient must be genetically susceptible to periodontitis for it to occur. The DNA that controls the expression of periodontitis has to be activated. The inflammatory processes associated with gingivitis act as the switch, igniting the DNA and facilitating periodontitis expression if a sufficient number of periodontal pathogens are present.
Gingivitis is generally regarded as an early form of periodontitis; however, this is not the case. It is the gatekeeper to it. Gingivitis is also generally regarded as a nonserious, reversible condition. This is also not the case. Research has shown that patients with pocketing of only 3 mm have an elevated risk of vascular disease; however, higher levels of periodontal disease carry greater risk of vascular disease.
Examination of the molecular and cellular events occurring during the immuno-inflammatory response can be expanded to the clinical level and provide insight into therapeutic strategies. For example, during an inflammatory response, a number of cells such as monocytes and neutrophils are attracted to the site of inflammation. These cells release a host of toxic chemicals including proteases, among others. These toxic compounds are destructive to the body and the pathogens. The net effect is to liquefy the surrounding tissue to reduce the likelihood of bacterial metastasis. The body is willing to sacrifice tissue in an attempt to control the microbes.
Another example involves the timing of the inflammatory response and the reproductive rate of the bacteria. The acute inflammatory response to a bacterial challenge occurs in a matter of minutes. Chronic inflammation takes days or weeks to fully develop in response to the persistence of the bacteria in the tissue. The bacteria, however, reproduce in a matter of hours. It is no surprise that the body is commonly battling uphill to catch up with the bacteria due to these differences in the timing of events.
One of the ways clinicians can address gingivitis is as a last-chance opportunity to avoid the noncurable nature of periodontitis, which will require patients to manage their disease every day forever. Periodontitis involves localized or generalized irreversible loss of the patient's jawbone. The bacterial and inflammatory events noted above provide insight into the critical need to intervene aggressively when a patient presents with, or progresses from, health to gingivitis. Resolution of inflammation is a time- and energy-consuming process that occurs through tissue remodeling. Gingivitis induces a low-grade inflammatory response, which can lead to chronic inflammation if the bacteria persist, potentially leading to irreversible loss of tissue and function.
Doing everything possible to prevent the progression of gingivitis to periodontitis is the most important and impactful thing clinicians can do for their patients. This primarily involves getting a power toothbrush in the patient's hands and the appropriate interdental biofilm-removing devices. A 2015 study concluded that flossing is only recommended for sites of gingival and periodontal health, where interdental brushes (IDBs) will not pass through the interproximal area without trauma, and that IDBs are the device of choice for interproximal plaque removal.1
It is common in the dental profession to be casual about gingivitis, as evidenced by the paucity of writing on the subject. This is a dangerous mindset. Patients are best served if gingivitis is considered the endpoint of disease progression and that intervention should be undertaken aggressively and expeditiously. Currently there is no code or treatment for gingivitis. For most patients, providing the biofilm removal tools they need is sufficient to revert to health. This is our most important responsibility.
Richard H. Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity.
1. Kapel IL, Van der Weijden F, Doerfer C, et al. Primary prevention of periodontitis: managing gingivitis. J Clin Periodontol. 2015;42 (suppl 42):S71-6.
GP Perio: The Oral-Systemic Connection Richard H. Nagelberg, DDS