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Park Ave. Periodontal Assocates

Newsletter 15

Simon says, "Take one giant step back!"

Central Park, Just a short stroll from the Phillips Club Even ten-year olds know what "halitosis" means. Everybody is concerned that they may have "bad breath" at one time or another. We are certainly aware of it in others. Manufacturers of breath mints, lozenges and mouthwashes have profited handsomely from this universal self-consciousness. It is no wonder that multitudes of scientists are employed to determine what the sources of these odors are, how they can be detected, and how they can be eliminated.

It turns out that the sources of halitosis are varied. Certainly disorders affecting the upper and lower respiratory tracts, and those that include the gastrointestinal tract can cause bad breath. Various systemic and neurological diseases and side effects to medications add to the list of offenders. But let's not forget the portal of our concern: the mouth. That's where and why dentists get involved.

The mouth is a veritable greenhouse filled with bacteria that metabolize and ferment food debris that release noxious odors…unless they are effectively removed. It's long been known and accepted that metabolic activity of bacteria that colonize the tongue and other surfaces of the mouth contribute to malodors. Old fillings (especially silver amalgams) deteriorate by corroding and expanding to the point where they are no longer well-fitting. Cracks, chips, and irregular edges turn into hard-to-clean areas, trapping food and contributing to this problem. In addition, patients with poor salivary flow (which is a side effect of many medications) often develop problems with their breath. The reason this happens is that saliva helps wash away loose debris and bacteria found in the mouth. As salivary flow diminishes, more detritus remains on the teeth, tongue, and in the nooks and crannies of fillings, only to ferment and contribute to bad breath.

Gum diseases also play a major role in contributing to oral malodor. This has been confirmed by a recent Brazilian study*. Here's what they did. Twenty-one test subjects (none of whom smoked, had systemic diseases, wore dentures, or used antibiotics) with untreated periodontal disease having pockets greater than 3 mm were compared to 20 subjects with healthy mouths. Oral malodor was assessed in two ways. One measured the concentration of volatile sulfide compounds (VSC) using a portable monitor. This was accomplished by placing a disposable plastic straw 4.0cm into an open mouth to test the ambient air. The other test for malodor consisted of an organoleptic rating system on a 0-5 scale. To accomplish this, trained odor judges placed their talented organs 10cm from each subject's face. The subjects kept their mouths closed for 60 seconds and then breathed out gently so the judges could go to work.

Measurements and tests for VSC and odors were performed once the test and control subjects had their supragingival (above the gum) plaque and calculus removed. Once their mouths were superficially "clean," samples were collected from the six worst pockets in each test subject, with worst being defined as the deepest pockets that bled. Plaque samples were analyzed for the presence of three major periodontal pathogens associated with progressive disease. Bacteria were also sampled from the tongue.

What did they find? The researchers discovered that there were statistically significant correlations between high measurements of oral malodor and the presence and concentration of the three periodontal pathogens in the "diseased" group. No significant correlations were found in the "healthy" subjects.

The authors concluded that the three major bacterial pathogens found in periodontal pockets are an important source of oral malodor by contributing to the volatile sulfide compounds found in the mouth. They also noted, that VSC were found in the "healthy" subjects, but not to the same extent as found in the patients with the worst disease and malodor problems. They went on to describe the important role the tongue plays in halitosis. It appears that "tongue coating" (which they did not measure in this study) accelerates the production of methyl mercaptan in the mouth, the latter being a major VSC metabolite. In the end, these authors stated that hydrolyzing bacteria found in subgingival plaque and the presence of gum inflammation both contribute to the presence and strength of bad breath.

The results of this study support the anecdotal response many patients report when they say that their "breath is better" after periodontal treatment. It seems intuitively obvious that a cleaner mouth will lead to "sweeter" breath. So now we can add that treatment of periodontal disease not only makes a mouth healthier and lets us keep our teeth longer and in good function, but it may also enhance social relationships.

*Figueiredo LC, Rosetti EP, Marcantonio E, Marcantonio RAC, and Salvador SL: The relationship of oral malodor in patients with or without periodontal disease. J Perio 73:1338-1342, 2002.

Hormone Replacement Therapy: does it play a role in periodontal disease?

Hormone replacement therapy (HRT) has been receiving negative news lately, but millions of women continue to use it to decrease the symptoms of menopause. One of the problems associated with the onset of menopause is that bone density decreases in the spinal column and long bones. Research to determine if this same loss of bone density occurs in the mandible and maxilla, which ultimately weakens tooth support, has provided conflicting results. A recent multi-center study published in the Journal of Periodontology* by a varied group of physicians and dentists sheds new light on this important issue.

A research team that initially established, in a previous study, that HRT vs. placebo improves post-cranial bone density and that there is a weak but positive correlation with changes in oral bone, now report 3-year results. Forty-nine (49) women on HRT were included in their study. Bone density was measured with dual energy absorptiometry and alveolar crest height was determined by measuring the distance from the alveolar crest to the CEJ on standardized dental X-rays. Measurements were made at the beginning and the end of the 3-year study period. Comparison of the measurements of bone density and alveolar crest height showed increased bone density of the lumbar spine and femurs, and a weak but statistically significant correlation with increase in alveolar crest height. The authors concluded that the positive change in alveolar crest height was generalized, and not isolated to specific sites.

In analyzing their results, it is important to note that none of the patients included in this study had moderate or advanced periodontal disease. At their worst, they suffered from mild inflammation and few periodontal problems. This translates into crestal bone that may have been osteopenic and demineralized, which would appear less dense on X-rays. The degree of bone density should not be confused with the presence of periodontal disease. If HRT increases bone density, then the ACH or alveolar crestal height in these subjects would appear to improve as a result of hormonal treatment. This does not imply improved periodontal health; it may mean that oral bone is slightly stronger and could possibly be more resistant to the minimal changes associated with mild periodontal inflammation. However, patients taking HRT are at the same risk for periodontal disease as those not taking this treatment.

*Hildebolt CF, Pilgram TK, Yokoyama-Crothers N, Vannier MW, et al: The pattern of alveolar crest height change in healthy postmenopausal women after 3 years of hormone/estrogen replacement therapy. J Perio 73:1279-1284, 2002

Trying to keep your stress under wraps? You can't fool your dentist!

"How did you know?" asked the surprised patient.

"It's obvious," answered the seemingly clairvoyant dentist.

Many of us have had the experience of examining a mouth and immediately sensing something was wrong (such as a divorce, the death of a spouse, loss of a job, a major health crisis, etc.) before being told by the patient that they were in the throes of, or had just experienced, a life-changing event. An association between periodontal disease and stress has long been suspected. Stress was established as a primary etiology for acute necrotizing ulcerative gingivitis (ANUG) suffered by the troops in the trenches during World War I.

Many researchers have reported that stress is a risk indicator for periodontal disease. If so, shouldn't we evaluate our patient's psychological and psychosocial stress to see how these factors relate to adult periodontal disease? Actually, this has been attempted many times, always concluding that psychological factors affect a patient's periodontal status. How this occurs is open to conjecture. One thought is that strategies for coping with stress vary in patients with periodontal disease when compared to patients with healthy dentitions and that the manner of coping with stressful events is more important to psychological and physical well being than the stressor itself. A group of researchers* decided to study if this were true. The results are illuminating.

Fifty-three women and 36 men ranging in age from 27-68 years old participated in this study. All subjects had significant amounts of periodontal disease, all were either securely employed or financially comfortable, and none had major health diseases. Sixty-three (63) healthy subjects were used as controls in this study. All subjects were evaluated and compared for smoking habits, educational levels, emotional status, and had detailed periodontal examinations. Presence or absence of disease was determined by clinical attachment loss (CAL) and subdivided according to severity.

All subjects were given an intensive questionnaire designed to measure and categorize stress coping mechanisms. Nineteen subsets of actional and intrapsychic coping strategies comprised 114 questions given to each participant. Actional coping strategies are designed to actively alter a stressful situation or an individual's reaction to it. These behaviors include attack, escape, social contact and withdrawal from a stressful state. Intrapsychic strategies include a subject's perception, thinking, imagination, and motivational-emotional processes such as distraction, denial, devaluation, and even the ability to overestimate one's own resources.

The stress questionnaire devised by these researchers documented a variety of coping measures as opposed to most studies that tested either one stressful event or tested stress in only a few dimensions. "Stress-enhancing" strategies were part of this study. This aspect of the test not only studied measures used by the subjects to reduce stress, but if these measures actually enhanced stress. Statistical methods were then used to determine correlations between the five stress coping mechanisms studied and severity of CAL.

Results. As expected, there were statistically significant differences in the types of coping mechanisms reported by "healthy" and "diseased" subjects. The "diseased" subjects were much more likely to use "defensive" coping mechanisms ("I have done no harm"), or to use pharmaceuticals, or aggression. The "healthy" subjects were much more likely to use "active" coping mechanisms such as positive self- instruction or to exhibit social skills that controlled a situation. These results second a second paper by Genco et al that concluded that coping skills are more relevant than levels of stress.

The mechanism by which stress modulates periodontal disease is still not known. There are two basic models. One is a "psycho-neuro-immunological" model, which hypothesizes a cascade of physiologic events that result in changes in the immune system. The other is a behavioral model, which hypothesizes that negative behavioral factors (e.g. smoking, self-neglect) result in clinical disease. What seems certain is that stress plays an important role in the periodontal health of our patients. While few dentists have any desire to be psychiatrists, we must be vigilant about the psychological status of our patients and incorporate that into our treatment decisions. It was suggested by the authors that how we approach describing a patient's condition matters as to how they will react to hearing this information. Wouldn't it be nice to have a simple profile that would enable us to present critical dental problems to patients in a way that allows them to process this information so they could do what is best for them? Add this to all of our other responsibilities in caring for patients sitting in a dental chair (and how stressful that is for many), and its no wonder that "stress" is part of a dentist's daily diet. Perhaps D.D.S. really stands for "Doctors of Dental Stress."

Wimmer G, Janda M, Wieselmann-Penkner K, Jakse N, et al: Coping with stress: its influence on periodontal disease. J Perio 73:1343-1351, 2002.

Comments. What's curious about both of the last two articles is that neither referred to Ken Kornman's seminal work published years ago. Kornman discovered that bacteria associated with periodontal disease preferred to metabolize a class of hormones known as estradiols as opposed to simple sugars found in the foods we consume. Estrogen, cortisone, and adrenaline are all estradiols. Estrogen is certainly involved in HRT and both cortisone and adrenaline are secreted in increased amounts when we are under stress. In each instance, estradiols have the capacity to alter one's periodontal status…and not for the better.

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