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doi: 10.1111/j.1875-595x.2008.tb00185.x.

Affiliation

¹ World Health Organization, Global Oral Health Programme, Department of Chronic Disease and Health Promotion, Geneva, Switzerland. petersenpe@who.int

doi: 10.1111/j.1875-595x.2008.tb00185.x.

Affiliation

¹ World Health Organization, Global Oral Health Programme, Department of Chronic Disease and Health Promotion, Geneva, Switzerland. petersenpe@who.int

Abstract

The World Health Organization (WHO) Global Oral Health Programme has worked hard over the past five years to increase the awareness of oral health worldwide as an important component of general health and quality of life. Meanwhile, oral disease is still a major public health problem in high income countries and the burden of oral disease is growing in many low- and middle income countries. In the World Oral Health Report 2003, the WHO Global Oral Health Programme formulated the policies and the necessary actions for the improvement of oral health. The strategy is that oral disease prevention and the promotion of oral health needs to be integrated with chronic disease prevention and general health promotion as the risks to health are linked. The World Health Assembly (WHA) and the Executive Board (EB) are supreme governance bodies of WHO and for the first time in 25 years oral health was subject to discussion by those bodies in 2007. At the EB120 and WHA60, the Member States agreed on an action plan for oral health and integrated disease prevention, thereby confirming the approach of the Oral Health Programme. The policy forms the basis for future development or adjustment of oral health programmes at national level.

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dental health services / organization & administration

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national center for biotechnology information

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World Health Organization global policy for improvement of oral health--World Health Assembly 2007 - PubMed

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The World Health Organization (WHO) Global Oral Health Programme has worked hard over the past five years to increase the awareness of oral health worldwide as an important component of general health and quality of life. Meanwhile, oral disease is still a major public health problem in high income ...

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Prevention of oral diseases in developing countries. | Semantic Scholar

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A strategy in keeping with the primary health care approach would be an integrated oral health care delivery system with prevention and health education as priorities, based on the philosophy of self-reliance. : Low caries prevalence, high rates of periodontal disease and widespread oral mucosal disease constitute the major oral health problems in the developing countries.

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AIM

To compare the dental disease experience of Indigenous and non-Indigenous children in South Australia's mid-north region (regional area) and to assess Indigenous oral health differences at a regional- and state-level.

METHODS

Data were collected from a School Dental Service based in an Aboriginal-owned medical health service and standard school dental clinics in the regional area from March 2001 to March 2006. State-level data were obtained over a 12-month period in 2003. Caries prevalence (per cent dmft or DMFT >0) and severity (mean dmft or DMFT, SiC and SiC10) measures were used to assess dental disease experience.

RESULTS

In the regional area, Indigenous children aged <10 years had 1.6, 1.9, 1.6 and 1.4 times the percent dmft >0, mean dmft, SiC primary and SiC(10) primary, respectively, of their non-Indigenous counterparts, while Indigenous children aged 6+ years had 1.3, 1.7, 1.7 and 1.6 times the percent DMFT > 0, mean DMFT, SiC permanent and SiC10 permanent, respectively, of non-Indigenous children. Indigenous children in the regional area had significantly higher caries prevalence and severity than Indigenous children at a state-level.

CONCLUSION

Indigenous children in South Australia's mid-north region are dentally disadvantaged in comparison with their non-Indigenous counterparts and with the general South Australian Indigenous child population.

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PRIME PubMed | Indigenous child oral health at a regional and state level

# data[].attributes.attachment_link.description
To compare the dental disease experience of Indigenous and non-Indigenous children in South Australia's mid-north region (regional area) and to assess Indigenous oral health differences at a regional- and state-level. Data were collected from a School Dental Service based in an Aboriginal-owned medical health service and standard school dental clinics in the regional area from March 2001 to March 2006.

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Bull World Health Organ. 2005 Jan; 83(1): 3.

Full Text

The Full Text of this article is available as a PDF (40K).

Articles from Bulletin of the World Health Organization are provided here courtesy of World Health Organization

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The burden of oral disease: challenges to improving oral health in the 21st century.

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Bull World Health Organ. 2005 Jan; 83(1): 3. The Full Text of this article is available as a PDF (40K). Articles from Bulletin of the World Health Organization are provided here courtesy of World Health Organization

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Tooth decay happens when acids wear away the tooth's hard surface layer, called enamel. Learn all about tooth decay symptoms and more.

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New Hampshire Center for Comprehensive Dentistry |

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Did you know...

...tooth decay (dental caries) continues to be the most common chronic disease in both adults and children in the United States, according to the latest study by the National Institutes of Health (NIH)? Ninety-two percent of adults age 20-64 have had tooth decay. Children age 2-11 have a 42% incidence and 59% of teens age 12-19 have had tooth decay in their permanent teeth.

...tooth decay is second only to the common cold as the most prevalent disease in humans?

...that too many missing teeth, lost due to tooth decay, was the most common reason for draft rejection in World War II?

...it wasn't until the 1970's that tooth decay was determined to be caused by bacteria?

...over 200-300 different kinds of bacteria are present in the adult mouth? Although only a few types of bacteria cause tooth decay, they form complex biofilms that coat tooth surfaces.

...tooth decay can be "caught"? An exchange of saliva from one mouth to another can transmit the decay-causing bacteria. Kissing, sharing eating utensils or anything that has had contact with saliva can be a mode of bacterial transfer.

...acids produced by the bacteria attack tooth enamel? When your natural tooth structure is damaged it will need to be restored and will require additional maintenance over your lifetime.

...tooth decay only becomes painful when the cavity extends close to the tooth pulp where the tooth's nerve supply is located?

...detecting early signs of tooth enamel demineralization, or breakdown, the application of fluoride and use of antimicrobial solutions can help stop the progression towards tooth decay?

...your level of risk for developing tooth decay can be measured by screening for certain habits and behaviors, and testing your saliva for the presence of certain bacterial species and pH?

We hope you learned some facts about tooth decay. For a disease that is largely preventable, take steps to discover your level of risk for tooth decay at your next visit. Ask about CAMBRA - Caries Management by Risk Assessment - now a part of the patient-centered preventive care at New Hampshire Center for Comprehensive Dentistry. Discuss prevention and treatment recommendations with your dentist and dental hygienist to help you create a healthy smile and stay cavity-free.

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Facts About Tooth Decay: Did You Know? | Dentist in Amherst, NH

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Did you know... ...tooth decay (dental caries) continues to be the most common chronic disease in both adults and children in the United States, according to the latest study by the National Institutes of Health (NIH)? Ninety-two percent of adults age 20-64 have had tooth decay.

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oral health charity dental advice uk national smile month mouth cancer action month

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10 JAN 2019 - Ten facts and five tips to help you and your family battle tooth decay.

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Main

Fluorides are found naturally throughout the world. The beneficial effects of fluoride on teeth were first observed in an area with naturally-fluoridated water. Clinical trials subsequently demonstrated that the same benefits could be obtained by adjusting the fluoride level of water supplies to an optimum level of 1 part per million.

Because early investigations into the prevention of caries with fluoride involved fluoride in water supplies, it was assumed that the benefit came about mainly through a strengthening of teeth during development. However, research has shown that fluoride's topical effect is equally or more important. Fluoride inhibits caries by encouraging the tooth to remineralise after attack by plaque acids.

This mechanism explains much of the improvement in dental health shown by the UK national surveys over the past 30 years. Throughout this period, most toothpaste has been fluoridated, with a resulting topical effect considerably greater than was expected when fluoride toothpastes were first developed. Fluoride toothpaste has made a major contribution to improved oral health in the UK.

The case for targeted water fluoridation

The success of toothpaste fluoridation in the UK has resulted in a reassessment of the role of water fluoridation. In some parts of the country, especially more affluent areas, decay levels are now very low, so that water fluoridation would bring little additional benefit. But in the major connurbations with areas of social deprivation, disease levels are much higher and water fluoridation remains an essential public health measure. Everyone's diet includes water so everyone benefits, including the most disadvantaged who may not have the benefit of regular fluoride toothpaste use.

The recent White Paper on public health seeks to narrow inequalities in health. For oral health, water fluoridation is the most effective way of doing this but the need is for targeted water fluoridation schemes. The BDA has proposed that 25% of the UK population should be drinking optimally-fluoridated water by 2005. Provided that new fluoridation schemes serve areas of greatest social and material inequality, even an increase from the current 10% to a coverage of 25% could produce major dental health improvements.

The need for continued use of fluoridated toothpaste

Alongside targeted water fluoridation schemes, the population must continue to use fluoride in other ways if recent improvements in dental health are to be maintained. Fluoride toothpaste has been comprehensively tested and shown to provide a benefit even in fluoridated areas. Its use must be regarded as an important public health measure in its own right.

Other fluoride delivery systems are available, including salt and milk fluoridation. Tests have shown them to be effective in reducing decay, if used regularly, but these methods of delivery are not generally available in the UK.

Fluoride exposure from multiple sources

If excessive fluoride is ingested while permanent teeth are still forming (up to about the age of 7 years) mild enamel opacities may result. Such opacities are normally not discernible to the untrained eye. There are many other causes of opacities in addition to the ingestion of fluoride. It is noteworthy that after 30 years of fluoride toothpaste availability, fluoride dietary supplementation and water fluoridation in some areas, enamel opacities raise minimal public interest or concern. The risk benefit equation is strongly in favour of continued fluoride toothpaste use alongside water fluoridation.

However, if the benefits of fluoride toothpaste use are to be maintained, and if progress is to be made with water fluoridation in areas where this measure is still needed, it is essential that public confidence in fluoride is maintained. Limitation on the amount of fluoride ingested by under 7s can be achieved by supervised brushing, use of a pea-sized amount of paste and, for children at low risk of decay, by the use of formulations containing around 500 ppmF. Caution is necessary in the use of fluoride dietary supplements which are not a public health measure and should only be used under dentist supervision.

Summary

Fluoride reduces the incidence of dental decay substantially.

Fluoride benefits all age-groups, because of its topical effect.

Water fluoridation needs to be targeted on high caries areas which are normally also areas of social and material deprivation.

Thorough brushing twice a day with a fluoride toothpaste is also crucial to the improvement of oral health.

Statement approved by the Representative Board of the British Dental Association on 6 November 1999, having been proposed by Dr Geoffrey Craig, on behalf of the Association's Health and Science Policy Group.

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Fluorides and the prevention of dental decay: a statement from the Representative Board of the British Dental Association* - British Dental Journal

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Fluorides are found naturally throughout the world. The beneficial effects of fluoride on teeth were first observed in an area with naturally-fluoridated water. Clinical trials subsequently demonstrated that the same benefits could be obtained by adjusting the fluoride level of water supplies to an optimum level of 1 part per million.

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Clujul Med. 2015; 88(2): 137-139.

Abstract

Health is a right that requires responsible individual actions. Oral health corresponds to an important part of general health, even if for a large majority of people healthy teeth are equal with beautiful teeth. For children and adolescents „having an attractive smile" is synonymous with social acceptance and success. Dental decay has a high incidence in children in our country and progress in decay prevention, diagnosis and treatment is not reflected in children and adolescents' oral health. It is established by studies conducted by dentists and psychologists that dental decay can affect the quality of life by engendering specific eating behaviors, particular ways of speech or smile and unfortunately pain.

The aim of this article is to emphasize the modern approach of dental decay in line with principles of non-invasive strategies. An important element to be considered - prophylactic methods - must be included in every treatment plan, in order to control individual caries risk. The time invested in prevention during childhood represents a real benefit for the future adult's oral health. Many a dental problems can be avoided if dental decay management relies on the link between medical science and every day practice.

Keywords: dental decay, prevention, remineralization, children

Oral health is a fundamental component of overall health. Dental decay has a complex determination and various etiological factors. Diet and bacteria in the dental plaque play an essential role in the development of caries. Interventions in children and adolescents are considered to be very effective, because the disease has a dynamic evolution in a group or in the same subject at different periods of life [ 1].

Preventive measures for dental caries should be included in the patient's treatment plan at any age, in order to preserve restorative treatment outcomes and reduce future caries risk [ 2, 3].

The aim of this article is to underline the modern approach of dental decay according to minimally invasive strategy principles.

Method

We performed searches on the following databases / websites: the American Academy of Pediatric Dentistry Policies and Guidelines, the European Academy of Pediatric Dentistry Archives and Guidelines, the International Association of Pediatric Dentistry Online Oral Health Resources and Haute Autorité de la Sante Recommandation; the search terms included "caries risk", "decay prevention", "minimally invasive treatment", "children and adolescents". In the evaluation of the articles and guidelines the following problems were addressed:

1. The points in time for caries risk increase in children and adolescents;

2. The specific criteria of minimally invasive dentistry for children and adolescents;

3. The role of prophylactic and preventive measures for dental decay in the patient treatment plan.

Results and discussion

Dental care and follow up for children, especially at young ages, have specific features:

1. Patient behavior and its management requires a trained medical team, in order to meet the children's particular needs;

2. Parents' lack of concern or knowledge to preserve the integrity of temporary teeth. If temporary teeth are neglected, permanent teeth will erupt in an oral environment with modified microbial and salivary parameters, a risk factor for caries;

3. absence or inconsistency regarding dental hygiene;

4. physiological characteristics of temporary and permanent teeth [ 4, 5, 6].

Caries risk and developmental stages

Caries risk is defined as the probability of an individual to develop a certain number of caries lesions during a specific period of time [ 1]. Risk assessment is an important step in decision-making and treatment planning [ 7]. In children and adolescents we defined specific stages of high risk for tooth decay, when it is essential to make use of preventive measures:

1-3 years:

diet evolution and diversification, preference for refined product that does not require an active mastication;

neglected or inconsistent oral hygiene at this stage of child development; following the example of adults, the child tries to use the toothbrush but does not have the skills to perform a correct routine. Parents will complete the brushing of their children, especially in less accessible areas of the dental arches.

5-7 years:

diet with high carbohydrate intake, individual selection of snacks;

the child acquires greater ability to use tooth brush and gradually can perform oral hygiene alone, although parents intervention is still necessary to oversee and control the routine;

first permanent molar eruption (often confounded per a temporary tooth).

11 to 14 years:

diet with high carbohydrate intake, advertising and group opinion can affect tooth friendly products selection;

puberty-somatic, hormonal and psychological changes;

unfavorable attitude relative to the basic rules of oral hygiene, dental care, dental check-up and treatment sessions [ 8, 9, 10, 11].

Dental decay management

Currently, treatment of dental caries is reconsidered. Modern methods of detection and early diagnosis allow the individualization of clinical stages that can benefit from remineralization, if oral ecosystem parameters changes in a positive manner. To achieve this, the treatment of dental caries should be approached in a holistic manner, positioned in a sequence that lay stress on preventive methods and patient active involvement [ 12, 13].

Modern management of dental decay uses of the following algorithm:

detection and dimensional valuation of caries (decay type, associated histo-pathological changes);

monitoring the lesion, determine whether restoration or remineralization treatment will be performed;

assessing individual carious risk;

diagnostic/prognostic/therapeutic measures - lesion treatment using methods belonging to restorative or preventive dentistry;

periodical follow up, monitoring [ 12, 14, 15].

Numerous studies have shown that an important factor in the positive or negative feedback of preventive measures is represented by the social context. Often patients are not informed on dental pathology, neglect regular dental check-up, attend the dental office only in case of an emergency and embrace a diet rich in sugars and fats [ 16].

The first consultation dentist-patient is crucial to establish adequate communication, the basis of effective treatment. The information provided by the physician to the child and parents should be tailored to their educational and cultural context. What may seem like a "waste of time" in the first treatment session is actually a true valuation of our profession, because in the absence of preventive attitudes, the long-term prognosis of dental restorations is unfavorable and may be a failure [ 17, 18]. Adequate oral health requires a collective effort of everyone involved: medical team, child, family, and teachers, and if we consider the heterogeneity of those involved in this process we can comprehend why it is so difficult to move forward effective programs for dental caries prevention and treatment [ 19].

The question remains which dental decay approach is more effective for children and adolescents? A possible answer may result from the comparative analysis of the two models proposed in literature ( table I ):

Table I

RESTORATIVE MODEL

PREVENTIVE MODEL

Treatment of all active carious lesions

Diagnosis of active and inactive carious lesions

Restorative treatment goal is to arrest caries progression

Remineralization-for non cavitary lesions limited to enamel

Decay treatment-cavity preparation and restoration

First treatment objective -remineralized incipient lesions. Restorations are made only if preventive approach failed

Extensive restorations - all dental tissues considered demineralized and infected will be eliminated

Minimally invasive restorations - for demineralized tissues the first therapeutic approach will be remineralization

These recommendations cannot be implemented literally; they must be adapted to the patient's caries risk, which may evolve over time and must be evaluated in the control session [ 16, 19, 20].

Conclusions

Compliance for dental care and regular dental follow up in the absence of subjective complaints indicate the interests of the child and family in favor of oral health. A minimum rate of 2-4 check-ups per year for children and adolescents would maintain the results of previous treatments, reversible forms diagnosis and treatment of dental caries with minimal tissue removal [ 12, 14, 20]. This goal requires close cooperation with children and family and in the particular case of our country it must overcome educational barriers.

References

4. McDonald RE, Avery DR, Dean JA. Dentistry for the child and adolescent. 8th ed. St. Louis: Mosby Inc; 2004. pp. 236-257.pp. 257-270.pp. 333-353.pp. 353-364. [ Google Scholar]

5. Blique M. Prophylaxie dentaire individuelle, nouvel outil pour le traitement du jeune enfant a risque carieux eleve. J Odontol Pediatr. 1999;9:9-14. [ Google Scholar]

6. Haute Autorité de Santé HAS. Appréciation du risque carieux et indication du scellement prophylactique des sillons des premières et deuxièmes molaires permanents chez les sujets au moins de 18 ans. Argumentaire. 2005:12-78. [ Google Scholar]

7. Oulis CJ, Raadal M, Martens L. Guidelines on the use of fluoride in children, an EAPD policy document. EJPD. 2000;1(1):7-12. [ Google Scholar]

13. American Academy of Paediatric Dentistry. American Academy of Paediatric Dentistry Reference Manual. Chicago: 2004. Clinical Guideline on Pediatric Restorative Dentistry; pp. 106-114. [ Google Scholar]

14. Rodd H, Wray A. Treatment Planning for the Developing Dentition. London: Quintessence publishing Co. Ltd; 2006. pp. 45-73. [ Google Scholar]

16. Ahovuo-Saloranta A, Hiiri A, Nordblad A, Mäkelä M, Worthington HV. Pit and fissure sealants for preventing dental decay in the permanent teeth of children and adolescents. Cochrane Database Syst Rev. 2008;(4):CD001830. [[ PubMed] Google Scholar]

Articles from Clujul Medical are provided here courtesy of Universty of Medicine and Pharmacy of Cluj-Napoca, Romania

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Modern management of dental decay in children and adolescents - a review

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Health is a right that requires responsible individual actions. Oral health corresponds to an important part of general health, even if for a large majority of people healthy teeth are equal with beautiful teeth. For children and adolescents „having ...

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Dental Caries (Decay)

Dental decay is due to the dissolution of tooth mineral (primarily hydroxyapatite, Ca ₁₀ (P0 ₄) ₆(0H) ₂) by acids derived from bacterial fermentation of sucrose and other dietary carbohydrates. These bacteria live in bacterial communities known as dental plaque which accumulates on the tooth surface. For almost a century it was believed that any bacterial community on the tooth surface could cause decay, and treatment was almost exclusively the mechanical cleaning of these surfaces by toothbrushing, using some type of mild abrasive. Such treatments based upon debridement and, in extreme cases, upon dietary carbohydrate restriction, were singularly unsuccessful in reducing dental decay. In fact, the prevalence of dental decay was so high among young men that it was the major cause of rejection from military service in World Wars I, II, and the Korean War. This staggering amount of dental morbidity led to the formation of dentistry as a separate health profession in the late 19th century; to the expectation that all people would, if they lived long enough, be edentulous (toothless); and to a dental health bill to the public of approximately 34 billion dollars per year in 1990.

Things have changed. Water fluoridation has proven to be a most cost-effective way of reducing decay; fluoride dentifrices were even more effective than initially projected; and research findings indicate that most carious lesions actually reflect a sucrose-dependent Streptococcus mutans infection. Individuals at risk for this infection can be diagnosed and treated by frequent mechanical intervention, by intensive application of prescription levels of fluorides or other antimicrobials (such as chlorhexidine), by restriction of ingestion of sucrose between meals, or by use of products that contain sucrose substitutes (such as xylitol). The net result is that dental decay in the late 20th century is a controllable infection and should be preventable in many individuals. Almost 50% of young children are caries-free, and the level of edentia among individuals over 65, has dropped from 50% to about 20%.

Etiology

Dental decay has been known since recorded history, but was not an important health problem until sucrose became a major component of the human diet. When sucrose is consumed frequently, an organism known as Streptococcus mutans emerges as the predominant organism, and it is this organism that has been uniquely associated with dental decay.

In 1924 S mutans was isolated from human carious lesions, but subsequently was not thoroughly studied until the 1960s when it was re-identified as the etiologic agent of a transmissible caries infection in rodent models. In these studies, all of Koch's postulates for infectivity were fulfilled in animal models. However, it proved difficult to show that S mutans was a human dental pathogen, because S mutans appears to be a member of the normal flora on the teeth, and it was difficult to show that an increase in S mutans actually preceded and/or coincided with the earliest clinical lesion.

Dental decay is measured clinically as a cavitation on the tooth surface ( Figure 99-1). However, cavitation is a late event in the pathogenesis of decay, being preceded by a clinically detectable subsurface lesion known as a white spot ( Figure 99-1), and prior to that by subsurface demineralization that can only be detected microscopically. From a diagnostic and treatment perspective, the lesion should be detected at the white spot stage. This usually cannot be done without rigorous descriptive criteria (not all white spots are due to the decay process) and because the white spot stage in the caries-prone fissures and approximal surfaces of the tooth cannot be directly visualized during a dental examination.

The prevalence of dental morbidity is documented in terms of the number of teeth (T) or tooth surfaces (S) that have obvious decay (D), contain a dental restoration or filling (F), or are missing (M). These DMF teeth (DMFT) and DMF surface (DMFS) scores do not discriminate as to the relative proportions of the score due to decay, versus fillings and extractions. This insensitivity of the DMFT and DMFS scores in quantitating the actual decay, independent of morbidity led in early clinical studies to unimpressive associations between S mutans and DMFT or DMFS scores. However, when the comparison was limited to individuals with decayed teeth or when the plaque samples were taken from a decayed tooth site, a significant association between S mutans and decay was evident.

This association is clearly seen in individuals who developed xerostomia secondary to radiation treatment of head and neck cancer. S mutans and lactobacilli are normally present in low numbers in the plaque of these individuals. When the salivary flow decreases, the pH in the plaque drops, leading to a selection for aciduric (acid-tolerant) bacteria, such as S mutans and lactobacilli. New decayed lesions become obvious within 3 months after radiotherapy and the patient may average one or more new decayed surfaces per post-radiation month. During the development of decay, the proportions of, first, S mutans and then lactobacilli increased significantly. This sequence of events indicated that S mutans was involved with the initiation of decay, whereas the lactobacilli were associated with the progression of the lesion.

This bacterial succession is illustrated in Figure 99-2, which shows the sequence of events occurring on the surface of a caries-free tooth that either becomes carious or remains caries free. In either case, the tooth surface initially represents a carrier state relative to harboring a primary cariogen, such as S mutans, in the plaque on a smooth surface. The proportion of the cariogen in the flora is similar in both cases, but the location of S mutans differs within the plaques. In the tooth destined to develop decay, S mutans is located on the enamel surface, whereas in the tooth destined to remain caries free, S mutans is confined to the saliva-plaque interface. Debriding procedures, such as toothbrushing and flossing, might remove most plaque organisms, but could leave untouched those bacteria either firmly attached to the enamel surface or sequestered in defects in the enamel surface. In surfaces destined to become carious, the residual organisms would include S mutans, whereas in surfaces destined to remain caries free, S mutans would be absent. Over time these caries-free surfaces might alternately acquire and lose S mutans, thereby having an intermittent carrier-state status. However, in those surfaces in which caries will eventually develop, S mutans becomes a dominant member of the flora, undoubtedly secondary to frequent sucrose ingestion.

The incipient or white spot lesion occurs when the acidogenic activity of the cariogen causes tooth mineral to be mobilized from the subsurface enamel to buffer the pH at the plaque-enamel interface. Bacteriologic sampling at this stage should reveal both a proportional and an absolute increase in the levels of S mutans. When the lesion progresses to the stage of cavitation, the organisms penetrate into the enamel crystals ( Fig. 99-2). Also, secondary cariogens, such as the lactobacilli, appear as a result of the selection for aciduric organisms in the plaque. When the lesion reaches the advanced clinical stage, conditions may be such that S mutans can no longer survive, and only secondary cariogens like the lactobacilli and opportunistic organisms can be found.

This model predicts that a bacterial succession occurs during the progression of a carious lesion and that the flora of the advanced lesion may bear little resemblance to the flora of the incipient lesion. Thus it was necessary to sample the plaque during the initial lesion or white spot stage to find the etiologic agents of decay. When this was done, S mutans dominated in the flora. However, for the lesion to progress to the stage of cavitation, lactobacilli seem necessary. Thus while S mutans could be isolated from both progressive and nonprogressive lesions, L casei could only be isolated from progressive lesions.

Pathogenesis

These clinical studies indicated that of the 200 to 300 species which can be isolated from plaque, only S mutans, and to a lesser extent the lactobacilli, can be consistently associated with dental decay. What makes these organisms cariogenic relative to all other bacterial types found in the plaque?

In the 19th century, microbial acid production from dietary substrates was linked to the etiology of dental decay in what was called the chemoparasitic theory of decay. But researchers were not able to associate any single acidogenic species with decay, and concluded that decay was bacteriologically nonspecific and due to the increased amounts of acid formed when bacteria accumulated in plaque on the tooth surfaces. It was noted that decay occurred at retentive sites on the teeth and recommended mechanical debridement of these sites as the best method of reducing decay. While the clinical observations were correct, there was no way of determining that the retentive sites were caries prone because they provide the micro-environment which selects for S mutans and lactobacilli. In this section we shall examine those attributes of S mutans and the lactobacilli that enable them to be successful on retentive sites and show that these attributes constitute, in effect, the virulence factors which make these organisms specific odontopathogens.

Sucrose in the diet

Considerable evidence from epidemiologic observations and animal experiments indicates that, shortly after sucrose is introduced into the diet, a notably higher incidence of decay occurs. The relationship between sucrose ingestion and dental caries is reasonably well understood. The supragingival plaque flora derives its nutrients from various sources that include diet, saliva, sloughed epithelial cells, dead microbes, and gingival crevice fluid or exudate. All sources, except the foods in the diet provide only small amounts of nutrients. Dietary components are normally high-molecular-weight polymers (such as starch and proteins) that are in the mouth for short periods. They have a minimal effect on plaque growth except in those instances when food is retained between and on the teeth. Sucrose, however, changes this pattern because it is a low-molecular-weight disaccharide that can be rapidly sequestered and utilized by the plaque flora. Plaque organisms capable of fermenting sucrose have a decided advantage over the non-sucrose fermenters in that they can proliferate during periods of sucrose ingestion and thereby become the dominant plaque organisms.

Sucrose fermentation produces a rapid drop in the pH, to 5.0 or lower, at the point of interface between plaque and enamel. When sucrose is ingested during meals, sufficient saliva is secreted to buffer the plaque pH and decay does not occur. In fact, studies show that as much as one-half of a pound of sucrose consumed daily at meals for two years was not associated with an increase in dental decay; however, when the same or lesser amounts of sucrose were ingested between meals, subjects developed new decay at the rate of about three to four tooth surfaces per year. The frequent ingestion of sucrose has been shown to increase the lengths of time that sucrose could be detected in the saliva. This means that if this sucrose were available for microbial fermentation in the plaque, low plaque pHs would be present for long periods each day. When the plaque pH value falls below 5.0-5.2, the salivary buffers are overwhelmed and as lactic acid diffuses into the tooth, enamel begins to dissolve, releasing Ca and PO ₄ ions from sites beneath the surface enamel ( Figure 99-3). Normally, the bathing saliva replenishes these minerals, but if the length of the flux from the enamel is great, repair does not occur and cavitation results. Thus, sucrose consumption per se does not cause decay, but the frequent ingestion of sucrose by prolonging the time period by which the plaque is acidic, is cariogenic.

Plaque bacteria that ferment sucrose produce acids, which in vitro lower the pH value to below 5.0. However, only S mutans of all these species reliably caused decay in germ-free animals fed a high-sucrose diet. This suggested that microbial acid production was not the exclusive determinant of decay and that S mutans had to possess other attributes which were responsible for its virulence. S mutans was subsequently shown to metabolize sucrose in a remarkably diverse fashion that is not matched by any other known plaque organism. The major pathway is concerned with energy metabolism; in this process, the enzyme invertase splits sucrose into its component glucose and fructose molecules, which are then converted to lactic acid by the glycolytic pathway. Other enzymes, called glucosyltransferases, split sucrose but transfer the glucose moiety to a glucose polymer known as a glucan. S mutans forms several complex glucans that differ in their core linkage, amount of branching, and molecular weight. The first glucan identified had a core linkage consisting of an a1-6 bond that classified it as a dextran. Later, a unique glucan having an a1-3 core linkage was identified and given the name mutan. S mutans also has enzymes that split sucrose and transfer the fructose moiety to a fructose polymer known as a fructan. Other plaque bacteria can use sucrose to synthesize one or more of these polymers, with the exception of mutan. Only S mutans can form all of them, a fact that led to an inquiry into the relationship between polymer production and caries formation.

A series of in vitro experiments showed that the glucans enable S mutans to adhere to surfaces. This suggested that in vivo these adhesive polymers would enable S mutans to adhere tenaciously to the tooth surface and to accumulate on these surfaces, thereby causing decay in the underlying surface.

Animal experiments in which rodents were infected with mutants of S mutans that lacked the ability to form either dextran or mutan, indicated that the absence of mutan was associated with a greater reduction in smooth surface decay than was the absence of dextran. In each instance, the amount of pit and fissure decay was not significantly affected by these mutations. Decay on smooth surfaces seems to depend on the retentive polymers formed by S mutans, whereas in sites where retention is provided by the anatomy of the teeth (pits, fissures, and contact points between teeth), these polymers are not as important. Accordingly, pit and fissure decay may be caused simply by any acidogenic organism that can survive in these retentive sites.

This nonspecific explanation does not seem completely satisfactory, because in animal models and in human caries, S mutans, again, is the dominant organism involved or associated with pit and fissure decay. A few other organisms, such as Lactobacillus casei and Streptococcus faecalis, can cause fissure decay in germ-free rats. These three organisms are all relatively aciduric compared to other plaque bacteria; that is, they not only produce acids, but they are relatively resistant to the resulting low pH caused by acid accumulation. Lactobacilli are the most aciduric of the plaque bacteria, but these organisms only predominate by the time the carious lesion has extended into the dentin. At the time the earliest carious lesion is detected, only S mutans has reached significant levels and proportions ( Figure 99-2). When S mutans, lactobacilli, and other plaque species were compared in vitro for their ability to ferment sucrose at different pH values, S mutans was found to be more active than the other bacteria at pH 5.0, and thus, it is probably most active in vivo at the very pH at which the teeth begin to demineralize.

This aciduricity best explains the involvement of both S mutans and lactobacilli in human decay. A retentive site is colonized by those organisms present in saliva. S mutans, although scarce in the initial inoculum (fewer than 0.1% of the initial colonizers), is selected for if the average pH value in the site is not well buffered by saliva. Frequent ingestion of sucrose-containing products predisposes toward lower pH values and thus selects for S mutans. When the pH remains in the vicinity of 5.0-5.5, tooth mineral is solubilized, thereby buffering the plaque and maintaining an environment suitable for growth of S mutans. Eventually, enough mineral is lost so that a cavitation occurs in the enamel, and if this enlarges so that it extends into the dentin, a semiclosed system is formed in which the pH value drops below 5.0. Under these acidic conditions, growth of lactobacilli is favored, and these organisms succeed as the predominant flora in the carious lesion.

Clinical Manifestation

Dental decay occurs at discrete sites on the surface of the enamel. Progress through the enamel is usually slow because of the remineralizing action of the saliva, and is asymptomatic. When decay spreads into the dentin, the process accelerates, most likely because the very low pH that can arise in this semiclosed environment denatures the collagen scaffold that holds the hydroxyapatite salts in place and rapidly solubilizes them. When the dentinal decay approaches the innervated tooth pulp, the pain can be intermittent or continuous, and dull or excruciating. Pain is the chief complaint of the patient.

Microbiologic Diagnosis

A microbiologic diagnosis for a S mutans/lactobacilli infection is rarely sought, primarily because the acute pain that brings the patient to the dentist is almost always relieved by a dental restoration or extraction. Thus, the knowledge of an underlying S mutans infection would not change the treatment. However, microbiologic diagnosis would be advantageous in the management of the patient to prevent or minimize future decay. Such situations would occur whenever an expensive treatment is planned, such as orthodontic treatment, or the placement of dental crowns and bridges to replace missing teeth. Microbiologic examination would also be useful at the end of any restorative treatment to determine the residual level of S mutans and lactobacilli colonization on the teeth.

Scandinavian investigators have empirically determined that 10 ⁶ CFU S mutans per milliliter of stimulated saliva can be associated with future caries activity. Accordingly, they have recommended active intervention with fluoride, dietary counseling, and antimicrobial agents in individuals so infected. They have designed simple chairside tests that can, in a semiquantitated manner provide information on the salivary levels of S mutans. All of these tests rely on the fact that S mutans is resistant to 5 ug/ml of bacitracin and that it will grow in the presence of 20% sucrose. In liquid media containing these additives, S mutans will form adherent colonies on the side of glass, plastic strips, or any other solid surfaces that are present.

In a practical application of these tests, the clinician would not place orthodontic bands on an individual with 10 ⁶ CFU of S mutans, because this individual would be apt to develop decay around the margins of the bands. Likewise an individual who is having extensive bridgework (the placing of dental restorations across an edentulous space) would be at risk of developing new decay around the margins of these restorations. In both instances, the patient needs to be treated for S mutans infection prior to the placement of the dental devices or restorations.

Prevention and Treatment

Conventional dental therapy has not yet incorporated any microbiologically-based strategy into its armamentarium. Instead, a treatment based on response to symptoms has prevailed. The bankruptcy of this approach, which depends on a turn-of-the-century biologic base, has been demonstrated in the Scandinavian countries, where a socialized dental delivery system has made quality dentistry available to everyone. Because of the emphasis on treatment rather than prevention, the results have only prolonged the life span of the tooth by about 10 years, a rather poor therapeutic result. In England, where the health care system also emphasized treatment rather than prevention, one-half of the people over 35 years of age were edentulous in the 1970s. The Scandinavians, especially in Sweden, have changed their approach and have instituted plaque prophylactic programs for children and adults. Thorough dental cleaning with a 5% fluoride paste given at 2-4 week intervals combined with oral hygiene education, has lowered dental decay in children by about 80%-90%, compared to youngsters receiving symptomatic treatment. (Symptomatic treatment involves placing dental restorations in an obviously carious tooth, and pulling teeth.) Similar success has been achieved in adults with and without periodontal disease.

Thorough cleaning with fluoride apparently selects for the more desirable bacterial types, such as S sanguis and S mitis, which are capable of rapidly colonizing the tooth surfaces. S mutans presumably does not have an opportunity to become dominant, because the frequent debridement neutralizes its ability to be selected for by the low pH values that characterize an undisturbed plaque. Also, the 5% fluoride paste has an immediate bacteriostatic effect on the plaque organisms.

Fluoride as an Antimicrobial Agent in Plaque

The mechanisms by which fluoride prevents decay are multiple, and the relative contributions of each mechanism are not fully understood. The 30%-50% reduction in decay that follows water fluoridation is generally attributed to the fluoride replacing hydroxyl groups in the tooth crystal, thereby forming fluorapatite ( Fig. 99-4). Fluorapatite is less soluble in acid than hydroxyapatite, which means that a tooth containing fluorapatite dissolves slowly in the low pH value found in plaque, and accordingly, remineralizes faster in the intervals between sugar ingestion. These explanations do not completely account for the proved efficacy of topically-applied fluorides and raises questions about other modes of fluoride action.

The fluoride ion (F ⁻) inhibits the bacterial enzyme enolase, thereby interfering with production of phosphoenolpyruvate (PEP). PEP is a key intermediate of the glycolytic pathway and, in many bacteria, is the source of energy and phosphate needed for sugar uptake. The presence of 10-100 ppm of F ⁻, inhibits acid production by most plaque bacteria ( Fig. 99-4). These levels are delivered easily by most prescription fluoride preparations, such as were used in the Swedish studies. Of equal interest is the finding that at acidic pH values (5.5 or below), low levels of F ⁻ (1-5 ppm) inhibit the oral streptococci. These levels are found in plaque, especially in individuals who drink fluoridated water or who use fluoridated dentifrices. If this plaque fluoride is derived from the tooth, an antibacterial mode of action, which involves a depot effect, can be postulated for systemic (water) and topical fluoride administration.

The depot effect comes about in this manner. Water fluoridation promotes the formation of fluorapatite, whereas topical fluorides cause a net retention by the enamel of fluoride as fluorapatite or as more labile calcium salts. Microbial acid production in the plaque may solubilize this enamel-bound fluoride, which at the prevailing low pH in the plaque microenvironment could become lethal for the acid-producing microbes. Such a sequence would discriminate against S mutans and lactobacilli because they, as a result of their aciduric nature, are most likely the numerically dominant acid producers at the plaque-enamel interface. The fluoridated tooth thus contains a depot of a potent antimicrobial agent that is not only released at an acid pH value but is most active at this pH value. This hypothesis, then, attributes some of the success of water fluoridation and topical fluorides to an antimicrobial effect. It further suggests that judicious use of topical fluorides would be effective in patients with highly active caries.

The most effective dose schedule and fluoride preparation have not been determined. Neutral 1.0% sodium fluoride given daily to adults, who normally would experience rampant caries secondary to a xerostomia following irradiation for jaw cancer, has resulted in few or no caries. Controls, who were given a placebo as well as the best available hygiene instruction, averaged over two new decayed surfaces per post-radiation month ( Table 99-1). When the control patients were placed on the daily fluoride regimen, their decay rate dropped almost to zero. In another study, 5- to 6-year-old children, who had 10 or more carious tooth surfaces, were given the necessary dental restorations and either 1.2% F ⁻ as a neutral sodium fluoride gel or a placebo gel. The gels were taken unsupervised at home, twice a day for 1 week. After 2 years, the fluoride group had about 40% less decay than the placebo group. Eleven of 20 of these formerly rampant caries children had no new decay in their permanent teeth. In these xerostomia and pediatric patients, the initially high proportions of S mutans were decreased by the fluoride treatments which resulted in reduced decay.

Sucrose Substitutes that Aid in Caries Control

Eating foods that contain sucrose between meals can be highly cariogenic. Dietary counseling, that instructs patients to avoid between meal snacks may help to decrease the incidence of dental decay, but only if the patients are compliant. Another dietary approach to caries control is to recommend that patients eat snack foods that contain compounds that provide the hedonistic appeal of sucrose, but are not fermented by the plaque flora to the low pH levels associated with enamel demineralization.

The least acidogenic sucrose substitutes are the polyols, such as sorbitol, mannitol, and xylitol. Few plaque bacteria can ferment these substances, and those that can ( S mutans and L. casei ferment sorbitol and mannitol) exhibit a slow fermentation, because glucose catabolite repression keeps the necessary degradative enzymes at minimum levels. Xylitol, the only polyol with a sweet taste comparable to that of sucrose, and the only one that cannot be fermented by S mutans, has been shown to be anticariogenic when substituted for sucrose in either foods or chewing gum. In a chewing gum study, young adults who consumed about 6 to 7 g of xylitol gum per day had, after one year, an 80% reduction in caries increment compared to a control group who consumed 6 to 7 g of sucrose gum per day. In later studies, this type of intensive use of a xylitol chewing gum was shown to decrease salivary and plaque levels of S mutans. When the between-meal sucrose supply is reduced, the levels of S mutans will decline, as the low plaque pH values that selected for them are not as dominant a factor in the plaque microecology. Thus, xylitol can satisfy the craving for sweets, discriminate against S mutans, and significantly reduce the incidence of dental decay.

Periodontal Disease

Periodontal disease is the general description applied to the inflammatory response of the gingiva and surrounding connective tissue to the bacterial or plaque accumulations on the teeth. These inflammatory responses are divided into two general groupings: gingivitis or periodontitis. Gingivitis is extremely common, and is manifested clinically as bleeding of the gingival or gum tissues without evidence of bone loss or deep periodontal pockets. Pocketing is the term given to the pathologic loss of tissue between the tooth and the gingiva, creating spaces that are filled by dental plaque ( Figure 99-1). Periodontitis occurs when the plaque-induced inflammatory response in the tissue results in actual loss of collagen attachment of the tooth to the bone, to loss of bone, and to deep periodontal pockets which, in some cases, can extend the entire length of the tooth root (15 to 20 mm).

Periodontitis is usually graded according to the severity of the tissue loss and the number of teeth involved. Periodontitis is not as prevalent as once thought: a recent survey of American adults revealed that only 8% of the population surveyed had one tooth site with attachment loss measuring 6 mm or more. This finding was surprising, given past surveys, which indicated that almost everyone would experience advanced forms of periodontal disease as they aged, but is in agreement with recent population surveys in other countries which show that from 5 to 15% of the population has periodontitis.

Etiology and Pathogenesis

The most important new finding concerning periodontal disease is the realization that these clinical entities are really specific infections. These infections are unusual in that massive or even obvious bacterial invasion of the tissues is rarely encountered. Rather, bacteria in the plaque touching the tissue elaborate various compounds, such as H ₂S, NH ₃, amines, endotoxins, enzymes (such as collagenases) and antigens, all of which penetrate the gingiva and elicit an inflammatory response. This inflammatory response, although overwhelmingly protective, appears to be responsible for a net loss of periodontal supporting tissue, and leads to periodontal pocket formation, loosening of the teeth, and eventual tooth loss. As will be described subsequently, neutrophils are extremely important in this inflammatory response and, if they are absent, as in various neutropenias, or compromised as a result of chemotherapy, an aggressive form of periodontitis is encountered. T4 helper cells play a role in this defense, as witnessed by the periodontitis encountered in patients with acquired immune deficiency syndrome.

Gingivitis

The simplest form of gingivitis is associated with the accumulation of supragingival plaque along the gingival margins of the teeth. This form of gingivitis has been extensively studied in human volunteers, and the sequence of events is well described. In these studies, individuals are brought to a state of health and then refrain from all forms of oral hygiene for a 3- to 4-week period. The initial colonizers of the teeth are streptococci, which proliferate and in turn become colonized by other bacteria present in saliva, such as various Actinomyces species and Veillonella. The greatest growth of the plaque occurs at the gingival margin, where plaque accumulations usually are visible after several days. This plaque may, in some instances, provoke a bleeding gingivitis in which spirochetes and Actinomyces viscosus are prominent members of the plaque flora. If this plaque remains undisturbed, the flora gradually shifts toward an anaerobic, Gram-negative flora that includes black pigmented bacteroides and several types of spirochetes. The increase in these anaerobic organisms can be explained by the low oxidation-reduction potential of the aged plaque and by nutrients derived from the inflammatory exudate at the site.

The gingivitis may resolve itself or fester subclinically for an indeterminate period; however, the potential for the formation of a periodontal pocket (periodontitis) exists at any time. When pockets are detected clinically, they usually are associated with calcified plaque deposits, called calculus, present on the tooth surfaces. For many years, calculus was thought to be the etiologic agent of periodontitis, because inflammation usually subsided when it was removed and the tooth surfaces were mechanically cleaned. However, calculus is always covered by plaque, and removal of calculus would be synonymous with debridement of plaque. The subgingival plaque flora associated with periodontitis is dominated by an anaerobic, Gram-negative flora in all cases but one, and that is a unique clinical entity formerly known as periodontosis, and now as localized juvenile periodontitis (LJP). LJP is an important clinical entity because of the understanding it has provided of the complex and dynamic interactions between the host and the flora in the pocket ecosystem.

Localized Juvenile Periodontitis (LJP)

LJP is different from all other periodontal infections, as it is not associated with plaque accumulations or calculus (in fact the absence of such led early investigators to consider it as a degenerative condition), is localized to certain anterior or front teeth and first molars, and is seen following puberty. It is a rather rare entity, occurring in about 0.1 to 0.5% of teenagers, but when found, is often clustered within families. This familial background suggested a genetic predisposition, which subsequently has been identified as a neutrophil defect associated with reduced chemotaxis. Bacterial examinations of subgingival plaque from affected teeth and adjacent healthy teeth, revealed that the diseased teeth were colonized by an essentially Gram-negative flora dominated by organisms subsequently identified as various Capnocytophaga and Wolinella species and Actinobacillus actinomycetemcomitans. It is A actinomycetemcomitans that appears to be the etiologic agent of LJP, and the arguments for its involvement are illustrative of the arguments made to implicate other species in other forms of periodontitis.

Once LJP has been recognized clinically, most of the tissue damage has already occurred, thereby permitting only a retrospective diagnosis of an A actinomycetemcomitans infection. A actinomycetemcomitans is found at a higher prevalence in tooth sites associated with LJP and at a lower prevalence in healthy sites in the same mouth, or at sites in periodontally healthy individuals. It is often found among other family members in a household with an LJP individual, and indeed among siblings at risk to LJP, there is suggestive data that colonization by A actinomycetemcomitans precedes the development of a pocket and subsequent bone loss. But what has been the most important reason for implicating A actinomycetemcomitans as a periodontopathogen, is its killing effect on neutrophils.

A actinomycetemcomitans produces a leukotoxin that kills neutrophils in vitro. It is clear that this leukotoxin is expressed in vivo, because patients with LJP have developed circulating antibodies which can neutralize this toxin in vitro. From this finding, a scenario can be developed that explains the localized nature of LJP. Children with a neutrophil chemotactic defect become colonized by A actinomycetemcomitans in early life, presumably by contact with infected household members. The colonization spreads to those permanent teeth that erupted at ages 5 to 7, but remains quiescent as an infection during the time that the primary or baby teeth are lost, and new permanent teeth appear at about ages 11 to 13. The individual entering puberty, has a dentition composed of first molars and incisors that are colonized by A actinomycetemcomitans and newly erupted teeth that either are not colonized or only minimally colonized.

Something then triggers the relative overgrowth of A actinomycetemcomitans in the subgingival plaque, and some of these organisms invade the gingival tissue and cause attachment and bone loss in the absence of an obvious inflammatory response. The latter can be explained by both a sluggish neutrophil response to the bacteria and by the leukotoxin inhibiting the neutrophils, and thereby preventing a protective host response in the pocket microenvironment. The leukotoxin is antigenic and elicits an antibody response which may neutralize the leukotoxin at other tooth sites, thereby limiting the infection to the originally colonized molars and incisors.

This scenario, while incomplete, does explain the localized nature of LJP, partially explains the absence of an inflammatory response in the tissue, and demonstrates the dynamic role of neutrophils and circulating antibodies in defending the periodontium. Presumably, this theme is operating in the more commonly found cases of adult periodontitis. Certainly, the central role of the neutrophils in host defense is unquestioned, as individuals with neutropenias, chronic granulomatous disease and various leukemias often present with advanced forms of periodontal disease.

Early-Onset Periodontitis (EOP) and Adult Periodontitis (AP)

The more common forms of periodontitis comprise at least two clinical entities, an early onset form in mainly young individuals and a chronic form seen in older adults. The early-onset periodontitis (EOP) is more aggressive looking, while the adult periodontitis (AP) may reflect a stable, but tenuous, stand-off between the host's defensive systems and the plaque bacteria. It is not clear whether these entities represent multiple types of infections with two clinical manifestations, or a single mixed anaerobic infection with different levels of host containment.

The inability to distinguish microbiologically between these two general patterns reflects methodologic procedures relating to the sampling of the subgingival plaque and the inability of any one culture medium and/or technique to give the total picture of the 200 to 300 bacterial species found in the plaque flora. For example, the spirochetes cannot be quantitatively cultured and may account for more than 40% of the flora in EOP and AP. They can be enumerated by microscopic examination of the plaque but would be ignored in cultural studies. These cultural studies, in turn, reveal a bewildering array of species, many of them either newly-described or as yet unspeciated. None of these cultivable species predominates in all disease-associated plaques. For example, Bacteroides forsythus, a nonpigmenting fusiform organism has been associated with the active periodontal lesion. B forsythus is present in 13% of the active sites and at 8% of the inactive sites, a difference which is hardly indicative of etiologic association. Yet the authors concluded that B forsythus is a probable periodontal pathogen because its levels, when present, were on the average 4 times higher in the active sites than in the inactive sites, i.e., 2.5% vs 0.6%. This difference is well within the error of the methods used to isolate the organisms.

Despite these problems in assigning virulence to any one species, it is clear that the bacterial communities at disease sites are different from the communities at healthy and successfully-treated periodontal sites ( Table 99-2). The diseased sites are dominated by anaerobes, and in particular, by spirochetes and black-pigmented bacteroides species, such as Porphyromonas gingivalis and Prevotella intermedia. Among the latter, P gingivalis most often is associated with EOP, whereas P intermedia is found in both EOP and AP. No species, except the ubiquitous spirochetes, are consistently found in all lesions. Among the spirochetes, Treponema denticola is the only species that can be reliably cultured. It has been shown to possess a wide array of enzymes, such as a collagenase, peptidases, hyaluronidase, and a keratinolytic enzyme, and to produce noxious end products, such as butyrate, NH ₃, H ₂S, and endotoxin, that could cause, if they entered the periodontal tissue, an inflammatory response. However, comparable enzymes occur in P gingivalis and other anaerobic species found in the plaque, so that it would be difficult to assign etiologic significance to any one of these organisms based on the production of these enzymes. This being the case, it may be best to consider that the collective overgrowth of all these anaerobic species in the plaque causes a mixed infection that is responsible for tissue loss in EOP and AP.

Clinical Manifestations

Periodontal disease is usually painless until late in the disease process, when the teeth are so loose that some discomfort may appear upon chewing. Retention of food in a pocket site may provoke a sudden burst of microbial growth which could result in a painful abscess. At other times, the anterior teeth may become so loose that they separate and the patient visits a dentist because of the resulting poor aesthetics. However, under ordinary circumstances, it is bleeding upon brushing and/or concern over halitosis that brings the patient to the dentist. A thorough dental examination should find any pockets which may exist. If these pockets bleed upon probing, such bleeding is synonymous with tissue inflammation and warrants therapeutic intervention.

Microbiological Diagnosis

Microbiologic diagnosis is not commonly used in the management of periodontal disease. Several methodologies are, or soon will be, available that permit identification and quantification of the periodontopathogens listed in Table 99-2. The oldest method is the use of darkfield and phase contrast microscopy to identify spirochetes and other motile organisms in plaque samples. However, as spirochetes are detectable in most plaques, it is necessary to establish some critical value above which a spirochetal infection can be diagnosed. Our experience suggests that ≥ 20% spirochetes in any plaque sample permits the diagnosis of an anaerobic infection.

A microscopic examination cannot distinguish the species of bacteria present unless one uses an immunologic staining reagent specific for the organism in question. Such immunodiagnostic reagents have been used to detect and quantitate the levels of P gingivalis, P intermedia, T denticola, and A actinomycetemcomitans in the plaque. Cultural methods can, if the appropriate nonselective and selective media are used, provide information on the levels of A actinomycetemcomitans, black pigmented species, Campylobacter species, and other periodontopathogens. Also, because viable organisms are available, antibiotic sensitivities of the isolated organisms can be determined, which may be useful in certain instances.

Other diagnostic reagents are being developed to detect, in plaque, specific microbes or metabolites or enzymes unique to inflammation or infection. For example, specific microbes can be demonstrated in plaque by the use of DNA probes. Probes for A actinomycetemcomitans, P intermedia and P gingivalis are commercially available for testing via a reference laboratory. Future diagnostic procedures may rely on the detection of hydroxyproline, a collagen degradation product; prostaglandin, an inflammatory mediator; and enzymes, derived from either the host or the microbes. A trypsin-like enzyme is present in T denticola, P gingivalis, and B forsythus and is absent from at least 60 other subgingival plaque organisms. This enzyme can be detected by the hydrolysis of the trypsin substrate benzoyl-DL-arginine naphthylamide (BANA). The ability of subgingival plaque to hydrolyze BANA was associated with elevated levels and proportions of spirochetes and with probing depths greater than 6 mm. Subsequently, BANA hydrolysis was shown to be related to the T denticola and P gingivalis content of the plaque and to the clinical diagnosis of health or disease. As T denticola, P gingivalis and B forsythus are anaerobes, a positive BANA test may be useful in the diagnosis of an anaerobic plaque infection.

When these identification procedures were performed on the same plaque samples, the DNA probes and immunological reagents were significantly more likely to detect P gingivalis, B forsythus, A actinomycetemcomitans and T denticola than was the traditional cultural approach. In fact, this study suggested that culturing may be the least accurate detection procedure for these plaque species. When the probes and immunological reagents were compared to the BANA test, the probes and antibodies were slightly more accurate, i.e., 88% vs. 83%. All three approaches were essentially comparable indicating that reliable non-cultural methods are available to aid in the microbiological diagnosis of periodontal infections. Because the BANA test detects an enzyme(s) found in three anaerobic species, it may be used to detect an anaerobic periodontal infection.

Prevention and Treatment

Gingivitis can be prevented by good oral hygiene and professional surveillance. Gingivitis can be effectively treated by debridement of the teeth, and, if needed, by short-term use of products containing chlorhexidine, stannous fluoride, or other antimicrobial agents. Mouth rinses, gels, and toothpastes, when used in conjunction with toothbrushing and flossing, are probably adequate to deliver any antimicrobial agents to subgingival sites that are 1 to 3 mm in depth. At probing depths greater than 3 mm, there may not be sufficient penetration of the agent to the bottom of the pocket, and infection may persist. Subgingival scaling (debridement) by a professional is indicated, and additional benefits can usually be obtained by the use of irrigating devices containing an antimicrobial agent.

There is rarely any need to use systemic antimicrobial agents to treat gingivitis associated with pocket depths of 1 to 4 mm, with the exception of an increasingly rare and painful condition known today as acute necrotizing ulcerative gingivitis (ANUG) and formerly as trench mouth. Cases of ANUG that are refractory to mechanical debridement and topical antimicrobial agents respond, quickly and dramatically, to systemic metronidazole. The recognition of metronidazole's efficacy in ANUG led to the discovery that metronidazole has bactericidal activity against anaerobes. ANUG is characterized by tissue invasion by spirochetes and possibly other anaerobes and by elevated plaque levels of spirochetes and P intermedia ( Table 99-2). ANUG thus resembles periodontitis in being an anaerobic infection.

Clinical dentistry has been about 80 to 85% successful in treating periodontitis by debridement and surgical procedures. However, surgery is labor intensive, and therefore costly. This limits the number of individuals who can be treated in a cost-efficient manner. However, if the majority of clinical cases of periodontitis represent specific bacterial infections, then an alternate treatment strategy would be to diagnose and treat the infection. It would seem that the crucial determination for the clinician in his treatment plan will be the diagnosis of either a micro-aerophilic infection, due to A actinomycetemcomitans, or an anaerobic infection characterized by the overgrowth of spirochetes and other anaerobic species.

A actinomycetemcomitans is sensitive to tetracycline, and early uncontrolled studies showed that tetracycline, scaling and root planing, periodontal flap surgery, and topical treatment with chlorhexidine were able, to save hopeless teeth in LJP patients. Additional studies, but none of a double-blind nature, confirm the usefulness of tetracycline in the treatment of LJP. Subsequently it was shown that tetracycline is concentrated in the fluid that seeps out of the periodontium into the pocket micro-environment. This fact, combined with the demonstration that A actinomycetemcomitans can be found in some plaques associated with EOP and AP ( Table 99-2), has led to the use of tetracycline in those clinical entities. Results have been equivocal, but this has not detracted from the popularity of tetracycline as a treatment for periodontitis.

Most bacteriologic studies implicate anaerobes as the etiologic agent(s) of EOP and AP, and this would point to the use of a drug such as metronidazole. However, early animal studies that employed lifetime feeding of extremely high dosages of metronidazole suggested that the drug might be tumorigenic. These studies have not been confirmed and, indeed, in 1981 the FDA approved metronidazole for treatment of anaerobic infections. In dentistry, this concern has caused a reluctance to use metronidazole, but has also allowed time for well controlled clinical trials of metronidazole.

Six double-blind studies have demonstrated that metronidazole, given for periods of time as short as 1 week, can significantly improve periodontal health. In all cases, the metronidazole was given in conjunction with professional debriding of the teeth. Maximal benefits were obtained when the metronidazole was given after the debridement. The best clinical response was often noted in patients with more advanced disease, in which the pocket depths were ≥ 6 mm, whereas there was only a moderate benefit when the pocket depths were from 4 to 6 mm. In these advanced cases some teeth, that were initially scheduled for extraction upon reexamination, were found no longer to need extraction and thus, in a sense, were saved.

Metronidazole has subsequently been evaluated to determine whether it can reduce the need for periodontal surgery. In three double-blind studies, the unsupervised usage of metronidazole for one week, when combined with the standard debridement procedures, was able to significantly reduce the number of teeth needing surgery when compared to the debridement procedures plus placebo treatment. This sparing effect on surgery has lasted for several years after the one-week period of systemic treatment.

The localized nature of the periodontal infection and the easy access of the teeth has prompted the development of delivery systems which release the antimicrobial agent directly into the periodontal pocket. The first of these delivery systems that is commercially available is a tetracycline impregnated cord which can be wrapped around the tooth below the gingival margin. This cord releases over 100μg of tetracycline per ml of gingival crevicular fluid during the entire period that it is in situ. In this manner, patient compliance is assured and the plaque microbes are constantly exposed to therapeutic levels of the agent.

These data from the double-blind metronidazole studies indicate that EOP and AP respond to treatment as if they were anaerobic infections and would seem to presage the more frequent usage of anti-anaerobic agents, such as metronidazole, in the future treatment of periodontal disease. Further developments of delivery systems which release antimicrobials directly into the periodontal pocket should assure that in the future, most periodontal infections will be medically managed.

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Microbiology of Dental Decay and Periodontal Disease

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The tooth surfaces are unique in that they are the only body part not subject to metabolic turnover. Once formed, the teeth are, under the correct conditions, essentially indestructible, as witnessed by their importance in fossil records and forensic medicine.

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