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PerioFrogz: Research Summaries and Implementation Strategies
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The objective of PerioFrogz is to help dental professionals stay current with on-going research; facilitate integration of research findings into daily practice, ultimately elevating the level of patient care.
“Inflammation and Bone Loss in Periodontal Disease.”
Source: J Periodontol. 2008 Aug;79(8):1669-76 [Suppl]
Author By: David L. Cochran
This article deals with the mechanism by which inflammation leads to periodontal bone resorption. Host response factors drive periodontal tissue destruction.
Summary of research:
  • Body’s initial response to gingival bacterial invasion is activation of immune system.
  • Initial immune response releases inflammatory mediators into gingival tissue.
  • Inflammatory mediators travel through soft gingival tissue towards alveolar bone.
  • Failure to confine immune system response to soft tissue results in periodontitis.
Results and Conclusions
  • Increased recognition of the importance of immuno-inflammatory response in periodontitis.
  • Spreading of inflammatory mediators through gingival soft tissue results in bone loss if these immune factors reach adjacent alveolar bone.
  • Confining inflammatory mediators to gingival tissue prevents gingivitis from developing into periodontitis.
Key take-away
Following bacterial invasion into gingival epithelium, the body mounts an immuno-inflammatory response with an initial release of inflammatory mediators into the gingiva, to combat the bacteria. The inflammatory mediators physically travel through the gingiva towards the adjacent alveolar bone. When they reach the bone, or very close to it, bone resorption and periodontitis occurs. In other words, failure to confine the inflammatory process within gingival soft tissue results in expansion to the alveolar bone and progression of gingivitis to periodontitis. Clinically, we need to monitor, treat and educate our patients with gingivitis about the critical importance of controlling the disease process to prevent gingivitis from progressing to periodontal disease and causing irreversible damage.
Implementation strategies:
This new understanding about ‘inflammation’ traveling to the alveolar bone, along with previous studies indicating the systemic effects of chronic inflammation, should change our entire approach to the treatment of gingivitis. A diagnosis of gingivitis is, more often than not, accompanied by our admonishment to the patient to do more at home. Brush better, floss better, use this aid, come back sooner… and with that, the patient is left to deal with the ‘inflammation of their gum tissue’ on their own.
Our clinical experience tells us that for a few patients this works, for most; however, the next recall is a repeat of the previous one. One only has to look at the patient chart notes to confirm this.
A quick review of research tells us:
  • Clinicians should attempt to eliminate inflammation prior to involvement of the alveolar bone.
  • Scaling a sulcus of 1-3 mm can actually cause attachment loss.
  • Pathogens such as Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf) and Treponema denticola (Td) are tissue invasive and replicate within the tissue and can cause permanent damage.
  • It takes up to one minutes per pocket with an ultrasonic instrument to eliminate pathogens.1-5
Taking all of this into consideration as well as guidelines from the American Academy of Periodontology and the JP Institute indicates that treatment should be open ended since all immune systems function differently according to the individual’s level of risk. As clinicians we must treat gingivitis more assertively than ever before.
Since we cannot change a patient’s gingivitis during the prophy visit, we must enroll the patient in their own care, including the potential need for additional treatment.
Consider the following the next time you have a ‘gingivitis’ patient in the chair:
  • Determine the patient’s level of risk. In addition to personal & family health history consider:
    o Compliance
    o Home care
    o Restorative needs
    o Occlusion / TMJ / TMD
    o Crowding
  • Allow enough visits to provide a thorough ultrasonic debridement of each sulcus. This may take up to one minute per bleeding area.
  • Estimate the number of treatment visits you think the patient will need to achieve disease remission / absence of inflammation in this case.
  • Leave the treatment open ended in case the patient doesn’t respond or follow through as you predict.
  • Finally, educate your patient. “Bob, right now you have a completely reversible condition. If you reverse the inflammation in the gum tissues now, you will never have to experience permanent loss to your jaw bone.”
References
  1. Cobb CM. Non-surgical pocket therapy: mechanical. Ann Periodontol. 1996;1:443-490.
  2. David L. Cochran , J Periodontol. 2008 Aug;79(8):1669-76 [Suppl]: Inflammation and Bone Loss in Periodontal Disease
  3. Chen C, Rich SK. Biofilm basics. Dimensions of Dental Hygiene. 2003;1(1):22-25.
  4. Matsuda SA. Instrumentation of biofilm. Dimensions of Dental Hygiene. 2003;1(1):26-30.
  5. Effects of ultrasonic and sonic scalers on dental plaque microflora in vitro and in vivo. J Clin Periodontol 1992;19:455-459

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