I was a young flower child of the 1960s, an era in which big flashy cars and the emergence of McDonald’s hamburgers were accompanied by a desire for speed and fast food service. As a young kid back then, my parents were able to trade in a very small ranch-style home for a larger home in the countryside. They were interested in finding a nice house in a grassy suburb, a bright open place far from hectic, crowded cities where happy families could grow and bask in the sunshine of home ownership. I still remember the day we drove to view the plot of land we eventually purchased; I ran around the grassy field and was having a glorious time running through the autumn weeds, wild grasses, and flowers.
On the way home, I couldn’t catch my breath, and my parents could hear a loud wheeze that was followed by a persistent nocturnal cough that would not quit. After telephoning the family doctor, my dad took me in the shower so I could breathe the warm, moist air and my parents placed me in a mist tent that was designed to break up the mucus in my wheezy bronchial airways.
After a series of debilitating upper respiratory tract infections, our family doctor eventually diagnosed extrinsic (allergic) asthma. Extrinsic asthma is caused by a type of immune system response to inhaled allergens such as pollen, animal dander, or dust mite particles. Allergic asthmatics, like me, respond quite well to the use of inhaled steroids and/or a short course of oral steroids that suppress the immune system, particularly in the lungs where the reaction is creating havoc.
What does extrinsic asthma and periodontal disease have in common? Both diseases are the result of complex interrelationships between infectious agents and host factors. Another way to look at the etiology is to understand that both allergic asthma and periodontitis result from an interaction between infectious agents and host immuno/inflammatory response. In the case of allergic asthma, the infectious agent is inhaled allergens like pollen or dust mites. In periodontitis, the infectious culprits are microorganisms that reside in subgingival biofilms and in the connective tissue.
Back in the 1960s, there were few medications that could reduce bronchial inflammation and open the bronchial airways that could become severely constricted. When asthma strikes and the airways constrict and fill up with mucus, the asthmatic individual feels as if he/she is breathing through a narrow straw. It’s a very scary feeling and sometimes a life-threatening one in untreated cases. Today, thanks to decades of scientific asthma/allergy research, there are oral and inhaled medications that dilate the bronchial tubes (which we now call a bronchial tree because of its many branches) and reduce airway inflammation.
In treating periodontal infections, we still have few evidence-based medications that can reduce host response to the overgrowth of mostly anaerobic bacterial species, but that may be changing. Besides 20 mg of low-dose doxycycline, taken twice a day, periodontal researchers are busy studying other agents that alter alveolar bone loss, such as NSAIDs and biophosphonates.1 Researchers have a long way to go, however, in determining the value of these and other agents in the future treatment of periodontal diseases. Therefore, don’t rush to tell your patients about new bone-altering agents until the safety and efficacy of these agents are well established.
To date, the only FDA-approved systemic anti-inflammatory agent available is low-dose doxycycline (taken bid). In the 35 or so percent of the patient population who have periodontal disease, researchers postulate that this disease results from a person’s faulty immune system where the body creates a fight with biofilm pathogens. As the battle continues, the body’s immunoinflammatory response results in alveolar bone loss.
An accumulation of evidence has shown that systemic antibiotics are of value in arresting bone loss in certain types of periodontal diseases such as generalized and localized aggressive periodontitis and refractory periodontitis. The mechanism of action by systemic antibiotics is related to the antibiotics’ antimicrobial effects.2
Bacteria are the dominant form of life on earth. There are more of them than there are of us. Part of their continuing success stems from their ability to divide rapidly and live in biofilm-protected environments.
Most bacteria are harmless to humans and many contribute to good health, while a large proportion of bacteria that can cause disease are only potentially pathogenic, meaning that the bugs only affect people who are already at risk for disease or who have a weakened immune system.
I recently read some new and fascinating information on bacterial flora in the healthy oral cavity. It turns out that some of the species that are commonly associated with periodontal disease such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola may not be present in healthy subgingival sites.3
As I put on my thinking cap in an attempt to unravel one of nature’s many elaborate puzzles, here’s what my weary and somewhat over-cluttered mind came up with: Perhaps the reason why the subgingival bacterial flora in periodontal disease seems to be dominated by anaerobic, gram-negative species is because the inflammatory response (which is abnormal in periodontal disease subjects) provides a nutrient-rich, happy environment for anaerobic bacteria. In other words, tissue inflammation and bleeding provide an ongoing feast for the anaerobes as they busily multiply at an incredible rate daily. I read somewhere that a single bacterium can produce billions of descendants a day! (Just imagine a life of continual munching on cheese nachos or fries whenever the mood strikes!)
So, if it’s really a bug’s life in a susceptible host, are systemic antibiotics of any use?
There is an impressive body of evidence suggesting that, when used adjunctively (in combination with nonsurgical mechanical debridement), systemic antibiotics can significantly improve periodontal treatment outcome.2 Not only can antibiotics kill or inactivate bacteria in hard-to-reach areas such as furcations and deep pockets, they can reduce the risk for refractory disease and the number of teeth that need periodontal surgery.2
In next month’s column, we’ll discuss in greater detail the rather intricate relationship between microorganisms and periodontal treatment outcome, and the appropriate use of systemic antibiotics. I’ll be reporting on my interview with a distinguished periodontal researcher who has devoted his entire career to studying the microbiology of gingival and periodontal diseases in humans.
References
1 Ciancio SG. Medications: a risk factor for periodontal disease diagnosis and treatment. J of Periodontol 2005: Nov 2005 (Supplement).
2 Winkelhoff AJ, Winkel EG. Microbiological diagnostics in periodontitis: biological significance and clinical validity. Periodontol 2000 : 39: 40-52.
3 Aas JA et al. Defining the normal bacterial flora of the oral cavity. J Clin Microbiol 2005: 43: 5721-5732.
