Periodontitis for medical practitionersBMJ 1998; 316 doi: https://doi.org/10.1136/bmj.316.7136.993 (Published 28 March 1998) Cite this as: BMJ 1998;316:993
- Trevor L P Watts (), senior lecturer in periodontology
- Department of Periodontology and Preventive Dentistry, United Medical and Dental Schools of Guy's and St Thomas's Hospitals, London SE1 9RT
- Correspondence to: Dr Watts
- Accepted 28 October 1997
Periodontitis is largely excluded from medical education, but general practitioners may well be consulted by patients who have this condition. Periodontitis is one of the best researched dental diseases; Medline lists 33 000 papers published under the heading Periodontal diseases between 1966 and 1996. However, misconceptions about periodontitis abound (box), some of which are perpetuated by medical correspondents in the national press. A basic understanding of the condition and of evidence based treatment will help general practitioners ensure that patients are not given misleading advice.
Periodontitis is primarily a disease of the periodontal ligament, not of bone
Bacterial plaque is the main cause of periodontitis
Smoking and diabetes are the principal exacerbating factors
Periodontitis is associated with a complex microbial environment
Success of treatment depends on the control of bacterial plaque; antimicrobial drugs have only an adjunctive role in a full treatment plan
This review is based on 25 years of undergraduate and postgraduate teaching of the subject. Selection of the few references from the huge number available is inevitably biased, and is intended to illustrate certain key points, but the views given are widely held consensus opinions.
Periodontitis—scene and the crime
On a tooth with healthy gingiva, inflammation caused by developing bacterial plaque occurs within 5-20 days. The junction between the tooth and the jaw (fig 1) is covered by epithelium that has a high turnover1 and is permeable to neutrophils and many molecules. Beneath the epithelium is the organ that may have the body's fastest turnover of collagen—the periodontal ligament. Fibres of the periodontal ligament are anchored in the thin cementum on the tooth root at one end and in alveolar bone or soft gingival connective tissue at the other. The tooth does not have to be anchored in bone for it to be clinically healthy, fully functional, and free from appreciable mobility.2 The appearance of the bone in periodontitis may be misleading, since bone will undergo resorption in the presence of inflammatory mediators or occlusal trauma (for example, from bruxism or parafunctional activity). What turns reversible inflammation (gingivitis) into irreversible, damaging periodontitis is destruction of the collagen fibres of the periodontal ligament. This is called loss of attachment—usually with the formation of periodontal pockets that break the peripheral seal around the tooth.
Since loss of attachment is always accompanied by inflammation it is difficult to separate the two clinically.3 Two theories on progression have been proposed—the “burst” theory, which claims that a sudden loss of a measurable amount of attachment occurs, and the continuous theory, which states that loss of attachment is gradual, almost imperceptible.4 Neither mechanism has been proved clinically, and each has a weakness. The continuous theory may be an artefact of averaged observations and the burst theory may be an artefact of measurement error. Both may be true in different situations.
Periodontitis is irreversible
Gingivitis is an inflammatory response to bacterial plaque on the teeth and is resolved by good plaque control. In periodontitis, the additional irreversible step of loss of attachment occurs. Periodontitis develops in specific sites—it does not occur in everyone with uncontrolled dental plaque, on all the teeth of susceptible people, or on all the surfaces of these teeth. If periodontitis progresses, abscesses or hypermobility may occur when a large amount of support has been lost, and teeth may drift or over erupt (fig 2).
Common misconceptions about periodontitis
Classification of periodontitis
Early onset aggressive periodontitis is present in about 0.1% of the population of the United Kingdom. This umbrella term covers the following disorders: prepubertal periodontitis (usually associated with severe systemic immune defects5); localised and generalised juvenile periodontitis (severe disease before age 25); and rapidly progressive periodontitis (most damage done in less than a year, usually before the age of 356). These diseases are often related to defects in neutrophils or monocytes,7 and in some studies seem commoner in Afro-Caribbean people.
Chronic adult periodontitis affects about 20% of the population, starts in the late teens or early 20s, and progresses slowly. Acute ulcerative gingivitis-type periodontitis is rare. However, some, but not all, cases of periodontitis in people with HIV will be of this type. Immunosuppression allows invasion of periodontopathogens, with necrosis of tissue and sequestration of bone.
Forty years ago Russell began studies on periodontitis. These showed that the major factors that correlated with periodontal destruction were age (reflecting irreversible attachment loss) and oral cleanliness.8 Another landmark investigation was a longitudinal study of age cohorts in a group of Tamil tea labourers in Sri Lanka, none of whom had important health problems or malnutrition.9 Subject were aged 15-33 years at the start of the study and were followed for 15 years. Plaque was practically undisturbed during the study. Furthermore, the unique study design enabled cross sectional comparison of the accuracy of examiners. An important result emerged. Subjects could be divided into three groups on the basis of the progression of periodontal disease—11% had no appreciable attachment loss, 81% had a slow rate of progression with moderate tooth loss, while 8% showed rapid progression and massive tooth loss. When these results are compared with more recent data from the United Kingdom (not, unfortunately, as complete as might be desired) the difference between a population with no plaque control and one with some plaque control becomes apparent. Corresponding figures for the United Kingdom are 80%, 20%, and 0.1% respectively. Many other investigations have incriminated smoking and diabetes as important risk factors in periodontitis.10–12
Much of the early microbiology of periodontitis suffered from the shifting sands of bacterial taxonomy. Moore et al from 1980 to 1985 defined the complex bacterial environment in which attachment loss occurs. More than 300 types of microorganism may be found in periodontal pockets.13 In the mid-1970s a hunt for important periodontopathogens was triggered by Loesche's definition of the specific plaque hypothesis.14 This holds that some organisms are more likely than others to cause attachment loss. Currently, the most researched organisms are probably Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis.
The specific plaque hypothesis is impossible to prove. Koch's postulates are of no value when dealing with up to 400 species, all of which may cause an inflammatory response, and many of which crop up in relatively harmless and potentially virulent strains. Socransky suggested a five point approach to establishing an aetiological relation, but five inadequate arguments do not make one good argument.15 The current consensus is that some periodontal organisms may have a more important role than others, but the central event is the destruction of periodontal attachment by host mechanisms in response to a wide range of organisms.
Appropriate periodontal treatment
A periodontal treatment plan has to consider several complex issues—uncertainty about whether the patient will adhere to advice, the probable outcome of treatment for individual teeth, and alternatives for tooth replacement such as partial dentures, bridges, and osseointegrated implants. Before embarking on definitive treatment, the patient's compliance with plaque control and tissue response to the simpler forms of treatment must be assessed. When the patient is unable to cooperate fully, a palliative approach may be more appropriate. Full cooperation may include giving up smoking, which both exacerbates periodontitis and affects adversely the outcome of treatment. Some patients may go to their general practitioner for help with quitting smoking.
Plaque control in treating periodontitis
Plaque control is the central principle of treatment
Patients must remove plaque daily on all accessible surfaces of teeth, including proximal surfaces
Where the patient cannot reach, an operator must remove plaque with appropriate instruments and perhaps surgical techniques
Removal of plaque enables tissues to heal up against the tooth over the next 6 to 12 weeks, provided the potential reservoir of bacterial plaque is controlled
Treatment gains are lost if plaque is not controlled subsequently
Treatment and prevention of all periodontal problems related to plaque begin with establishing thorough plaque control by the patient. Control is needed to contain the bacterial reservoir from which any periodontitis pockets might quickly be repopulated. In healthy subjects, complete plaque removal every 48 hours may be sufficient for gingival health, but daily removal may help establish a regular simple habit.16 One method of oral hygiene—widely advocated, but not proved better than several others—was described first by Bass, and includes vertical movement of dental floss on proximal tooth surfaces (fig 3).17 Establishing good oral hygiene should resolve superficial inflammation and reduce slightly the depth of pockets.
Root surface debridement
Along with establishment of thorough plaque control by the patient, an attempt is made to remove plaque from all pockets. Where plaque has become calcified, this entails removal of the calculus, which is only damaging because of its surface layer of bacterial plaque.18 Many studies have shown that root planing resolves inflammation, reduces pockets, and also improves clinical attachment.19 The main side effects of all successful periodontal treatment are root hypersensitivity, which usually declines, and gum recession, which may not be aesthetically pleasing.
Most antiplaque mouth rinses have an effect—albeit limited—on gingival inflammation However, the teeth must first be cleaned of all visible plaque deposits. A 0.2% chlorhexidine mouth rinse (by far the most effective) used for two minutes every 12 hours will prevent plaque accumulating on a clean tooth surface.20 Deposits of bacterial plaque have a highly insoluble matrix, and even a chlorhexidine mouth rinse penetrates only a fraction of a millimetre. This mouth rinse may, however, replace mechanical oral hygiene during healing after surgery, when the teeth have been thoroughly cleaned.21
The principal systemic adjunctive drugs are tetracyclines (favoured in periodontitis of early onset), and metronidazole (in slower adult forms). Penicillin is of no benefit in treating chronic inflammatory periodontal diseases. Tetracyclines were introduced as a possible treatment for disease related to facultative organisms. Studies also showed a separate anticollagenolytic effect of tetracycline on host tissue, which may be important.22 Use of tetracyclines in the early onset forms of disease may enhance non-surgical treatments by 80-100%.23
Metronidazole has a profound effect on obligate anaerobes and is virtually free from acquired bacterial resistance. With non-surgical treatment, studies have shown small adjunctive effects, but there is no clinically important effect in the absence of other periodontal treatment.24 Metronidazole may also be used for acute ulcerative gingivitis or as an alternative to penicillin for acute periodontal abscesses, but in both cases there must be prompt and effective periodontal follow up treatment.
Metronidazole and tetracycline are available in forms that can be delivered locally. They are placed in a periodontal pocket after root planing, with the intention of enhancing the local effect. Some preparations may be very expensive, and most studies have been short term. At present, prescribing an antibacterial drug for gingivitis or periodontitis as sole treatment is not indicated.
The principal objectives of periodontal surgery are to enable access for more effective subgingival debridement by the operator, and to alter the form of the tissues so that the patient has a realistic chance of achieving good dental hygiene. Over the past 15 years, guided tissue regeneration techniques have been developed with the aim of reconstructing periodontal attachment.25 However, these techniques may not have a clinical advantage over others. The first clinical trial of enamel matrix derivative that is painted on tooth roots at surgery has recently shown promising adjunctive effects.26
Techniques of bone grafting and bone substitute implanting are largely unused in the United Kingdom for several reasons. Bone loss accompanies periodontitis, but it is not the essential change in the disease. A bone graft held firmly next to a tooth may cause resorption of the root. However, some bone regeneration occurs after successful treatment in any case, without grafts or substitutes (fig 4).27 Regeneration of bone is the best way of showing that inflammation caused by plaque is controlled, but is not essential to a successful outcome.
Surgical versus non-surgical treatment
Trials have compared the effects of the main methods of periodontal surgery with each other and with non-surgical treatment. Non-surgical methods may achieve similar overall results in many situations, but they have to be repeated and so treatment takes longer. The longest duration of follow up in comparative surgical studies has been eight years,28 although there are longer follow up periods in cohort studies. Provided the patient maintains good plaque control and effective professional support is available every three months, the principal surgical techniques achieve results that can be maintained. Several studies have indicated that a surgical approach is more effective in treating deeper periodontal pockets. In all forms of periodontal treatment, success demands a high level of plaque control.29
Osseointegrated implants have acquired a place in periodontal treatment over the past 15 years. The system against which all implant success is measured was developed by Brånemark, a Swedish orthopaedic surgeon. The procedure usually entails two stages. Osseointegration is the first objective, and crowns, bridges, or dentures on the implant structures are provided about six months later. Long term studies show success rates of 85-90% for maxillary fixtures and 95-99% for mandibular fixtures. Factors that increase the risk of failure include smoking, poor control of plaque, one particular type of bone structure, and removable rather than fixed prostheses.
Conflict of interest: None.