Guidance

Chapter 5: Periodontal diseases

Updated 9 November 2021

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.

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Introduction

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)^{[footnote 1]}. The early stages of disease may be symptom-free, but the impact on peoples’ lives of later stage disease are more serious^{[footnote 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^{[footnote 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.

Definitions

The 2017 World Workshop classification of periodontal and peri-implant conditions^{[footnote 3][footnote 4]}, can be summarised as follows.

Periodontal health

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

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

Periodontitis is a microbially-associated, host-mediated inflammation that results in loss of periodontal attachment. A patient is said to have periodontitis if:

• interdental clinical attachment loss (CAL) is detectable at ≥2 non-adjacent teeth

or

• buccal or oral CAL ≥3 mm with pocketing ≥3 mm is detectable at ≥2 teeth, where the lost clinical attachment cannot be ascribed to another cause

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^{[footnote 4]}. This chronic and inflammatory disease is caused by a complex interplay of risk factors, with dental plaque being the most important^{[footnote 4]}.

Epidemiology

Some level of irreversible periodontitis affects almost half of UK adults^{[footnote 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^{[footnote 6]}. The peak in prevalence occurs between 60 and 64 years of age^{[footnote 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^{[footnote 7][footnote 8][footnote 9][footnote 10][footnote 11]}, particularly when people can undertake the necessary self-care and are able to visit the dental team.

Risk or susceptibility and protective factors

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^{[footnote 12][footnote 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^{[footnote 14]}.

There is ongoing debate about the role of periodontitis in cardiovascular diseases^{[footnote 15][footnote 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^{[footnote 17]}. Likewise, the evidence linking lifestyle factors such as stress^{[footnote 18][footnote 19]}, poor diet^{[footnote 20][footnote 21]}, being overweight^{[footnote 22]}, or cannabis use^{[footnote 23]}, is insufficient to suggest a clear association with periodontal diseases.

Plaque

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^{[footnote 1]}.

Tobacco

Tobacco smoking and use of smokeless tobacco products have a profound effect on the risk of developing periodontitis^{[footnote 24][footnote 25]}. They also impair the treatment response. Cessation of tobacco use can prevent further deterioration of periodontal health (Chapter 2: Table 2; Chapter 11).

Vaping

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^{[footnote 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).

Alcohol

There is emerging low-certainty evidence that alcohol consumption is associated with periodontitis^{[footnote 27][footnote 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.

Diabetes

Glycaemia in those without a diagnosis of diabetes, and hyperglycaemia in those with diabetes are both risk factors for poor periodontal health^{[footnote 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^{[footnote 30]}.

Medications

Several medications may affect periodontal health, which underlines the importance of a comprehensive and up-to-date medical history.

Medications may cause:

• dry mouth – antidepressants^{[footnote 31]}, and other drugs can cause dry mouth
• gingival enlargement – most commonly seen with calcium channel blockers for cardiovascular disease^{[footnote 32]}, although other drugs can also have this effect

Therefore, it is good practice to check the possible side-effects of patient medications in a formulary.

Primary prevention of periodontitis

Risk factor control

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^{[footnote 33]}, and thereafter tooth loss^{[footnote 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^{[footnote 35][footnote 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^{[footnote 37]}.

Plaque control

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^{[footnote 38][footnote 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^{[footnote 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 (PDF, 116KB) relating to managing patient self-care.

Whilst brief behaviour change interventions have the potential to improve plaque control over traditional oral hygiene instruction alone^{[footnote 41][footnote 42]}, the evidence to date is not robust^{[footnote 41]}. There is low to moderate certainty evidence that motivational methods, involving plaque disclosure and repeated OHI reduce plaque^{[footnote 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^{[footnote 43][footnote 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^{[footnote 45][footnote 46]}.

Removal of plaque retention factors

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.

Smoking cessation

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.

Alcohol risk reduction

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)^{[footnote 47]}.

Diabetes control

The following actions are advised^{[footnote 13][footnote 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 (PDF, 190KB). It is worth noting that people may be set different threshold units by their team; thus dental teams should explore this with each patient^{[footnote 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^{[footnote 14]}.

Medication management

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

Ask people on medication if they experience dry mouth or swollen gums.

Assess

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.

Action

You should:

• explain findings and assess possible need to change medication
• contact physician to request consideration for medication change where appropriate regarding gingival enlargement – download template letter
• consider short-term use of chlorhexidine mouthrinse in addition to usual plaque control methods
• consider increasing frequency of reviews and of scaling (professional mechanical plaque removal)

Secondary prevention of periodontitis

Early detection and management pathways: basic periodontal examination

Early detection and treatment of periodontitis increases the likelihood of tooth retention^{[footnote 49]}. One screening tool that is well known and quick to use is the Basic Periodontal Examination (BPE)^{[footnote 50]}. The BPE uses the WHO BPE probe and is suitable for routine assessment of all dentate adults (Table 5.1).

Table 5.1. BPE codes

Code	Observation
0	Healthy gingival condition with no bleeding on probing
1	Bleeding on probing
2	Plaque retention factor present (for example calculus, overhanging restoration)
3	Black band extending 3.5mm to 5.5mm is partially obscured (indicates pocket 4mm to 5.5mm)
4	Black band extending 3.5mm to 5.5mm is completely obscured (indicates pocket of 6mm or greater)
*	Furcation involvement

Detailed advice on the use of the BPE is provided in the Greater Manchester Local Dental Network’s (2019) Healthy Gums Do Matter^{[footnote 51]} and the British Society for Periodontology and Implant Dentistry (BSP) BPE guidelines^{[footnote 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^{[footnote 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.

Table 5.2. BPE summary guidance for children and adolescents (British Society of Periodontology, 2012)^{[footnote 52]}

Age		Teeth to assess
7 to 11 years	Gum disease is difficult to identify unless looked for	6   1/      6[footnote 87] 6     /1    6 BPE codes to use: 0,1,2 (only)
12 to 17 years	Gum disease is difficult to identify unless looked for	6   1/      6[footnote 87] 6     /1    6 BPE codes to use: 0,1,2,3,4 and * BPE = 0-2 as above BPE = 3 in 1 or more sextant: treat and review after 3 months BPE = 4 or * in any sextant: full periodontal assessment and normally arrange referral

Managing periodontitis

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^{[footnote 50]}. Plaque scores may identify areas with specific oral hygiene problems to be managed^{[footnote 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^{[footnote 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^{[footnote 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^{[footnote 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.

New classification of periodontitis

The new classification of periodontitis^{[footnote 3][footnote 54]} describes the historical degree of periodontal breakdown (stage) and the speed of the breakdown (grade)^{[footnote 54]}. It was adapted for implementation in the UK healthcare system by the BSP^{[footnote 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^{[footnote 54]}.

Table 5.3. Staging and grading of periodontitis

Staging of periodontitis
	Stage I (early/mild)	Stage II (moderate)	Stage III (severe)	Stage IV (very severe)
Interproximal bone loss*	<15% or <2 mm**	Coronal third of root	Mid third of root	Apical third of root
Extent	Describe as: • localised (up to 30% of teeth) • generalised (more than 30% of teeth) • molar/incisor pattern
Grading of periodontitis
	Grade A (slow)	Grade B (moderate)	Grade C (rapid)
% bone loss / age	<0.5	0.5–1.0	>1.0

*Maximum bone loss in percentage of root length. **Measurement in mm from cemento-enamel junction (CEJ) if only bitewing radiograph available (bone loss) or no radiographs clinically justified (CAL).

Sources: see ^{[footnote 54][footnote 55]}.

Notes:

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.

Tertiary prevention of periodontitis

Supportive periodontal care (SPC) after treatment for periodontitis

Periodontitis is a chronic disease that will recur and worsen without good plaque control^{[footnote 8][footnote 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^{[footnote 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^{[footnote 58]}. Some patients preferred ultrasonic compared to hand instrumentation because it took less time.

Components of SPC include:^{[footnote 59][footnote 60]}

• setting expectations – advice about the importance of SPC and the commitment required and need for patient adherence
• regular monitoring of
  • plaque and gingival inflammation to guide oral hygiene advice
  • probing depths and bleeding on probing to guide:
    • evaluation of health and stability
    • treatment
• oral hygiene advice Chapter 8 and behaviour change Chapter 3 intervention as appropriate (covered above)
• debridement or professional mechanical plaque removal (PMPR):
  • removal of supra and subgingival plaque and calculus (PMPR)
  • root surface debridement of pockets 5mm and deeper with bleeding on probing

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^{[footnote 37]}.

In patients with type 2 diabetes, there is moderate certainty evidence that SPC improves metabolic control and reduces systemic inflammation^{[footnote 61]}. These findings have been supported by several systematic reviews. However, the certainty of the evidence and the amount of reduction in HbA1c varies^{[footnote 62][footnote 63][footnote 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^{[footnote 65]}.

Management of periodontitis: summary

Table 5.4 summarises the possible management options for periodontitis in adults in relation to BPE scores.

Table 5.4. BPE and possible management options in adults

Code	Observation	Management
0	Healthy gingival condition	Risk factor control Recalls as low risk
1	Bleeding on probing	Risk factor control Recalls as low risk depending on extent of bleeding
2	Plaque retention factors	Consider removing retention factor Recalls as low risk depending on extent of bleeding
3	Pockets 4mm to 5.5mm	Risk factor control Remove retention factors Detailed assessment, including pocket charting in affected segments, radiographs, classification, and grading Active treatment Supportive Periodontal Care
4	Pockets of 6mm or greater	As Code 3 above and additionally Detailed assessment, including full-mouth pocket charting, radiographs, classification, and grading
*	Furcation involvement	As Code 4 above

Mouthrinses, mouthwashes and sprays

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^{[footnote 66][footnote 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^{[footnote 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^{[footnote 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^{[footnote 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^{[footnote 69]}. Similar results were shown for other reviews involving herbal^{[footnote 70]}, aloe vera^{[footnote 71][footnote 72]}, green tea^{[footnote 73]} and polyphenol^{[footnote 74]} rinses.

Peri-implant health

Dental implants may be used to replace missing teeth. However, the soft tissues and bone around dental implants^{[footnote 75]}, are at the same risk of inflammation and progressive disease as those around natural teeth^{[footnote 38]}. Among patients with implants the prevalence of peri-implant mucositis and peri-implantitis are approximately 43% and 22% respectively^{[footnote 76]}.

Superficial inflammation (peri-implant mucositis) and true breakdown (peri-implantitis) around dental implants are common^{[footnote 75]}, and evidenced by bleeding on gentle probing, erythema, swelling and/or suppuration^{[footnote 2]}.

Poor oral hygiene, a history of periodontitis, smoking, diabetes, and lack of supportive care appear to be risk factors for peri-implant disease^{[footnote 2][footnote 77][footnote 78]}. Whilst previous systematic reviews have shown limited or conflicting evidence regarding the role of smoking as a risk factor for peri-implantitis^{[footnote 78][footnote 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)^{[footnote 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^{[footnote 81]}.

Definitions

Peri-implant health

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^{[footnote 4][footnote 82]}.

Peri-implant mucositis

The main clinical characteristic of peri‐implant mucositis is bleeding on gentle probing. Erythema, swelling and/or suppuration may also be present^{[footnote 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^{[footnote 4][footnote 82]}.

Peri-implantitis

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^{[footnote 2][footnote 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’^{[footnote 2]}.

Prevention of peri-implantitis

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^{[footnote 83][footnote 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^{[footnote 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^{[footnote 82]}.

At each visit:

• monitor plaque and marginal inflammation
• monitor probing depths and compare them to baseline (following placement of prosthesis) and previous visits, bleeding, and presence of pus
• take appropriate radiographs as indicated and compare with the time of prosthesis placement and subsequent films
• debride all supra and submucosal plaque and calculus
• consider early referral to specialist for unresponsive deepened pockets with bleeding, or pus and progressive bone loss
• decide on recall interval based on peri-implant and periodontal status

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^{[footnote 85][footnote 86]}.

Resources

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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