The iceberg tip: a bit more may soon be showing

While the numbers have changed through the years depending on which paper is being quoted, it is estimated that there are some 50 billion bacteria in the mouth, made up of some 500 different species. We've identified about 30 of these 500 species, and about 8 of these have some role in periodontal disease. Think of the magnitude of what we don't know! So it stands to reason that one day we should be able to identify more of these elusive buggers, and it's reasonable to assume that some of them will play a role in the etiology of periodontal disease. So regardless of current breakthroughs, potential vaccines or magic bullets to shove into pockets, periodontal disease is not disappearing in the near future.

While most of these potential pathogens have resisted being cultured in the laboratory environment to date, researchers* at Boston's Northeastern University theorized that more microorganisms would grow in an environment that simulated their natural setting. To test this theory they grew bacteria in diffusion chambers in a specially designed aquarium. They discovered that this simulated oral environment yielded larger numbers of colonies than in traditional technical-grade mediums. The net result was that a co-culturing system developed among bacterial species and that this cross-feeding grew previously uncultivable microorganisms. So while we are still witnessing the proverbial tip of the microbiological iceberg relative to the oral cavity, it won't be long before new species are discovered and we will better understand the causes and how to control (and perhaps prevent) periodontal disease.

*Kaeberlein T, Lewis K, Epstein SS. Isolating uncultivable microorganisms in pure culture in a simulated natural environment. Science 296:1127-1129, 2002.

When swollen gums just won't go away

We've written about it before and it deserves being written about again: calcium channel blockers induce the gums to swell…and stay swollen. Calcium channel blockers, like nifedipine, are effective long-acting vasodilators. They are particularly effective in treating hypertension. Their most common side effect is gingival overgrowth (swollen gums) accompanied by chronic inflammation.

To understand how and why this drug causes gum problems, it is helpful to review the life and death of an epithelial cell. Epithelium consists of keratinocytes. Cells emerge from the proliferation compartment in the basal cell layer and continue to differentiate while migrating through the various stratified squamous cell layers. The end of this life cycle is cell death known as apoptosis. Apoptosis plays an integral part in controlling tissue thickness. When apoptosis is suppressed, gingival growth rate is altered and gums become thicker. While we know that nifedipine affects the apoptosis of gingival keratinocytes, does it affect other tissues besides the gums? Researchers at a Japanese dental school tried to learn more about this*

Methods and materials. Specially bred rats were given a diet supplemented with nifedipine and then sacrificed on days 8, 15, and 30. Sections of the mandibular gingival and the palatal mucosa were removed and histologically studied for different aspects of cell death compared to control samples.

Results. Nifedipine-induced changes were noted as early as day 15. In addition, the researchers found that the nifedipine inhibited the apoptosis of keratinocytes before gingival hyperplasia could be detected on day 15. They also determined that nifedipine prolonged cell lifetime but did not alter cell proliferation activity. No such observations were made on palatal mucosa.

Discussion and conclusions. Cellular homeostasis (i.e. tissue remodeling) is a balancing act between mitosis and apoptosis. Altering the rate of apoptosis results in gingival overgrowth. This study demonstrated that nifedipine-induced hyperplasia occurs before clinical changes can be observed. In addition, the authors discovered that nifedipine does not increase keratinocyte proliferation but prolongs cell life by inhibiting keratinocyte apoptosis.

Comment. This study does not mention the clinical ramification of nifedipine-induced hyperplasia. In our experience, it may range from mild with slight papillary swellings to severe gingival overgrowths. It is not dose-related but may be influenced by the patient's plaque (or lack of) control. In severe cases, gingival surgery is necessary to control huge overgrowths that are unsightly and have a tendency to abscess. Once surgery is performed and patients practice improved oral hygiene measures, overgrowths may reappear but often to a lesser and more manageable extent. Switching from one calcium channel blocker to another does not necessarily reduce or alter gingival hyperplasia. Only in the severest cases, do we ask physicians to consider changing the medication.

*Shimizu Y, Kataoka M, Seto H, Kido J, and Nagata T. Nifedipine induces gingival epithelial hyperplasia in rats through inhibition of apoptosis. J Perio 73:861-867, 2002.

Are bleeding gums a sign of a problem? Not always!

When examining a patient's gums, dentists and hygienists usually use bleeding on probing (BOP) as a sign of periodontal disease. Conversely, they use the lack of bleeding as a sign of periodontal health. Treatment decisions are then based on these findings as well as on other clinical parameters. But is BOP necessarily an accurate indicator of a problem? What happens when patients take aspirin to prevent cerebrovascular and cardiovascular diseases? Does aspirin therapy affect BOP? And in turn, are treatment decisions being made based on a parameter that is drug-induced? To find answers, a double-blind experiment* studied the effects of short-term daily aspirin ingestion on BOP.

Methods and materials. Forty-six periodontally healthy patients were included in this study. Sixteen (16) were given a placebo, 15 were given low-dose aspirin (81mg) and 15 were given a daily regular-dose aspirin (325 mg). A variety of clinical parameters were measured including BOP before the experiment began and 7 days after administration of the aspirin or placebo.

Results. The patient's percentage of BOP prior to the start of the experiment appeared to affect the outcome. Patients with <20% BOP sites at baseline did not have a statistically significant number of bleeding sites (BOP) after aspirin exposure. Most significantly, subjects with >20% BOP were affected by a daily aspirin (325 mg) but NOT the 81mg dose. Curiously, this result was independent of the subject's gingival health and oral hygiene.

Discussion and conclusion. Ingesting aspirin (325mg) daily may affect the outcome of BOP, especially if the patient had >20% bleeding sites prior to beginning this preventive cardiovascular/cerebrovascular therapy. For these patients, clinicians need to use additional parameters besides BOP to determine if periodontal intervention is needed.

Comment. It would be interesting to know if long-term use of 325mg of aspirin therapy results in an increase/worsening of a patient's periodontal status. Previously published papers have noted the benefits of non-steroidal anti-inflammatory drugs on preventing periodontal breakdown as well as the classic papers of Geiger and Wasserman that demonstrated no correlation to bleeding and periodontal breakdown. Maybe the importance of BOP needs to be reassessed.

*Schrodi J, Recio L, Fiorellini J, Howell H, Goodson M, and Karimbux N. The effect of aspirin on the periodontal parameter bleeding on probing. J Perio 73:871-876, 2002.

Single-tooth implants = safe and predictable*

While it's been twenty years since osseointegrated implants were introduced worldwide and nearly fifteen years since the American Dental Association graduated them from "experimental" to "accepted" dental therapy, it is important to present studies that validate what has become everyday procedures for dental clinicians. While it is always impressive and rewarding to provide enough implants that replace a complete or removable denture (or avoid the need for a patient to ever need one), replacing a single tooth comes with special challenges all its own. Not only are the esthetic stakes raised when replacing a single missing tooth, but also a solitary implant needs to withstand occlusal stresses without being able to distribute these forces onto other implants or teeth.

Methods and materials. Fifty-nine patients, with ages ranging from 19 to 73, had 71 single implants placed. The subjects had a variety of medical conditions that did not preclude implant placement, including hormone replacement therapy, thyroid conditions, hypertension, hypercholestemia and Crohn's disease. Forty-seven implants were placed in the maxilla, 24 in the mandible. Thirty-two implants were placed in the anterior region, 39 in the posterior.

Implant lengths (all were 3i dual-acid etched) ranged from 10-20mm, and the widths from 3.25-6.0mm. While most subjects had normal bone densities, equal numbers of implants were placed in soft and hard bone, too (11% and 15.5% respectively). Nineteen cases required bone augmentation (the type was left up to the clinician) and 2 required sinus lifts. Four were placed in immediate extraction sites. Results. Only 1 implant failed, for a success rate of 98.6%. All other implants were immobile, free of bone loss, and without signs or symptoms of any pathology. The implants in this study were evaluated from 30.9 to 60 months.

Discussion. This study is important because it includes implants of different sizes and widths, placed anteriorly and posteriorly, and in different types of bone densities by 3 different clinicians. Given the variables, the success rate for this dual-acid etched implant was 98.6% for up to five years. The authors compared their results, in a comprehensive literature review, to other articles that describe the success of single-tooth replacement implants and those of short-span fixed bridges.

Conclusions. Single-tooth implant replacements have a predictable outcome.

*Mayer TM, Hawley CE, Gunsolley JC, and Feldman S. The single-tooth implant: a variable alternative for single-tooth replacement. J Perio 73:687-693, 2002.

Are powered toothbrushes worth the money?

It depends. Ads make you think powered toothbrushes are more effective than manual ones, so do a lot of dentists and hygienists. So what's the scoop? Researchers at Marquette School of Dentistry* (this study was sponsored by Braun/Oral B, Boston, MA) studied 172 subjects who had mild to moderate gingivitis and at least 20 teeth. Subjects were included who had never used a power toothbrush before, and no formal instruction was given as to the correct toothbrushing technique. One hundred and fifty-seven completed the study.

Methods. The subjects were divided into 2 groups; one used a power toothbrush, the other a manual one. Those using the power toothbrush were asked to read and follow the directions in the manufacturer's instruction booklet; those using the manual toothbrush were given a brochure on proper brushing technique from the ADA. Both groups brushed twice daily for 2 minutes. A variety of clinical parameters were measured, including pocket depths, attachment levels, crevicular fluid, gingival inflammation, calculus, amount of tooth stain, and more.

Results. After 3 months, inflammation was reduced in both groups and there were no noticeable differences between the two groups with regard to the amount of stain on the teeth. Plaque and calculus were reduced more significantly at the end of the study in subjects using the power toothbrush. However the attachment levels and gingival recession were the same in both groups.

Conclusions. While there was some statistical advantage to using the power over the manual toothbrush, it is arguable how clinically significant are the results. It is safe to say that without formal instructions, the power toothbrush can safely be used. Furthermore, it is probable that formal instructions achieve better results with both devices.

Comment. It is evident, to us, that effective oral hygiene is predicated on how effective the hygienist or dentist is, and on the patient's motivation to improve their oral health. While not a whole lot better, patients often perform better with the power toothbrush because it is inherently an effective motivating instrument.

Dentino AR, Derderian G, Wolf, MA, Cugini MA et al. Six-month comparison of powered versus manual toothbrushing for safety and efficacy in the absence of professional instruction in mechanical plaque control. J Perio 73:770-778, 2002

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