Acute necrotizing ulcerative gingivitis

So your dentist has just informed you that you have "gum disease," and your proposed course of treatment sounds more like wedding vows than an appointment to fill a cavity. You may even have been referred to a gum specialist, or periodontist. Unfortunately, you're not alone. Both older people and those a generation younger -- who grew up drinking fluoridated water and therefore escaped the "cavity-prone years" relatively unscathed -- find themselves facing gum problems.

Horror stories abound: hours of sitting with gloved fingers and sharp instruments crammed into one's mouth; endless horrible scraping sounds. And although the expectation of ripping pain at any moment is never fulfilled, anxiety returns with each new appointment.

Fortunately, it doesn't have to be this way. Sensitive new diagnostic tests that can sound an early warning, an increased understanding of prevention, and innovative drug-delivery strategies give cause for optimism.

Open wide

Although we seldom think of them in this way, teeth are living tissues that have blood and nerve supplies. They are surrounded by several anatomically distinct structures. The gingiva (as gums are officially know) is teh pink tissue visible to the eye. Out of sight, underneath the gingiva, the periodontall ligament attaches each tooth to alveolar bone. The gingiva is also attached directly to the teeth, and above this attachment is a small sulcus, or moat. (See illustration.)

Because the gingival sulcus is the playing field where health and disease meet head-to-head, regular, thorough cleansing of it is vital. The gingival sulcus is also central to the diagnosis and treatment of periodontal disease.

The term "periodontal disease" may refer to problems of the gingiva or disorders of the deeper structures, such as the underlying bone and connective tissue. Gingivitis, or inflammation of the gum tissue, is the most frequently encountered one. Characterized by red, swollen, bleeding gums, this is the mildest periodontal disease and is relatively amenable to treatment. Some other forms of gingivitis, such as acute necrotizing ulcerative gingivitis (formerly called trench mouth or Vincent's infection) are more painful and difficult to cure. Patients infected with human immunodeficiency virus can have HIV-associated gingivitis, a particularly aggressive form of the disease.

Periodontitis, a more serious condition, involves the inflammation -- and eventual destruction -- of the periodontal ligament and the alveolar bone. Symptoms, if present, vary widely and include sore, bleeding gums, halitosis, teeth sensitive to heat and cold, and abscesses.

The extent of tissue loss is determined by inserting a probe into the gingival sulcus to measure the depth of the pocket and the level at which the tooth is attached to the gum. The greater the loss of attachment, the more severe the disease. Dental x-rays can also estimate the amount of periodontal destruction. Exposed roots, which have no protective coating of enamel, are at increased risk for cavities. And if enough ligament and bone are lost, the teeth loosen and may need to be extracted.

The most common form of this disease is adult periodontitis; others occur in youngsters and in people with AIDS.

The plaque plague

The primary cause of both gingivitis and periodontitis is bacterial dental plaque, which is composed of 200-300 species of organisms. The link between plaque and gum disease was forged in 1965, when Harald Loe and coworkers published the results of their classic experimental gingivitis study. Twelve healthy people were paid to abandon all oral-hygiene measures. Deposits of soft debris built up very quickly in their dirty mouths, and the bacteria population soared. Gingivitis developed within ten days in three people, and within 15-21 days in the others. When the volunteers resumed brushing, their gums and bacteria counts soon returned to normal.

For several years following Loe's experiment the "nonspecific plaque" hypothesis prevailed, directly connecting the amount of bacterial plaque in the mouth to the presence of periodontal disease. However, that interpretation did not explain why some patients with large amounts of plaque had relatively little inflammation, while others with fairly clean mouths suffered from advanced periodontal disease.

Since the late 1970s, various bacterial species that inhabit the mouth have been linked to particular periodontal diseases, and the "specific plaque" hypothesis has come to the forefront. Certain bacteria are found in the plaque of people with healthy gums, others are associated with gingivitis, and several more-virulent strains have been linked with periodintitis.

The bacteria that are the most troublesome produce enzymes capable of destroying connective tissue and cells. The progression of periodontal disease depends not just on which organisms are present, but also on a person's immunologic reaction to them. Some individuals mount a more effective immune reaction to these invaders than do others. In certain people, unfortunately, the body's own immune cells both attack the bacteria and produce enzymes and other factors that can help destroy the periodontal ligament and alveolar bone.

How many of us have it?

A survey recently completed by the National Institute of Dental Research showed that in the U.S. 44% of employed adults had some amount of gingivitis, and 14% had at least moderate periodontitis. As high as these numbers seem, they may actually be underestimates. The study sampled only employed people, and the abbreviated examination performed by investigators did not probe for gum disease in some sites where it often occurs.

The Harvard School of Dental Medicine and the New England Research Institute just finished a survey of people over age 70 living in New England. Investigators found a much higher level of gum disorders in this population than would have been expected based on results of other surveys. Of the elders with teeth, 86% had at least moderate periodontal disease.

The molecular mouth exam

Until very recently, dentists could diagnose periodontal disease only by looking at the gums, examining dental x-rays, and exploring in the gingival sulcus. Newer techniques that detect the bacteria thought to cause the problems -- or the host reaction to them -- are becoming available. Tests employing DNA probes have been in use since 1985. Here the dentist samples the fluid in the gingival sulcus with absorbent paper. The specimen is sent to a specialized laboratory, where technicians expose it to DNA probes that can determine whether certain disease-producing bacteria are present. Companies are working to develop testing kits that dentists can use to produce immediate results in the office. Another new assay is based on the ability of sampled bacteria to cleave a peptide, releasing a substance that reacts with a variety of dyes. The disadvantage of these molecular tests is that they are designed to identify only a limited array of bacteria and may miss a causative species not included in their repertoire.

That problem may be sidestepped by assays that look at enzymes breakdown products created when the body is attacked by any disease-producing agent. One particularly promising test measures aspartate aminostransferase (AST), an enzyme released when cells die. A kit for rapid in-office determination of AST levels is currently being developed. Similar kits for collagenase (an enzyme that destroys ligamentous tissue) are already available, and assays for other enzymes are sure to follow.

Gum-control measures

If gingivitis or periodontitis has been diagnosed -- or better yet, to prevent these problems from developing -- the most important thing a person can do is to maintain meticulous oral hygiene. Brushing the teeth properly is essential. (A scrubbing action, like what is used to clean bathroom tiles, is out because it damages the gums.) A dentist or hygienist can demonstrate how to brush the teeth gently and concentrate on that all-important gingival sulcus. In addition, daily flossing is in order for any teeth a person wishes to keep. These procedures minimize formation of plaque by removing food debris. If gum recession has exposed roots, the dentist may prescribe a fluoride gel to decrease sensitivity and protect from decay.

Antimicrobial or antiseptic mouthrinses are also helpful in reducing gingivitis. Effective over-the-counter products contain essential oils, sanguinarine, or -- for shsort-term use -- hydrogen peroxide. Good prescription agents include chlorhexidine gluconate and stannous fluoride.

For most people with adequate dexterity, all that's required is brushing, flossing, and perhaps a few hygiene aids such as a rubber tip, a floss holder, or an interproximal brush that cleans between the teeth (all available in drug-stores). For people who have trouble with these, however, an electric toothbrush is worthwhile. Look for one with a stationary grip and revolving tufts of bristles, and avoid the old-fashioned kind where the whole device vibrates. Again, a scrubbing action should not be used. Home irrigators are excellent for anyone showing signs of periodontal disease. The best ones have tips that direct fluid deep into the sulcus and flush out debris. Antimicrobial or antiseptic rinses can be put into these devices.

The mainstay of periodontal therapy is mechanical removal of both the causative bacterial plaque and the tartar buildup that can trap it. For relatively mild cases and as a first step in more severe ones, the hygienist or dentist will scrape these concretions from the tooth and smooth the root surface, a procedure called scaling and root planing. Follow-up care involves better oral hygiene, often coupled with antibiotics, antimicrobial rinses, and/or return office visits to have the sulcus irrigated.

When this approach is not enough, periodontal -- or "flap" -- surgery may be necessary. Here the gums are temporarily raised away from the teeth and bone to allow deeper access. In years past, the dentist would simply clean out the area and pull the gums back together with sutures. Today a major goal is regenerating the lost structures. Freeze-dried bone or synthetic materials can be packed into bone defects. Or physical barriers such as Gore-Tex can be draped over eroded areas to prevent gum tissue from growing into them, thus allowing periodontal tissue and bone cells to grow. Barriers now in use must be removed in a second surgical procedure. Researchers are currently investigating other ways to stimulate regeneration, including use of growth factors,s as well as barriers that can be absorbed by the body.

A glimpse at the future

New therapies are aimed at increasing the concentration of bacteria-fighting agents right where they are needed -- in the gingival sulcus -- and thereby eliminating side effects of systemic antibiotics. This is accomplished through techniques collectively called "local delivery." The most extensive research in this field has been done by investigators at the Forsyth Dental Center in Boston. Initial clinical results are very promising for experiments in which tetracy-cline-impregnated fibers were packed around a tooth. Fibers bearing other antibiotic and antimicrobial combinations are also being studied. In addition, researchers are trying to develop drug carriers that dissolve as easily as some sutures do. To date, all of these systems are still experimental, and none has been approved by the Food and Drug Administration.

Dentists hope that new diagnostic technology and improved delivery of medications to the sulcus will reduce the number of patients facing periodontal surgery or losing teeth to gum problems. The ultimate goal is to minimize the occurrence of such diseases, much as water fluoridation has blocked the development of dental cavities.

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