Showing papers in "Periodontology 2000 in 1997"

The pathogenesis of human periodontitis: an introduction

Abstract: The pathogenesis of human periodontitis was placed on a rational footing for the first time by Page & Schroeder in 1976 (7). Although the details were scanty, the general principles and the overall conclusions reached in that article, which became a citation classic, are still largely acceptable today. An enormous amount has been learned about all aspects of human periodontitis, including its pathogenesis, since 1976. Several reviews of the pathogenesis have been written during that time (1, 3-6, 9-11), but with one possible exception (4), no publication has summarized currently available data and organized it into a relatively complete and rational picture. There are good reasons for this. Whereas the amount of information available in 1976 was limited and all relevant information could be accommodated in a single lengthy article, this is no longer the case. Although much of the detail is still missing, a far more complete and compelling picture of the pathogenesis is now emerging. Indeed, it is possible to approach the pathogenesis not only from the cellular level as was done in 1976 but to extend the story to the molecular level and to some extent to the genetic level. A staggering amount of information is available about the pathogenesis of human periodontitis. The information derives from a broad range of fields and disciplines, and much of it is highly specialized. We enthusiastically accepted the invitation to lead the effort to create a volume of PERIODONTOLOGY 2000 devoted completely to the pathogenesis of human periodontitis. Such a volume provides sufficient space for an inclusive, highly integrated result and, equally important, it provides the opportunity to include many of the world’s experts, whose collective efforts far surpass those that could have been achieved by any one or two individuals. Even with this format, we could not be all-inclusive, and many recognized experts could not be included. Our goals for this volume are to provide chapters that collectively present the current understanding of the pathogenesis of periodontitis in a userfriendly manner. Although the individual chapters are intended to be able to stand alone, they are all highly interrelated and integrated and the total is far greater than the sum of the parts. We have chosen the final chapter as a discussion section in which we summarize highlights of all the chapters, emphasize broad concepts, make clinical application where appropriate, speculate based on the data and point out future directions of the field. Experts agree that human periodontitis is initiated and perpetuated by a small group of predominantly gram-negative, anaerobic or microaerophilic bacteria that colonize the subgingival area. Indeed, at the 1996 World Workshop on Clinical Periodontics, the relevant working group concluded (2) that most human periodontitis is caused by Porphyrornonas gingivalis, Bacteroides forsythus and Actinobacillus actinornyceterncornitans. During the 1970s and 1980s, great strides were made in elucidating the infectious nature of human periodontitis; in the 1990s we have come to realize that, although bacteria are essential, they are insufficient for the disease to occur. Host factors such as inheritance, tobacco smoking and various other risk factors may even outweigh the bacteria as determinants of whether the disease occurs and of the severity of clinical outcome. These observations have led to major changes in ideas and concepts about pathogenesis, prevention and treatment. Over the past 10 to 15 years, substantial new information has been obtained about how these bacteria cause the formation of periodontal pockets, conversion of junctional epithelium to pocket epithelium and destruction of the alveolar bone and connective tissues of the gingiva and periodontal ligament. Bacteria mostly cause the observed tissue destruction indirectly, and they do so by activating various components of the host defense systems in such a manner that destruction ensues. It is enigmatic that the same host systems that provide protection and de-

Chlorhexidine: is it still the gold standard?

Abstract: After 20 years of use by the dental profession, chlorhexidine is recognized as the gold standard against which other antiplaque and gingivitis agents are measured. Chlorhexidine's antiplaque effect is a result of the dicationic nature of the chlorhexidine molecule, which affords the agent the property of persistence of antimicrobial effect at the tooth surface, through both bactericidal and bacteriostatic effects. Although other antiplaque agents may show either purely immediate effect, or limited persistence, the degree of chlorhexidine's persistence of effect at the tooth surface is the basis of its clinical efficacy. Similarly, the cationic nature of the chlorhexidine molecule is the basis of the most common side effect associated with the use of the agent--extrinsic tooth staining. Such tooth staining seems to be the result of a local precipitation reaction between tooth-bound chlorhexidine and chromogens found within foodstuffs and beverages. The cationic nature of the chlorhexidine molecule also means that the activity of the agent is rapidly reduced in the presence of anionic agents, specifically those found within certain types of toothpaste; thus care is required when using normal toothbrushing alongside chlorhexidine. By understanding how the chemical properties of the chlorhexidine molecule can explain the plethora of clinical efficacy and safety data, the use of chlorhexidine can be optimally aimed towards the patient groups who would most benefit from the superior therapeutic effect of the agent. Specifically, chlorhexidine would seem to be of most value to patients in whom the ability to perform adequate oral hygiene procedures has been compromised. In these individuals the delivery of the correct dose of chlorhexidine to the tooth surface can be optimized through the judicial use of the several different chlorhexidine formulations now available. Thus, by understanding the properties and limitations of the chlorhexidine molecule, the dental profession can ensure that the efficacy of the agent is maximized, and the side effects associated with the agent are minimized, allowing chlorhexidine to rightly remain the gold standard against which other antiplaque agents are measured.

The history of oral hygiene products: how far have we come in 6000 years?

Abstract: How far have we come in the past six millennia? Numerous dental epidemiological studies indicate that people are keeping their teeth longer than over before in this century. Agents and devices have evolved, by custom and by research, to enable people, with professional assistance, to maintain good oral health. Our diets, our lifestyles and our professional colleagues have "conspired" as pathogenic influences on oral health. The profession has met the challenge by developing and perfecting a myriad of devices and agents to thwart these pathogenic factors. Patient motivation and professional acceptance of preventive dentistry procedures still remain challenges. We certainly eat well, speak well, look fine and "smell fresh"--but we also have plaque, gingivitis and dental caries. The reader can determine how much progress has been made by reflecting on his or her personal oral health status!

Induction of the immune response to periodontopathic bacteria and its role in the pathogenesis of periodontitis

Abstract: Periodontitis results from infection with subgingival plaque-forming bacteria followed by host immune responses. Recent data indicate that Porphyromonas gingivalis, Actinobacillus actinomycetemcornitans and Bacteroides forsythus initiate and progress periodontitis (1). Pgingivalisis mostly found in deep periodontal pockets and especially in active sites (111, 212, 239). A. actinomycetemcomitans is found in pockets from patients with localized juvenile periodontitis as well as advanced adult periodontitis (72). B. forsythus seems to be related to disease activity (46, 235). Progress of the disease is arrested or slowed and the clinical condition is ameliorated by eliminating or decreasing the numbers of these bacteria (187). Bacterial ecology and immune responses in periodontal pockets are complex. Therefore, it is unlikely that only these three bacteria are the causative agents of periodontitis. However, exceeding a particular threshold or a rapid increase in the number of these three types of bacteria are closely related to the breakdown of periodontal tissues. The objective of this chapter is to summarize current understanding of the immune response induced by these bacteria and its role in the pathogenesis of periodontitis.

Evaluation of oral hygiene products: science is true; don't be misled by the facts.

Abstract: Most people in industrialized countries use oral hygiene products. When an oral health benefit is expected, it is important that sufficient scientific evidence exist to support such claims. Ideally, data should be cumulative derived from studies in vitro and in vivo. The data should be available to the profession for evaluation by publication in refereed scientific journals. Terms and phrases require clarification, and claims made by implication or derived by inference must be avoided. Similarity in products is not necessarily proof per se of efficacy. Studies in vitro and in vivo should follow the basic principles of scientific research. Studies must be ethical, avoid bias and be suitably controlled. A choice of controls will vary depending on whether an agent or a whole product is evaluated and the development stage of a formulation. Where appropriate, new products should be compared with products already available and used by the general public. Conformity with the guidelines for good clinical practice appears to be a useful way of validating studies and a valuable guide to the profession. Studies should be designed with sufficient power to detect statistically significant differences if these exist. However, consideration must be given to the clinical significance of statistically significant differences between formulations since these are not necessarily the same. Studies in vitro provide supportive data but extrapolation to clinical effect is difficult and even misleading, and such data should not stand alone as proof of efficacy of a product. Short-term studies in vivo provide useful information, particularly at the development stage. Ideally, however, products should be proved effective when used in the circumstances for which they are developed. Nevertheless, a variety of variable influence the outcome of home-use studies, and the influence of the variable cannot usually be calculated. Although rarely considered, the cost-benefit ratio of some oral hygiene products needs to be considered.

Is the chemical prevention of gingivitis necessary to prevent severe periodontitis

Abstract: Gingival inflammation seldom causes discomfort, social embarrassment or loss of function. As most sites with gingival inflammation do not progress to severe periodontal disease, gingivitis should not be considered a public health problem. Periodontitis is always preceded by gingivitis. But most gingivitis remains stable for years without progressing to periodontitis. The number of gingivitis sites that do convert is small. The levels of oral cleanliness achieved by the majority of populations in industrialized countries are below the threshold for severe destructive periodontal disease of personal and public health concern. Because methods of measuring the progression of periodontal disease are unreliable, definitive answers regarding conversion of gingivitis to severe periodontitis are lacking. Gingival inflammation frequently remains contained; most gingivitis remains stable for years without progressing to periodontitis. Decreasing gingivitis does reduce shallow pocketing, but the effect on severe periodontitis is not clear. Although the underlying justification for the reduction of plaque is to reduce gingival inflammation to prevent or reduce severe periodontitis and tooth loss, the basis for the approach is equivocal. A reasonably high level of plaque appears to be compatible with acceptably low levels of periodontal disease. Reducing nonspecific plaque levels to such levels is therefore a rational goal. The conventional methods of controlling periodontal disease involve mechanical removal of plaque and calculus. A complimentary ecological approach, using chemicals, would be to alter the environment of the pocket to prevent growth of putative pathogens. Any ecological approach should be sensitive to the dangers of disrupting the natural ecology of dental plaque. Some antimicrobial and antimetabolic agents such as fluoride, chlorhexidine and triclosan and zinc citrate can selectively suppress certain organisms or inhibit bacterial proteases implicated in tissue damage. The uncertainties about factors that convert gingival inflammation into periodontitis and periodontitis into severe periodontitis coupled with insufficient data from controlled clinical trials on the effectiveness of chemical reduction of gingivitis to prevent severe periodontitis leads one to conclude that more research is required before the need for the chemical prevention of gingivitis to prevent severe periodontitis can be justified.

Gum health product formulations: what is in them and why?

Abstract: Two dominant factors dictate which ingredients are used in formulating toothpaste and mouthwashes. The major one is the type of active ingredient chosen, especially cationic active ingredients such as chlorhexidine; the other factor is the needs of the consumer. Apart from gum health benefits, the consumer expects to obtain from gum health toothpaste and mouthwashes other benefits of clean teeth (abrasive and detergent), fresh breath (antimicrobial agents and flavor) and protection from caries and possibly tartar. Exhaustive testing involving experimental design and validated laboratory and clinical tests is essential to ensure that all these benefits are delivered. Unless products are developed systematically, then products with relatively poor activity can find their way on to the market.

Supragingival calculus and periodontal disease

Abstract: Supragingival calculus predisposes to the development of periodontal disease by providing a retentive surface for plaque bacteria and impeding attempts to maintain an effective level of plaque control (47). Although the presence of calculus and gingival inflammation, as evidenced by bleeding on probing, are not always coincident (1) the close proximity of supragingival calculus to the gingiva ensures that its superficial layer of plaque bacteria is maintained in contact with the gingival tissues. The finding that oral hygiene instruction alone resulted in significant improvements in the gingival health of individuals with large amounts of calculus supports the primary role of plaque bacteria (21). Recent studies have investigated the relationship between supragingival calculus and gingival recession (59). A selected sample of Thai children and adolescents were examined, and the amount of supragingival calculus and gingival recession was measured on the six lower anterior teeth. A significant association was observed between total calculus levels and the presence and extent of gingival recession. Two clinical studies, again involving Thai children and adolescents, demonstrated that subjects who used an anticalculus dentifrice for 1 year had significantly less supragingival calculus and gingival recession than those who used a placebo dentifrice or continued to use their customary oral hygiene procedures (60, 81). Supragingival calculus is relatively porous and becomes stained by dietary constituents and tobacco, and its removal is generally appreciated by the individual. Although toothbrushing with a conventional toothpaste containing abrasives and detergents may interfere with its formation, the widespread prevalence of supragingival calculus clearly indicates that such measures are not generally very effective. The dental profession spends a considerable amount of time removing supragingival calculus. In England and Wales periodontal treatment comprises approximately 23% of the treatment provided by the National Health Service (NHS) general dental services. In 1988-1989, single-visit scale and polishes cost GBP 120 million, approximately 12% of the total costs. The professional removal of supragingival calculus is frequently undertaken as part of a more comprehensive program to remove tooth deposits and provide instruction and advice regarding the maintenance of effective oral hygiene. Many factors influence how often supragingival calculus is removed, including the rate of supragingival calculus formation and whether the costs are borne by the patient or some other form of health care system. The implications of scaling and polishing have been considered in a previous review (2). Since supragingival calculus is a predisposing factor in the development of gingivitis and recession the development of clinically proven products that reduce its formation benefits both the profession and consumers. Anticalculus products comprise a significant sector of the oral hygiene market in many countries. For example, in the United States, anticalculus toothpaste accounted for approximately one quarter of total toothpaste sales in 1995.