What is chronic inflammatory periodontal disease (CIPD)?

Many dental workers don't even measure blood pressure regularly, let alone provide advice to patients about obesity or blood sugar. To make matters worse, we in the dental community have become complacent with the erroneous assumption that some forms of periodontal disease are normal or tolerable. Let us step up our action, especially for patients who already have risk factors for CIPD and related systemic diseases, and do more than just clean their teeth twice a year. We should accurately diagnose oral disease, provide treatment to maximize oral disease resolution, and then help patients stay that way.

rice: You talked about sites in CIPD treatment. Can you tell me about your philosophy and the science associated with it?

Donley: CIPD is a systemic disease with site-specific manifestations. We can describe the degree and rate of progression at a patient level through staging and grading. However, the preferred level of oral health is teeth that are fully functional, aesthetically pleasing to the patient, relatively free of any diseased sites, and inherently maintainable.

We need to diagnose, treat, reassess and manage CIPD at field level. We now have an evidence-based definition of what constitutes a healthy website. Periodontal health is defined as a site with no evidence of inflammation, no ongoing attachment loss, and optimal probing depth (a depth of probing that is accessible to the clinical team and maintainable to the patient). In short, we process sites that do not meet this definition.

We may develop treatment plans and coding procedures on a sextant or quadrant basis, but we never lose sight of the fact that CIPD is a systemic disease with site-specific manifestations. That’s not my philosophy – that’s what current science says. This requires clinicians to understand what a healthy site is every time they insert a probe into the gingival sulcus. There should be no hesitation about which areas require treatment.

rice: I like that you talk about eliminating and interrupting the cause. Please share more.

Donley: It's no longer just about removing plaque and tartar. CIPD occurs when biofilms become dysbiosis. Biofilms are microscopic. Only when a biofilm grows to the point where we can recognize it clinically do we call it a plaque. Yes, plaque calcifies and forms tartar, but calculus itself is also a microscopic term. Only when the calcified biofilm grows to the extent that we can detect it clinically does we call it “dental calculus.”

Not all biofilms form plaques, not all plaques calcify, and not all calcified biofilms grow into clinically apparent calculus. You can remove clinical evidence of plaque and tartar and restore the health of an area. If you want to maximize your chances of healthy recovery, you need to eliminate any clinical cause and then expose the affected surface (the adjacent tooth surface that meets the disease site definition) to a method or combination of methods that will also disrupt any microscopic cause.

While we can use visual and tactile evidence to determine the presence of plaque and detectable calculus, it is currently impossible to determine whether a microscopic cause is present. Until we have better diagnostic methods, we should assume that the surface adjacent to the site where the disease is present is covered with a microscopic cause and treat it as described above. Therefore, the only way we can be sure that the microscopic etiology has been sufficiently disrupted is if we expose every square millimeter of the affected surface to a method or combination of methods that is capable of interrupting the microscopic etiology.

We no longer want to actively (or inadvertently) remove tooth structure. We've known for at least 30 years that we don't want a glass-smooth surface. Science has proven that what we want is the opposite of what many of us have been trained to achieve. We wanted to preserve the cementum because the biofilm is not embedded as deeply into the cementum as originally thought, but rather in the outer 40 microns. We also know that preserving cementum provides better potential for tissue reattachment. We hope to interrupt any microscopic cause without removing cementum. At present, it seems reasonable to consider a two-step approach to adequate debridement in the field:

  • step 1: Remove any clinically detectable biofilm without removing excessive cementum.
  • Step two: Interrupting any underlying microscopic etiology by exposing every square millimeter of the tooth/root surface involved to a method or combination of methods capable of interrupting any microscopic etiology that may be present without removing excess cementum.

Use actual defined debridement endpoints, rather than deep beliefs about debridement methods, to determine what to use. When deciding between manual or ultrasound, or laser and topical antibiotic delivery, the mindset should be:

  • What would give you the best chance of removing any clinically detectable cause without also removing the cementum?
  • What would give you the best chance of interrupting any underlying microscopic cause without removing cementum?

The answers to these questions will guide your choice of debridement method.

rice: There is much more to think about and challenge yourself when choosing a protocol. Our final segment next month will discuss the cardiology research Dr. Donley is involved in and our ideas for setting up shop in their practice. He will share his thoughts on the future of the industry and the need to help the public understand oral system health and dentistry.

Editor’s note: This article appeared in the October 2023 print edition RDH Magazine. Dental hygienists in North America are eligible for a free print subscription. Register here.

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