by Lynne H. Slim, MS, RDH
On Mother’s Day I was excited about cooking for my Mom. In preparing for her arrival, I bathed my four dogs and brushed their biofilm-laden teeth. Nellie, my youngest dachshund, was loaded with Georgia ticks, so I plucked them off and placed them on a towel. With a few minutes to spare, I amused myself by observing these bloodsucking parasites and their grasping limbs that help them position themselves correctly to sink their mouths into a dog’s flesh. The ticks were off my precious dog and confused when they couldn’t find nourishment from a towel.
One sure way to put me to sleep is to shove a periodontal journal under my nose and tell me to read about periodontal inflammation. I’ve made a valiant effort to read about it this week and consequently, I’m feeling bright-eyed and bushy-tailed because of my extra sleep! Chronic wounds are a lot like localized inflamed periodontal pockets in that they both possess elevated proinflammatory cytokines, high protease levels, and an excessive accumulation of neutrophils.1,2 Wound care specialists are now paying close attention to wound biofilm, which hijacks the host immune response, and RDHs are doing exactly the same in their efforts to manage oral biofilm.
Biofilm is an ancient multicellular form. The biofilm slime contains polysaccharides, proteins, and DNA. Bacteria organize themselves and direct biofilm activity by quorum sensing so they can eat, defend themselves, and reproduce, just like other species.1
Periodontal pathogens in subgingival biofilm are continuously commandeering the host immune response in order to acquire a steady state of hyper-inflammation. In other words, some of these pathogens, like P. gingivalis, are hijacking the immune system so they can thrive. Biofilm must have a stable parasitic relationship with the host tissue to survive and thrive. Just like the vampirelike Georgia ticks that suck blood for nourishment, oral biofilm is continuously sucking up nutrients from the pocket environment.
Evidence suggests that P. gingivalis is a major etiological agent for severe forms of chronic periodontitis.2 P. gingivalis was found in 85.75% of subgingival biofilm samples from patients with chronic periodontitis, and it is rarely recovered at significant levels from patients without periodontal destruction. In addition, a reduction in the level of P. gingivalis at a diseased site was associated with disease resolution at that site. Subgingival implantation of P. gingivalis in mice and nonhuman primates has been shown to induce periodontal bone loss.2
The presence of biofilm perpetuates inflammation and promotes chronic conditions. Periodontal pathogens like P. gingivalis have specific virulence factors that make them invincible. Think of P. gingivalis as an army tank plowing its way through the tissue, invading host defenses, and even manipulating the immune system to provide continued nourishment for the troops. The major antigen of P. gingivalis induces an overall inflammatory response that can be compared to a cannon ball that is discharged to destroy the enemy. P gingivalis even has appendages that are like caterpillar treads on army tanks that manipulate the host immune system to its advantage. These appendages (called adhesions) attach to host cells. They even find ways to feed themselves via the host’s circulatory system. A yummy treat for them is nutrient-rich plasma and iron from lysed blood cells.
How do we explain biofilm-induced periodontal inflammation to our patients? Try explaining in a simple manner that sticky biofilm slime forms on teeth and creeps under the gums if it is not adequately removed. The slime eventually forms sophisticated communities (like nests, hives, or ant hills). As the slime matures, population shifts take place and certain “bad” bugs take up residence. Some of these more sophisticated bugs are like army tanks. They are powerful enemies that want only one thing, to survive, and they do so by neutralizing the body’s defenses and destroying surrounding tissue and bone.
In biofilm infections, there is a steady interaction between the biofilm and the host. Just like the tiny but mighty Georgia tick, individual biofilms are parasitic and manipulate the host to get adequate nutrition and thrive. The host remains frustrated with a localized hyperinflammatory response and is unable to overwhelm the biofilm.1
Managing a chronic periodontal biofilm infection requires a rock-solid protocol and a commitment to excellence. Suppressing subgingival biofilm is no easy task! Work hard to provide meticulous debridement and suppression of the immune response, along with consistent self-care measures and periodontal maintenance. Always refer to a periodontist in severe, aggressive, and refractory cases, and develop written criteria for referral.
1. Wolcott RD, Rhoads DD, Dowd SE. Biofilms and chronic wound inflammation. Retrieved May 11, 2010 from the World Wide Web: http://184.108.40.206/~woundcar/wp-content/uploads/2009/07/biofilmwoundinflammation.pdf
2. Pathirana RD, O’Brien S, Reynolds EC. Host immune responses to Porphyromonas gingivalis antigens. Periodontol 2000 2010: 52: 218-237.
Lynne H. Slim, RDH, MS, RDH, is an award-winning writer who has published extensively in dental/dental hygiene journals. Lynne is the CEO of Perio C Dent, a dental practice management company that specializes in the incorporation of conservative periodontal therapy into the hygiene department of dental practices. Lynne is also the owner and moderator of the periotherapist yahoo group: www.yahoogroups.com/group/periotherapist. Lynne speaks on the topic of conservative periodontal therapy and other dental hygiene-related topics. She can be reached at [email protected] or www.periocdent.com.