March 27, 2023

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21 April 1926 to 8 September 2022
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This guidance is issued jointly by the Department of Health and Social Care, the Welsh Government, the Department of Health Northern Ireland, Public Health England, NHS England and NHS Improvement and with the support of the British Association for the Study of Community Dentistry.
Delivering Better Oral Health has been developed with the support of the 4 UK Chief Dental Officers.
Whilst this guidance seeks to ensure a consistent UK wide approach to prevention of oral diseases, some differences in operational delivery and organisational responsibilities may apply in Wales, Northern Ireland and England. In Scotland the guidance will be used to inform oral health improvement policy.
Whilst several conditions may affect the tooth-supporting tissues referred to as the periodontium or gums, the following sections focus on the most common forms of periodontal diseases, called ‘gingivitis’ (inflammation of the gums that can be reversed) and ‘periodontitis’ (inflammation that results in loss of periodontal attachment) (1). The early stages of disease may be symptom-free, but the impact on peoples’ lives of later stage disease are more serious (1), particularly as the disease is irreversible.
Gingivitis and periodontitis are separate conditions, although both are initiated by plaque in susceptible people. Gingivitis is a risk factor for periodontitis, although not all people or sites with gingivitis go on to develop periodontitis. The prevention and management of periodontitis is described here in terms of primary, secondary, and tertiary prevention as shown in Chapter 1 (Table 1.1). Because both conditions are initiated by plaque, the primary prevention of periodontitis will also prevent gingivitis.
As the use of dental implants to replace missing teeth has increased, 2 new conditions, peri-implant mucositis and peri-implantitis, have become apparent (2). These conditions may be analogous to gingivitis and periodontitis. Additional advice for the prevention of these conditions is provided at the end of this chapter.
The 2017 World Workshop classification of periodontal and peri-implant conditions (3, 4), can be summarised as follows.
Periodontal health is the absence of clinically detectable inflammation (<10% of sites bleeding on probing), on an intact periodontium, or a reduced periodontium where attachment loss has resulted from anything other than periodontitis.
Gingivitis is an inflammatory condition resulting from interactions between the dental plaque and the host’s immune response, which remains contained within the gingiva and does not extend to the periodontal attachment (cementum, periodontal ligament, and alveolar bone). Such inflammation is reversible by reducing levels of dental plaque at and below the gingival margin.
Periodontitis is a microbially-associated, host-mediated inflammation that results in loss of periodontal attachment. A patient is said to have periodontitis if:
Periodontitis causes progressive destruction of the tooth‐supporting tissues. Signs of the disease include clinical attachment loss, manifested as interdental recession and/or periodontal pocketing and alveolar bone loss (4). This chronic and inflammatory disease is caused by a complex interplay of risk factors, with dental plaque being the most important (4).
Some level of irreversible periodontitis affects almost half of UK adults (5), although this might underestimate true disease levels.
Similar levels of periodontal diseases are present globally, with the latest evidence suggesting that around 10% of the world’s population (8.2 to 11.4% age standardised) has evidence of severe disease (6). The peak in prevalence occurs between 60 and 64 years of age (6), and there are marked inequalities by socio-economic status. About half of all adults have some evidence of moderate disease and thus, it is one of the most common chronic inflammatory diseases globally.
Age need not be a barrier to good periodontal health (7 to 11), particularly when people can undertake the necessary self-care and are able to visit the dental team.
In addition to plaque build-up, tobacco (smoking or chewing) and alcohol use, several general health conditions are risk factors for periodontal diseases. Conversely, there are risks to general health resulting from having active periodontal diseases.
Some systemic disorders, such as diabetes and cardiovascular diseases, share similar genetic and/or environmental influences with periodontal diseases, thus affected people may have signs of either or both conditions (12, 13).
International consensus of joint dental and medical experts, based upon evidence from systematic reviews, recommends the importance of periodontal therapy in reducing the risks of diabetes and its complications (14).
There is ongoing debate about the role of periodontitis in cardiovascular diseases (15, 16), but at present no firm conclusions can be drawn. Also, there is insufficient information to determine the true relationship between rheumatoid arthritis and periodontitis. (17) Likewise, the evidence linking lifestyle factors such as stress (18, 19), poor diet (20, 21), being overweight (22), or cannabis use (23), is insufficient to suggest a clear association with periodontal diseases.
Dental plaque is a highly organised and specialised film of bacteria in an organic matrix that forms on the teeth. The intercellular matrix consists of various micro‐organisms and their by‐products. The bacteria mutually support each other, using chemical messengers, in a complex and highly evolved community, that can protect them from an individual’s immune system and chemical agents.
Normally, small amounts of bacteria cause only minimal inflammation, but a disruption in the balance (dysbiosis) between the plaque and person’s immune system can lead to the initiation of gingivitis and progression to periodontitis (1).
Tobacco smoking and use of smokeless tobacco products have a profound effect on the risk of developing periodontitis (24, 25). They also impair the treatment response. Cessation of tobacco use can prevent further deterioration of periodontal health (Chapter 2: Table 2; Chapter 11).
Evidence suggests that although not risk free, using an e-cigarette (vaping), is far less harmful to health than smoking. Findings about the impact of vaping on periodontal health are inconsistent but suggest people who vape are at greater risk for periodontal diseases compared to non-smokers (26). However, it is helpful to recognise that most people who vape are former smokers and will have experienced the effect of smoking on their periodontal health. It will take time to build a clear picture of their longer-term periodontal health through longitudinal research. E-cigarettes may, however, have a lower risk of periodontitis than tobacco and therefore provide a helpful transition to cessation for smokers (Chapter 11).
There is emerging low-certainty evidence that alcohol consumption is associated with periodontitis (27, 28). Possible mechanisms of action may be related to alcohol’s negative impact on bone density and saliva secretion. Advice on managing alcohol risk reduction is presented in Chapter 12: Alcohol.
Glycaemia in those without a diagnosis of diabetes, and hyperglycaemia in those with diabetes are both risk factors for poor periodontal health (29) and also impair the response to its treatment. While well-controlled diabetes is not a risk factor, many people oscillate between different levels of control. Therefore, it is best to assume an increased risk of periodontal diseases for anyone who has diabetes (30).
Several medications may affect periodontal health, which underlines the importance of a comprehensive and up-to-date medical history.
Medications may cause:
Therefore, it is good practice to check the possible side-effects of patient medications in a formulary.
The primary prevention of periodontitis and gingivitis involves control of any risk factors. An overview of risk factors and their management is presented in Chapter 2: Table 2. As gingivitis is a predictor of developing periodontitis (33), and thereafter tooth loss (34), its prevention also helps in the primary prevention of periodontitis. Importantly, risk factor control is also the mainstay of the management of established gingivitis and periodontitis (that is, secondary and tertiary prevention (35, 36)).
In view of the chronic nature of the disease and risk of the irreversible bone-loss, self-care is vitally important. For everybody, the primary preventive goals are to develop good plaque removal skills and to avoid tobacco. Effective and regular toothbrushing from infancy and interdental plaque removal from 18 years of age (beforehand if evident disease) are therefore the main skills required from an early age (Chapter 8). All dental team members play a major role in assessing, coaching, and supporting patients with self-care. Whilst professional intervention plays an important role for people with advanced disease, no clinical benefits of ‘routine scale and polish’ have been demonstrated for adults with good periodontal health (37).
The central role of plaque in the pathogenesis of periodontitis means that its control is essential in the maintenance of periodontal health. Comprehensive advice on oral hygiene instruction (OHI) is outlined in Chapter 8 on oral hygiene.
The importance of behaviour change approaches in support of plaque control is increasingly recognised (38, 39) within periodontal care. Contemporary approaches encourage patients to understand how oral hygiene might benefit them, to develop confidence in their oral hygiene abilities, to set targets for change that they feel able to achieve and to challenge perceived barriers to performance. Some of these methods address common barriers to an effective oral hygiene routine that may have been missed during traditional instruction.
Useful resources include the Oral Hygiene TIPPS video (40), which was devised by the Scottish Dental Clinical Effectiveness Programme. Oral Hygiene TIPPS (Talk, Instruct, Practice, Plan, Support) is a behaviour change strategy for dental teams helping them to increase patients’ confidence in their ability to perform effective plaque removal and help them plan how and when they will look after their teeth and gums. Behaviour change is covered in detail in Chapter 3, which has case studies relating to managing patient self-care.
Whilst brief behaviour change interventions have the potential to improve plaque control over traditional oral hygiene instruction alone (41, 42), the evidence to date is not robust (41). There is low to moderate certainty evidence that motivational methods, involving plaque disclosure and repeated OHI reduce plaque (39); and, very low to low certainty evidence that motivational methods reduce gingivitis. Amongst teenagers receiving orthodontic care, there is moderate certainty evidence that reminders reduce plaque and gingivitis in the short term, and very low certainty evidence that they do so over a 3-month period (43, 44).
The potential for m-Health (mobile phone messages) to support oral hygiene in mothers, children and orthodontic patients is being tested, but to date there is insufficient evidence to make firm recommendations (45, 46).
In sites where calculus and overhanging restorations with ledges prevent plaque removal (BPE Code 2), the retentive factor can be removed. This may not be necessary where there are no signs of gingivitis but may be required if there is evidence of disease.
Cessation of tobacco use can prevent further deterioration of periodontal health. Information about checking patients’ smoking status and for helping people to quit is provided in the chapter on tobacco and smoking (Chapter 11). Smoking should be managed by Asking, Advising and Acting in line with the strong evidence on brief interventions outlined in the oral cancer text to be found in Chapter 2: Table 4.
To keep health risks from alcohol to a low level it is safer not to drink more than 14 units a week on a regular basis (see Chapter 12: Alcohol). (47).
The following actions are advised (13, 30).
In addition to usual good practice for periodontal diseases prevention, people with diabetes should be informed of the implications for their periodontal health.
Discuss how diabetes control affects periodontal health and ask about their level of glycaemic control, also known as HbA1c. Levels consistently below 7.0% (8.6 mmol/L) indicate good control. The target HbA1c value for most people with diabetes is 6.5% or below in line with IFCC (International Federation of Clinical Chemistry) or 48mmol/mol (or below) DCCT (diabetes control and complications trial). Units are increasingly calculated in mmmol/mol. It is worth noting that people may be set different threshold units by their team; thus dental teams should explore this with each patient (48).
Encourage people to maintain good diabetes control (including diet, medication, exercise and so on) and to follow up with the diabetes physician regularly.
Write to the diabetes physician for guidance on a patient’s diabetes status and health, particularly HbA1c levels. Download template letter.
Inform the physician about the patient’s periodontitis status, which may help the physician to tailor diabetes care and advice appropriately and support the person with diabetes in maintaining more effective control.
Periodontal treatment may improve diabetes control among affected people and it is associated with reduced complications of diabetes (14).
Members of the dental team will be used to enquiring about their patients’ medications as part of a medical history. Specific assessments and actions are relevant to periodontal health.
Ask people on medication if they experience dry mouth or swollen gums.
Assess the oral cavity for any impact of medication, for example, dry mouth, mucosal changes, caries, extensive plaque deposits or candida infection or gum swelling.
You should:
Early detection and treatment of periodontitis increases the likelihood of tooth retention (49). One screening tool that is well known and quick to use is the Basic Periodontal Examination (BPE) (50). The BPE uses the WHO BPE probe and is suitable for routine assessment of all dentate adults (Table 5.1).
Detailed advice on the use of the BPE is provided in the Greater Manchester Local Dental Network’s (2019) Healthy Gums Do Matter (51) and the British Society for Periodontology and Implant Dentistry (BSP) BPE guidelines (50). It is important to note that the BPE does not provide a diagnosis, nor does it assess the response to treatment, as pockets do not always reduce, even in successful treatment.
The BPE has also been adapted for early detection of periodontal diseases in children, as periodontitis can manifest in childhood and adolescence, but is difficult to detect without probing (52). Therefore, all children from the age of 7 years onwards should be examined with a modified BPE. The BSP summary guidance indicates how to do this in 2 age bands: 7 to 11 years and 12 to 17 years as presented in Table 5.2.
As for any disease, the management of periodontitis will depend on its extent, severity and rate of progression. An overview of risk factors and their management is presented in Chapter 2: Table 2.
Patients with BPE scores of 0 to 2 are deemed not to have periodontitis and therefore only require primary prevention. As periodontitis and gingivitis have common risk factors, prevention of one will prevent the other. As set out above, primary prevention involves plaque control, the removal of plaque retention factors and management of other risk factors that either increase the risk of developing periodontitis or complicate its successful care.
Patients with BPE scores of 3 or 4 may have periodontitis. Preventive care may therefore involve secondary (detecting the early stages of periodontitis and intervening before full symptoms develop) or tertiary prevention (softening the impact of periodontitis by helping people manage its long-term consequences with Supportive Periodontal Care (SPC)).
Secondary prevention will involve more detailed periodontal charting to identify affected sites, as patients with these BPE codes will have pockets of ≥4mm or ≥6mm respectively (50). Plaque scores may identify areas with specific oral hygiene problems to be managed (53).
The European Federation of Periodontology has developed S3 level evidence-based clinical practice treatment guidelines for periodontitis, which have been adapted and adopted by the BSP for implementation in the UK (53). Once the patient has an established diagnosis of periodontitis, it may be managed by a stepwise approach to therapy as outlined in the guidance (53).
Sextants coded 3 should receive initial therapy including self-care advice (oral hygiene instruction and risk factor control). After the patient has had time to respond to this, a 6-point pocket chart should be recorded in the affected sextant to monitor progress and advise the patient accordingly.
If there is a code 4 in any sextant then record a 6-point pocket chart to identify affected sites throughout the entire dentition. Tertiary prevention in patients who have undergone initial therapy for periodontitis, and who are now in the maintenance phase of care will require full probing depths throughout the entire dentition recorded at least annually. It is important to support patients with clear advice as part of supportive periodontal care Chapter 2: Table 2.
The 2017 World Workshop on Classification of Periodontitis (3), is useful in classifying the stage and speed of breakdown of periodontitis as part of the detailed assessment required in patients with the disease.
The new classification of periodontitis (3, 54) describes the historical degree of periodontal breakdown (stage) and the speed of the breakdown (grade) (54). It was adapted for implementation in the UK healthcare system by the BSP (55). An overview is presented in Table 5.3.
The BSP adaptation classifies the disease into 4 stages based on severity (I, II, III or IV) and 3 grades based on disease susceptibility (A, B or C). The stage of periodontitis cannot reduce, because the bone loss is largely irreversible, but may increase (54).
Sources: (54, 55).
If a patient has interproximal attachment loss but BPE codes of only 0, 1 and 2, (for example, a previously treated, stable periodontitis patient), and radiographs are not available or justifiable, staging and grading should be performed on the basis of measuring attachment loss in mm from the CEJ and estimation of concomitant bone loss.
If a patient is known to have lost teeth due to bone loss likely to have been within the apical third of the root, stage IV may be assigned.
Periodontitis is a chronic disease that will recur and worsen without good plaque control (8, 56). This is the basis for providing SPC, which involves a long-term commitment from the patient and an intensive level of support, monitoring and care from the dental team. Trials have compared different types of SPC, with inconclusive results, but to date there have been no randomised controlled trials comparing SPC to no SPC (57). The evidence for the clinical efficacy of subgingival air polishing compared with ultrasonic debridement for systemically healthy patients in periodontal maintenance is still limited and remains inconclusive (58). Some patients preferred ultrasonic compared to hand instrumentation because it took less time.
Components of SPC include: (59, 60):
Patient adherence to plaque control is central to periodontal care as removal of supra and subgingival plaque and calculus is of limited value in the absence of high standards of plaque control (37).
In patients with type 2 diabetes, there is moderate certainty evidence that SPC improves metabolic control and reduces systemic inflammation (61). These findings have been supported by several systematic reviews. However, the certainty of the evidence and the amount of reduction in HbA1c varies (62 to 64); there is insufficient evidence to determine if this effect is maintained beyond 4 months.
Findings for any benefit of periodontal therapy on hypertension remain inconclusive (65).
Table 5.4 summarises the possible management options for periodontitis in adults in relation to BPE scores.
There is a range of mouthrinses, mouthwashes and sprays available to the public, in addition to mechanical plaque control with dentifrices, for longer or short-term use.
The body of available evidence suggests that of the products evaluated, there is high certainty evidence for the use of chlorhexidine mouthrinse to reduce dental plaque and gingivitis (66, 67). Both 0.1 and 0.2% chlorhexidine gluconate mouthwashes are effective for preventing plaque formation and reducing gingival inflammation during the early healing period after periodontal and implant surgery (66). Plaque scores (very low certainty evidence) and gingivitis scores (moderate certainty evidence) are reduced to a similar degree, whether using chlorhexidine mouthrinse containing sodium fluoride or chlorhexidine alone (67). It is important to note that chlorhexidine gluconate may be incompatible with some ingredients in toothpaste and therefore it is important to rinse the mouth thoroughly with water between using toothpaste and chlorhexidine-containing products. Longer term use of chlorhexidine mouthrinse has adverse effects including extrinsic tooth staining; taste disturbance or alteration; effects on the oral mucosa including soreness, irritation, mild desquamation, and mucosal ulceration or erosions; general burning sensation or a burning tongue. This product is, therefore, advised for short-term use.
There is very little reliable evidence available to draw conclusions about effects of chlorhexidine antiseptic sprays on plaque and gingivitis (68). There is, however, low to moderate certainty evidence that adjunctive antiseptics in mouthrinses, including essential oils and cetylpyridinium chloride (CPC) provide statistically significant reductions in gingival, bleeding and plaque indices when compared to mechanical plaque control alone (69). Similar results were shown for other reviews involving herbal (70), aloe vera (71, 72), green tea (73), and polyphenol (74) rinses.
Dental implants may be used to replace missing teeth. However, the soft tissues and bone around dental implants (75), are at the same risk of inflammation and progressive disease as those around natural teeth (38). Among patients with implants the prevalence of peri-implant mucositis and peri-implantitis are approximately 43% and 22% respectively (76).
Superficial inflammation (peri-implant mucositis) and true breakdown (peri-implantitis) around dental implants are common (75), and evidenced by bleeding on gentle probing, erythema, swelling and/or suppuration (2).
Poor oral hygiene, a history of periodontitis, smoking, diabetes, and lack of supportive care appear to be risk factors for peri-implant disease (2, 77, 78). Whilst previous systematic reviews have shown limited or conflicting evidence regarding the role of smoking as a risk factor for peri-implantitis (78, 79), a more recent systematic review provides low certainty evidence from 8 cross-sectional surveys of a significant association (OR 1.7, 95% CI 1.25‐2.3) (80). There is also low certainty evidence that the placement of implants in smokers is associated with implant failure, postoperative infection, and marginal bone loss (81).
The main clinical characteristics of peri-implant health is an absence of clinical signs of inflammation, absence of bleeding and/or suppuration on gentle probing, no increase in probing depth compared to previous examinations and absence of bone loss beyond crestal bone level changes resulting from initial bone remodelling (4, 82).
The main clinical characteristic of peri‐implant mucositis is bleeding on gentle probing. Erythema, swelling and/or suppuration may also be present (82). The diagnosis is based on the presence of bleeding and/or suppuration on gentle probing with or without increased probing depth compared to previous examinations and absence of bone loss beyond crestal bone level changes resulting from initial bone remodelling (4, 82).
Peri‐implantitis is a plaque‐associated disease of the tissues around dental implants, characterised by inflammation of the mucosa and progressive loss of supporting bone (2, 82). Diagnosis of peri-implantitis includes presence of bleeding and/or suppuration on gentle probing, increased probing depth compared to previous examinations and the presence of bone loss beyond crestal bone level changes resulting from initial bone remodelling.
In the absence of data from a previous examination the diagnosis of peri‐implantitis is based on a ‘combination of presence of bleeding and/or suppuration on gentle probing, probing depths of ≥6 mm and bone levels ≥3 mm apical of most coronal portion of intraosseous part of implant’ (2).
The principles of prevention around implants are the same as for teeth and focus on effective control of plaque and management of other risk factors (83, 84). However, plaque control around implants is more challenging due to the circumferential nature of peri-implantitis lesions, as well as plaque retention around cemented restorations and the design of super-structures that hinder access to the implant surface for brushing. An overview of risk factors and their management is presented in Chapter 2: Table 2.
Monitoring of implants includes regular checking of soft tissue health visually and by probing. Radiographs are required to monitor bone stability over time (82). Unresponsive pockets with bleeding, pus and/or progressive bone loss (as indicated by presence of bone loss beyond crestal bone level changes resulting from initial bone remodelling) indicate peri-implantitis (82).
At each visit:
There is low certainty evidence that SPC can potentially maintain peri‐implant health measured in terms of implant success rates, and prevent peri‐implant mucositis, and/or peri‐implantitis (85, 86).
Greater Manchester Local Dental Network. Healthy Gums do Matter. Practitioner’s Toolkit. 2019. Second Edition.
BSP Clinical Guidelines including flowchart implementing the 2017 classification of periodontal diseases.
BSP UK version of the S3 Treatment Guidelines for Periodontitis.
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The teeth to assess are all 4 permanent first molars, the upper right first permanent incisor and the lower left first permanent incisor.  2
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