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.
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:
- interdental clinical attachment loss (CAL) is detectable at ≥2 non-adjacent teeth
- 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 (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.
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 (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:
- dry mouth – antidepressants (31), and other drugs can cause dry mouth
- gingival enlargement – most commonly seen with calcium channel blockers for cardiovascular disease (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 (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).
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.
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
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.
- 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 (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).
Table 5.1. BPE codes
|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)|
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.
Table 5.2. BPE summary guidance for children and adolescents (British Society of Periodontology, 2012) (52)
|Age||Teeth to assess|
|7 to 11 years||Gum disease is difficult to identify unless looked for||
6 1/ 6[footnote 1]
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 1]
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
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.
New classification of periodontitis
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).
Table 5.3. Staging and grading of periodontitis
|Staging of periodontitis|
|Interproximal bone loss*||<15% or <2 mm**||Coronal third of root||Mid third of root||Apical third of root|
• localised (up to 30% of teeth)
• generalised (more than 30% of teeth)
• molar/incisor pattern
|Grading of periodontitis|
|% 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).
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 (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.
- 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
- 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 (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).
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
|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
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 (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).
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 (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:
- 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
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.
1. Kinane DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nature Reviews Disease Primers. 2017;3(1):17038.
2. Berglundh T, Armitage G, Araujo MG, Avila-Ortiz G, Blanco J, Camargo PM and others. Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. Journal of Clinical Periodontology. 2018;45(S20):S286-S91.
3. Kornman KS, Tonetti MS. Special Issue: Proceedings of the World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions. Journal of Clinical Periodontology. 2018;45: i-v, S1-S291.
4. Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH and others. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. Journal of Clinical Periodontology. 2018;45 Suppl 20:S162-s70.
5. NHS Digital. Adult Dental Health Survey 2009 – Summary report and thematic series [NS] London: The Health and Social Care Information Centre; 2011.
6. Bernabe E, Marcenes W, Hernandez CR, Bailey J, Abreu LG, Alipour V and others. Global, Regional, and National Levels and Trends in Burden of Oral Conditions from 1990 to 2017: A Systematic Analysis for the Global Burden of Disease 2017 Study. Journal of Dental Research. 2020;99(4):362-73.
7. Lindhe J, Socransky S, Nyman S, Westfelt E, Haffajee A. Effect of age on healing following periodontal therapy. Journal of Clinical Periodontology. 1985;12(9):774-87.
8. Axelsson P, Nystrom B, Lindhe J. The long-term effect of a plaque control program on tooth mortality, caries and periodontal disease in adults. Results after 30 years of maintenance. Journal of Clinical Periodontology. 2004;31(9):749-57.
9. Axelsson P, Lindhe J, Nyström B. On the prevention of caries and periodontal disease. Results of a 15-year longitudinal study in adults. Journal of Clinical Periodontology. 1991;18(3):182 to 189.
10. Needleman IG. Ageing and the periodontal tissues. In: Newman M, Takei H, Klokkevold P, Carranza F, editors. Carranza’s Clinical Periodontology. 11th ed. St Louis, Missouri: Elsevier Saunders; 2011. p. 28-33.
11. Wennström JL. Treatment of periodontal disease in older adults. Periodontology 2000. 1998;16(1):106-12.
12. Liu W, Cao Y, Dong L, Zhu Y, Wu Y, Lv Z and others. Periodontal therapy for primary or secondary prevention of cardiovascular disease in people with periodontitis. Cochrane Database of Systematic Reviews. 2019(12).
13. Albandar JM, Susin C, Hughes FJ. Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: Case definitions and diagnostic considerations. Journal of Clinical Periodontology. 2018;45(S20):S171-S89.
14. Sanz M, Ceriello A, Buysschaert M, Chapple I, Demmer RT, Graziani F and others. Scientific evidence on the links between periodontal diseases and diabetes: Consensus report and guidelines of the joint workshop on periodontal diseases and diabetes by the International Diabetes Federation and the European Federation of Periodontology. Journal of Clinical Periodontology. 2018;45(2):138-49.
15. Sanz M, Marco Del Castillo A, Jepsen S, Gonzalez‐Juanatey JR, D’Aiuto F, Bouchard P and others. Periodontitis and cardiovascular diseases: Consensus report. Journal of Clinical Periodontology. 2020;47(3):268-88.
16. Lavigne SE, Forrest JL. An umbrella review of systematic reviews of the evidence of a causal relationship between periodontal disease and cardiovascular diseases: position paper from the Canadian Dental Hygienists Association. Canadian journal of dental hygiene 54(1): 32-41. 2020;54:32-41.
17. Calderaro DC, Corrêa JD, Ferreira GA, Barbosa IG, Martins CC, Silva TA and others. Influence of periodontal treatment on rheumatoid arthritis: a systematic review and meta-analysis. Revista Brasileira de Reumatologia (English Edition). 2017;57(3):238-44.
18. Decker A, Askar H, Tattan M, Taichman R, Wang H-L. The assessment of stress, depression, and inflammation as a collective risk factor for periodontal diseases: a systematic review. Clinical Oral Investigations. 2020;24(1):1-12.
19. Ferreira R, Corrêa M, Magno M, Almeida A, Fagundes N, Rosing C and others. Physical Activity Reduces the Prevalence of Periodontal Disease: Systematic Review and Meta-Analysis. Frontiers in Physiology. 2019;10:234.
20. Chapple ILC, Bouchard P, Cagetti MG, Campus G, Carra M-C, Cocco F and others. Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases. Journal of Clinical Periodontology. 2017;44(S18):S39-S51.
21. Akram Z, Shafqat SS, Aati S, Kujan O, Fawzy A. Clinical efficacy of probiotics in the treatment of gingivitis: A systematic review and meta-analysis. Australian Dental Journal. 2020;65(1):12-20.
22. Khan S, Barrington G, Bettiol S, Barnett T, Crocombe L. Is overweight/obesity a risk factor for periodontitis in young adults and adolescents?: a systematic review. Obesity Reviews. 2018;19(6):852-83.
23. Keboa MT, Enriquez N, Martel M, Nicolau B, Macdonald ME. Oral Health Implications of Cannabis Smoking: A Rapid Evidence Review. Journal of the Canadian Dental Association. 2020;86:k2.
24. Aminoshariae A, Kulild J, Gutmann J. The association between smoking and periapical periodontitis: a systematic review. Clinical Oral Investigations. 2020;24(2):533-45.
25. Leite FRM, Nascimento GG, Scheutz F, López R. Effect of Smoking on Periodontitis: A Systematic Review and Meta-regression. American Journal of Preventive Medicine. 2018;54(6):831-41.
26. Yang I, Sandeep S, Rodriguez J. The oral health impact of electronic cigarette use: a systematic review. Critical Reviews in Toxicology. 2020;50(2):97-127.
27. Pulikkotil SJ, Nath S, Muthukumaraswamy, Dharamarajan L, Jing KT, Vaithilingam RD. Alcohol consumption is associated with periodontitis. A systematic review and meta-analysis of observational studies. Community dental health. 2020 2020/02//; 37(1):[12-21 pp.].
28. Amaral Cda S, Vettore MV, Leão A. The relationship of alcohol dependence and alcohol consumption with periodontitis: a systematic review. Journal of Dentistry. 2009;37(9):643-51.
29. Nascimento GG, Leite FRM, Vestergaard P, Scheutz F, López R. Does diabetes increase the risk of periodontitis? A systematic review and meta-regression analysis of longitudinal prospective studies. Acta Diabetologica. 2018;55(7):653-67.
30. NHS England, NHS Improvement. Dental Care for People with Diabetes. Version number: 1.0 First published: July 2019. London: NHS England; 2019. Contract No.: 000078.
31. Cappetta K, Beyer C, Johnson JA, Bloch MH. Meta-analysis: Risk of dry mouth with second generation antidepressants. Progress in Neuropsychopharmacology and Biological Psychiatry. 2018;84(Pt A):282-93.
32. Vidal F, de Souza RC, Ferreira DC, Fischer RG, Gonçalves LS. Influence of 3 calcium channel blockers on gingival overgrowth in a population of severe refractory hypertensive patients. Journal of Periodontal Research. 2018;53(5):721-6.
33. Murakami S, Mealey BL, Mariotti A, Chapple ILC. Dental plaque-induced gingival conditions. Journal of Clinical Periodontology. 2018;45(S20):S17-S27.
34. Lang NP, Schätzle MA, Löe H. Gingivitis as a risk factor in periodontal disease. Journal of Clinical Periodontology. 2009;36(s10):3-8.
35. Local Government Assocation. Prevention London: LGA; 2020 [05.11.2020].
36. Tonetti MS, Eickholz P, Loos BG, Papapanou P, van der Velden U, Armitage G and others. Principles in prevention of periodontal diseases. Journal of Clinical Periodontology. 2015;42(S16):S5-S11.
37. Lamont T, Worthington HV, Clarkson JE, Beirne PV. Routine scale and polish for periodontal health in adults. Cochrane Database of Systematic Reviews. 2018(12).
38. Sanz M, Herrera D, Kebschull M, Chapple I, Jepsen S, Beglundh T and others. Treatment of Stage I-III Periodontitis – The EFP S3 Level Clinical Practice Guideline. Journal of Clinical Periodontology in Europe. 2020.
39. Huang J, Yao Y, Jiang J, Li C. Effects of motivational methods on oral hygiene of orthodontic patients: A systematic review and meta-analysis. Medicine (Baltimore). 2018;97(47):e13182.
40. SDCEP. Oral Hygiene TIPPS video: Scottish Dental Clinical Effectiveness Programme; [29.05.2020].
41. Järvinen M, Stolt M, Honkala E, Leino-Kilpi H, Pöllänen M. Behavioural interventions that have the potential to improve self-care in adults with periodontitis: a systematic review. Acta Odontologica Scandinavica. 2018;76(8):612-20.
42. Carra MC, Detzen L, Kitzmann J, Woelber JP, Ramseier CA, Bouchard P. Promoting behavioural changes to improve oral hygiene in patients with periodontal diseases: a systematic review. Journal of Clinical Periodontology. 2020.
43. Mohammed H, Rizk MZ, Wafaie K, Ulhaq A, Almuzian M. Reminders improve oral hygiene and adherence to appointments in orthodontic patients: a systematic review and meta-analysis. European Journal of Orthodontics. 2018;41(2):204-13.
44. Lima IFP, de Andrade Vieira W, de Macedo Bernardino Í, Costa PA, Lima APB, Pithon MM and others. Influence of reminder therapy for controlling bacterial plaque in patients undergoing orthodontic treatment: A systematic review and meta-analysis. Angle Orthodontist. 2018;88(4):483-93.
45. Sharif MO, Newton T, Cunningham SJ. A systematic review to assess interventions delivered by mobile phones in improving adherence to oral hygiene advice for children and adolescents. British Dental Journal. 2019;227(5):375-82.
46. Toniazzo MP, Nodari D, Muniz F, Weidlich P. Effect of mHealth in improving oral hygiene: A systematic review with meta-analysis. Journal of Clinical Periodontology. 2019;46(3):297-309.
47. UK Chief Medical Officers. Alcohol consumption: advice on low risk drinking. Department of Health and Social Care: UK Government; 2016.
49. Rosling B, Serino G, Hellstrom MK, Socransky SS, Lindhe J. Longitudinal periodontal tissue alterations during supportive therapy. Findings from subjects with normal and high susceptibility to periodontal disease. 2001;28(3):241-9.
50. BSP. Basic Periodontal Examination (BPE). British Society of Periodontology; 2019.
51. Greater Manchester Local Dental Network. Healthy Gums do Matter: Practitioner’s Toolkit. 2019.
52. BSP. Guidelines for periodontal screening and management of children and adolescents under 18 years of age. British Society of Periodontology; 2012.
53. West N, Chapple I, Claydon N, D’Aiuto F, Donos N, Ide M and others. BSP implementation of European S3 – level evidence-based treatment guidelines for stage I-III periodontitis in UK clinical practice. Journal of Dentistry. 2021;106:103562.
54. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: Framework and proposal of a new classification and case definition. Journal of Periodontology. 2018;89 Suppl 1:S159-s72.
55. Dietrich T, Ower P, Tank M, West NX, Walter C, Needleman I and others. Periodontal diagnosis in the context of the 2017 classification system of periodontal diseases and conditions – implementation in clinical practice. British Dental Journal. 2019;226(1):16-22.
56. Needleman I, Suvan J, Moles DR, Pimlott J. A systematic review of professional mechanical plaque removal for prevention of periodontal diseases. Journal of Clinical Periodontology. 2005;32 Suppl 6:229-82.
57. Manresa C, Sanz‐Miralles EC, Twigg J, Bravo M. Supportive periodontal therapy (SPT) for maintaining the dentition in adults treated for periodontitis. Cochrane Database of Systematic Reviews. 2018(1).
58. Zhang J, Liu J, Li J, Chen B, Li H, Yan F. The Clinical Efficacy of Subgingival Debridement by Ultrasonic Instrumentation Compared With Subgingival Air Polishing During Periodontal Maintenance: A Systematic Review. Journal of Evidence Based Dental Practice. 2019;19(4):101314.
59. Sanz M, Herrera D, Kebschull M, Chapple I, Jepsen S, Beglundh T and others. Treatment of stage I-III periodontitis-The EFP S3 level clinical practice guideline. Journal of Clinical Periodontology. 2020;47 Suppl 22:4-60.
60. BSP Implementation of Treatment of Stage I-III Periodontitis –The EFP S3 Level Clinical Practice Guideline.
61. Baeza M, Morales A, Cisterna C, Cavalla F, Jara G, Isamitt Y and others. Effect of periodontal treatment in patients with periodontitis and diabetes: systematic review and meta-analysis. Journal of Applied Oral Sciences. 2020;28:e20190248-e.
62. Simpson TC, Weldon JC, Worthington HV, Needleman I, Wild SH, Moles DR and others. Treatment of periodontal disease for glycaemic control in people with diabetes mellitus. Cochrane Database of Systematic Reviews. 2015;2015(11):Cd004714.
63. Cao R, Li Q, Wu Q, Yao M, Chen Y, Zhou H. Effect of non-surgical periodontal therapy on glycemic control of type 2 diabetes mellitus: a systematic review and Bayesian network meta-analysis. BMC Oral Health. 2019;19(1):176.
64. Jain A, Gupta J, Bansal D, Sood S, Gupta S, Jain A. Effect of scaling and root planing as monotherapy on glycemic control in patients of Type 2 diabetes with chronic periodontitis: A systematic review and meta-analysis. Journal of Indian Society of Periodontology. 2019;23(4):303-10.
65. Muñoz Aguilera E, Suvan J, Buti J, Czesnikiewicz-Guzik M, Barbosa Ribeiro A, Orlandi M and others. Periodontitis is associated with hypertension: a systematic review and meta-analysis. Cardiovascular Research. 2020;116(1):28-39.
66. Chye RML, Perrotti V, Piattelli A, Iaculli F, Quaranta A. Effectiveness of Different Commercial Chlorhexidine-Based Mouthwashes After Periodontal and Implant Surgery: A Systematic Review. Implant Dentistry. 2019;28(1):74-85.
67. Elkerbout T, Slot D, Van Loveren C, Van der Weijden G. Will a chlorhexidine-fluoride mouthwash reduce plaque and gingivitis? International Journal of Dental Hygiene. 2019;17(1):3-15.
68. Zhang J, Ab Malik N, McGrath C, Lam O. The effect of antiseptic oral sprays on dental plaque and gingival inflammation: A systematic review and meta-analysis. International Journal of Dental Hygiene. 2019;17(1):16-26.
69. Figuero E, Roldán S, Serrano J, Escribano M, Martín C, Preshaw PM. Efficacy of adjunctive therapies in patients with gingival inflammation: A systematic review and meta-analysis. Journal of Clinical Periodontology. 2020;47(S22):125-43.
70. Cai H, Chen J, Panagodage Perera NK, Liang X. Effects of Herbal Mouthwashes on Plaque and Inflammation Control for Patients with Gingivitis: A Systematic Review and Meta-Analysis of Randomised Controlled Trials. Evidence-Based Complementary and Alternative Medicine. 2020;2020:2829854.
71. Al-Maweri SA, Nassani MZ, Alaizari N, Kalakonda B, Al-Shamiri HM, Alhajj MN and others. Efficacy of aloe vera mouthwash versus chlorhexidine on plaque and gingivitis: A systematic review. International Journal of Dental Hygiene. 2020;18(1):44-51.
72. Giri P, DivyaLalitha N, Prabu D, Bharathwaj V, Manipal S, Rajmohan M. A Systematic Review on the Efficacy of Aloe Vera Mouthwash on Periodontal Health. 2019;11:3217-22.
73. Gartenmann SJ, Steppacher SL, von Weydlich Y, Heumann C, Attin T, Schmidlin PR. The Effect of Green Tea on plaque and gingival inflammation: A systematic review. Journal of Herbal Medicine. 2020;21:100337.
74. Bunte K, Hensel A, Beikler T. Polyphenols in the prevention and treatment of periodontal disease: A systematic review of in vivo, ex vivo and in vitro studies. Fitoterapia. 2019;132:30-9.
75. Atieh MA, Alsabeeha NH, Faggion CM, Jr., Duncan WJ. The frequency of peri-implant diseases: a systematic review and meta-analysis. Journal of Periodontology. 2013;84(11):1586-98.
76. Derks J, Tomasi C. Peri-implant health and disease. A systematic review of current epidemiology. Journal of Clinical Periodontology. 2015;42:S158-S71.
77. Sousa V, Mardas N, Farias B, Petrie A, Needleman I, Spratt D and others. A systematic review of implant outcomes in treated periodontitis patients. Clinical Oral Implants Research. 2016;27(7):787-844.
78. Turri A, Rossetti PH, Canullo L, Grusovin MG, Dahlin C. Prevalence of Peri-implantitis in Medically Compromised Patients and Smokers: A Systematic Review. International Journal of Oral and Maxillofacial Implants. 2016;31(1):111-8.
79. Stacchi C, Berton F, Perinetti G, Frassetto A, Lombardi T, Khoury A and others. Risk Factors for Peri-Implantitis: Effect of History of Periodontal Disease and Smoking Habits. A Systematic Review and Meta-Analysis. Journal of Oral and Maxillofacial Research. 2016;7(3):e3.
80. Dreyer H, Grischke J, Tiede C, Eberhard J, Schweitzer A, Toikkanen SE and others. Epidemiology and risk factors of peri-implantitis: A systematic review. Journal of Periodontal Research. 2018;53(5):657-81.
81. Chrcanovic BR, Albrektsson T, Wennerberg A. Smoking and dental implants: A systematic review and meta-analysis. J Dent. 2015;43(5):487-98.
82. Schwarz F, Derks J, Monje A, Wang H-L. Peri-implantitis. Journal of Clinical Periodontology. 2018;45(S20):S246-S66.
83. Heitz-Mayfield LJ, Needleman I, Salvi GE, Pjetursson BE. Consensus statements and clinical recommendations for prevention and management of biologic and technical implant complications. International Journal of Oral and Maxillofacial Implants. 2014;29 Suppl:346-50.
84. Heitz‐Mayfield LJA, Heitz F, Lang NP. Implant Disease Risk Assessment IDRA–a tool for preventing peri‐implant disease. Clinical Oral Implants Research. 2020;31(4):397-403.
85. Lin CY, Chen Z, Pan WL, Wang HL. The effect of supportive care in preventing peri-implant diseases and implant loss: A systematic review and meta-analysis. Clinical Oral Implants Research. 2019;30(8):714-24.
86. Monje A, Aranda L, Diaz KT, Alarcón MA, Bagramian RA, Wang HL and others. Impact of Maintenance Therapy for the Prevention of Peri-implant Diseases. Journal of Dental Research. 2016;95(4):372-9.