Periodontal disease and alcohol consumption: The relationship, dental management, and role of the dentist

Abstract

Periodontal disease is a chronic multifactorial disease of the periodontium, involving inflammation and destruction of the supporting structures of the teeth including the gingiva, periodontal ligaments, root cementum and the alveolar bone. Alcohol has been found to have a negative impact within the oral cavity and more specifically on periodontal health. Although alcohol has been shown to further the progression and severity of periodontal disease, more research is required to further investigate the strength of this relationship and the mechanisms involved. Additionally, this paper discusses the dental management of periodontal disease, emphasizing the important role that dental professionals can play in the management of patients who consume alcohol.

Alcohol is one of the most widely used substances in the world today, and is also one of the most commonly abused. Due to its long and widespread use, alcohol has also been studied extensively. However, although it has been extensively researched, an understudied area in the dental field is the relationship between alcohol consumption and periodontal disease. It is well known that alcohol has effects on many of our body’s major systems and functions, including our nervous system, gastrointestinal system, and endocrine system, as well as exhibits cross-reactivity with many common drugs. According to the 2019 Canadian Alcohol and Drugs Survey (CADS), 76% of Canadians consumed an alcoholic beverage in the past year.¹ This is relevant to the field of dentistry as alcohol is known to have negative effects on the oral cavity.

Periodontitis is a chronic multifactorial inflammatory disease of the periodontium that results in the destruction of sound oral tissues that support the teeth. It causes progressive destruction of the periodontal ligament and alveolar bone due to the extension of inflammation from the gingiva.² Periodontal disease involves complex interactions between certain bacterial pathogens, destructive host immune responses, and environmental factors such as smoking and alcohol use.^3,4 There are well over 300 species of bacteria that may be colonized in the oral cavity, and some of which are the primary etiological agents associated with the disease. Although pathogenic biofilm is a necessary prerequisite for periodontal disease, it is important to note that they are insufficient to cause the disease.⁵ Finally, it is a multiphase disease that may exacerbate certain systemic diseases and may associate itself with various organ systems including the cardiovascular, endocrine, reproductive and the respiratory system.²

According to the 2019 Canadian Alcohol and Drugs Survey (CADS), males reported higher alcohol use than females (78% or 12 million males and 75% or 11.7 million females).¹ The age range that reported the highest use of alcohol were those aged 20 to 24 (84%), followed by those aged 25 years and older (78%), and then by those aged 15 to 19 (46%).¹ It was also reported that these results are consistent with the previous 2017 CADS, with only the alcohol consumption of those aged 14-19 seeing a decrease from 57%.¹ Of those surveyed, 21% reported experiencing at least one alcohol-related harm in that year.¹

The purpose of this paper is to investigate the relationship between alcohol consumption and periodontal disease, including the impact of alcohol on oral and systemic health, as well as the management and prevention of alcohol-related periodontal disease including the important role that dentists can play.

Periodontal disease

Etiology

Periodontitis is one of the most chronic infectious diseases and is characterized by progressive inflammation and destruction of periodontal tissue which includes the gingiva, periodontal ligaments, root cementum and the alveolar bone.² The oral cavity houses up to 700 different species of bacteria, and this ultimately forms the oral microbiome.⁶ Throughout the years, there have been numerous hypotheses about the progression of pathogens and formation of periodontal disease; however, the one shown to be most plausible was the Ecological Plaque Hypothesis proposed by Marsh (1994).⁷ This hypothesis states that changes in the local oral environment can preferentially select dental plaque microorganisms and thus predispose a site to disease due to the alteration of the protective microbial homeostatic mechanism.⁸

When homeostatic mechanisms are altered this results in an unfavorable disruption of the microbiota composition also known as dysbiosis. This dysbiotic environment leads to the deviation and transition within the polymicrobial community from gram-positive commensal microorganisms to gram-negative bacteria which inevitably results in a pathogenic relationship between the oral microbiome and the host.⁹ The first microbial complex associated with the disease is the orange complex which includes: P. intermedia, P. nigrescens, P. micros, and F. nucleatum. With disease progression, this complex gradually progresses to a more pathogenic form known as red complex bacteria which consists of T. forsythia, P. gingivalis, and T. denticola.⁹ Contrary to popular belief, although a necessary prerequisite, pathogenic biofilm is not merely enough to cause periodontal disease on its own. It is the highly complex interactions between both the biofilm and the inflammatory host immune response that leads to the formation and progression of periodontal disease.⁵

The mechanism of disease will begin with an exaggerated and inappropriate hyperinflammatory response, which will lead to production of cytokines, matrix metalloproteinases (MMPs), and high levels of oxidative stress.¹⁰ Monocytes exhibit toll-like receptors (TLR) which respond and recognize to the antigen LPS present on gram-negative bacteria.¹¹ Upon binding, monocytes become activated and differentiate to macrophages and produce proinflammatory cytokines such as IL-1β and TNF-α. It is the production of these cytokines that initiate the differentiation of osteoclasts that eventually lead to bone loss.¹⁰ Derived from neutrophils, MMPs and in particular MMP-8 makes up 80% of the collagenase protein that is located within the gingival crevicular fluid (GCF).¹² These matrix metalloproteinases will lead to the destruction of the periodontium, and degradation of both gingival and periodontal ligament collagen.¹² During the hyperinflammatory state, the oral environment will undergo oxidative stress and lead to the production of reactive-oxygen species, which is the body’s defense mechanism against pathogen invasion.¹⁰ Although beneficial to some degree, it induces and exacerbates periodontal disease pathogenesis by causing oxidative damage and destruction of host tissue.¹³ The body’s ability to defend itself against foreign invasion is highly complex, and although the initiation and excessive host inflammation is one of many mechanisms used, it is a double edged sword in the sense that although on one hand it is defending the host, it is simultaneously harming and destroying its own tissues.

Pathogenesis and clinical presentation

The initiation and exacerbation of periodontitis involves many factors. The presence of pathogenic biofilm is a necessary prerequisite; however, it is the addition of an exaggerated and inappropriate host immune response that ultimately leads to periodontitis. Although there must be dysbiosis and disruption of homeostatic mechanisms, it is solely not enough for the development of periodontitis. The host response in dental plaque can be described as four lesions as per Page and Schroeder (1976).¹⁴ These lesions are listed as initial, early, established and advanced (Table 1). Although outdated, it still remains fundamentally relevant regarding the order of lesion appearance as well as the primary cellular players involved in the disease process.⁵ The initial lesion appears 2-4 days after the accumulation of plaque localized at or near the gingival sulcus. It involves acute exudative vasculitis within gingival tissue and the infiltration of polymorphonuclear (PMN) cells into the junctional and sulcular epithelium.¹⁵ The early lesion develops within 4-7 days after plaque accumulation and correlates to early gingivitis. It is characterized by T- lymphocyte infiltration and the pathological alteration of fibroblasts along with erythema and bleeding on probing. The established lesion forms within 2-3 weeks after plaque accumulation and is characterized by the predominance of plasma cells and the increased loss of gingival connective tissue matrix with the establishment of a gingival pocket. Destruction at this point is still reversible. Finally, the advanced lesion correlates to periodontitis, and is irreversible. It is characterized by dense inflammatory infiltrate made up of macrophages and plasma cells, the loss of collagen attachment, and resorption of alveolar bone.¹⁵

Table 1: Pathogenesis of periodontal disease

Lesion Type	Manifestation and Clinical Presentation
1. Initial lesion	– Manifests 2-4 days post-plaque accumulation – Acute exudative vasculitis within gingival tissue – Predominant immune cells are PMNs – No clinical presentation
2. Early lesion	– Manifests 4-7 days post-plaque accumulation – Pathological alteration of fibroblasts – Predominant immune cells are T lymphocytes – Erythema and bleeding on probing present
3. Established lesion	– Manifests 2-3 weeks post-plaque accumulation – Loss of marginal gingival connective tissue matrix – Predominant immune cells are B cells (plasma cells) – Gingival pocket formation and erythema – Destruction is reversible at this stage
4. Advanced lesion	– Correlates to peridontitis – Destruction of gingival tissue architecture, alveolar bone loss, and periodontal ligament – Predominant immune cells are B cells (plasma cells) -Irreversible damage

Pharmacology of alcohol

Alcohol, also known as ethyl alcohol or ethanol is a colourless and volatile fluid which is produced by yeast fermentation to break down sugars from plants and fruits into ethanol and carbon dioxide.¹⁶ The three primary types of alcoholic beverages are beer, wine, and spirits. These alcoholic beverages differ in the amount of ethanol they contain in their % alcohol by volume (ABV). Liquor drinks are 35-45% ABV, wines are 8-12% ABV, and beers are 3-9% ABV.¹⁷

Like any drug, the pharmacokinetics of alcohol may be broken down into four categories, which include absorption, distribution, metabolism, and excretion. Absorption can be described as the process by which a drug passes from the site of administration into the bloodstream for transport. The absorption rate of alcohol is a first-order kinetic process, and the rate is proportional to the concentration of alcohol within the stomach.¹⁷ Given that alcohol is an uncharged molecule, it is able to cross biological membranes with ease via passive diffusion. Alcohol is almost completely absorbed from the intestine (duodenum), and the rate of absorption is fastest when the alcoholic contents enter the duodenum and jejunum. The rate of absorption of alcohol differs among individuals and is highly variable due to a plethora of factors. These factors may include but are not limited to food, drinking on an empty stomach, gender, and alcohol concentration.¹⁷ After the alcohol has been absorbed, the alcohol will pass through the hepatic vein towards the heart, enter the lungs, going back to the heart before being pumped and distributed and entering systemic circulation. Alcohol is distributed into the total body water compartment (TBW), which signifies about 50-60% of body weight for an individual weighing 85kg. This means that after alcohol has been equilibrated in body fluids and tissues, its concentration is highest in biofluids with the most water. For example, this would mean that saliva, sweat, and urine have the highest concentrations in comparison to blood, plasma, and serum.¹⁸ There are statistically significant differences in gender regarding their TBW. These differences are due to height, size, weight and the fact that females have a lower proportion of TBW. Hence, females tend to have higher blood alcohol levels compared to their male counterparts given that the amount of alcohol has been consumed.¹⁷ The metabolism of alcohol occurs primarily in the liver and can essentially be broken down into two steps. The first step involves alcohol being oxidized into acetaldehyde by the enzyme alcohol dehydrogenase. It is in fact the breakdown product acetaldehyde that is the highly toxic component within humans and is more carcinogenic than ethanol itself.¹⁶ It is acetaldehyde that also causes symptoms such as headaches, facial flushing, dizziness, and nausea and vomiting.¹⁶ The second step of alcohol metabolism is the conversion of acetaldehyde into harmless acetate or acetic acid by the enzyme aldehyde dehydrogenase, which can then further be utilized in the citric acid cycle. Finally, when it comes to excretion, most of the alcohol is removed and eliminated by oxidative metabolism and the remaining alcohol tends to be eliminated by excretion via the lungs, kidneys and skin.¹⁷

Pharmacodynamics is the action or effect of a drug on the body. With moderate alcohol consumption, alcohol acts on the neurotransmitters GABA, glutamate and dopamine. Alcohol will suppress the excitatory effects of glutamate, and will simulate GABA to induce calmness, relaxation and stress reduction.¹⁶ Alcohol simultaneously enhances dopamine release which amplifies pleasurable effects. Apart from neurotransmitters, the consumption of alcohol has also been extensively studied and has been shown to be associated with many diseases such as cardiovascular disease, type 2 diabetes, addiction, dementia and many more.¹⁶ Although one of the most widely used substances globally, the consumption and overconsumption of alcohol has been shown time and time again to pose no benefit to the human body, and is evidently the culprit for many diseases and pathologic deficits.

Periodontal disease and alcohol consumption

Alcohol is one of the most widely consumed substances globally and can be attributed to numerous negative outcomes and a wide variety of diseases.¹⁹ Alcohol is a very strong risk factor for many injuries and diseases and is responsible for about 4% of deaths worldwide.¹⁹ Alcohol has been extensively researched; however, its relationship to periodontal disease should be further investigated.

Alcohol and its contents are primarily consumed via oral consumption and therefore negatively affects the oral cavity and the oral mucosa.²⁰ Although the development of periodontal disease is highly complex and multifactorial, certain behaviors such as alcohol consumption can alter the host’s homeostatic mechanisms and increase susceptibility to the disease.^21,22 It was determined in a study performed by Szabo et al., (1999)²³ that consumption of alcohol does impair T-cell function as well as chemotaxis performed by neutrophils, and can therefore alter various immune responses and increase the risk of periodontitis. In a study performed by Lages et al., they attempted to investigate the effect of alcohol consumption and dependence on the quantification of both orange and red complex bacteria such as P. gingivalis, P. intermedia, F. nucleatum etc., as well as the presence of proinflammatory cytokines IL-1β and TNF-α within gingival fluid among individuals with and without periodontitis.²⁴ Out of 1010 individuals in the study, 468 were excluded due to not meeting the inclusion criteria. Of the remaining 542 individuals, 155 were selected by lottery and volunteered for microbiologic and immunologic examinations. Ultimately, 88 individuals were used in the observational study and were stratified into four different groups: individuals with alcohol dependence who had and did not have periodontitis, and individuals who occasionally consume or don’t consume alcohol who had and did not have periodontitis. Results from the study showed that the group with periodontitis who were dependent on alcohol presented with a significantly worse case of periodontal status compared to the other remaining three groups. Additionally, individuals in the group without periodontitis but who were dependent on alcohol had significantly higher plaque index, percentage of sites with bleeding on probing (BOP), percentage of CAL≥4mm, and less teeth compared to the group of individuals without periodontitis and who did not consume or occasionally consumed alcohol.²¹ Microbiologic results showed a significant difference between the study groups. The pathogens P. intermedia, E. corrodens, and F. nucleatum had significantly higher numbers in the periodontitis groups, in particular the group with periodontitis who were dependent on alcohol. However, there was no significant difference quantitatively with P. gingivalis and A. actinomycetmcomitans. The proinflammatory cytokine analysis showed no significant difference among the groups for TNF-α. However, a significant difference was seen in IL-1β for the group with periodontitis who were alcohol dependent compared to the other three groups. Finally, results showed a higher percentage of BOP, accompanied by higher E. corrodens and higher IL-1β levels. It is evident from this study that severity of periodontitis increases among alcohol users, and that the occurrence of disease is proportional to the frequency of alcohol consumption.^21,24 This study also highlighted that individuals with a dependence on alcohol showed higher plaque index levels and a higher severity of periodontitis. Although not highlighted in this study, it is important to be mindful that excessive amounts of alcohol consumption may increase biofilm formation and accumulation in the oral cavity due to alcohols ability to reduce salivary flow and cause dehydration.^21,25

In a more recent study performed by Gay et al., (2018),²⁶ the aim was to investigate the association between alcohol consumption and periodontitis in individuals 30 years or older living in the USA. This study used data from the National Health and National Examination Survey, and 7602 participants were included in the study who met the CDC American Academy of Periodontology periodontitis case definitions. This meant only dentate individuals with two or more teeth and with complete periodontal examinations were included. Results showed that of the 7602 participants, 3884 had periodontitis and was more prevalent among participants who were older, male, hispanic or black, with low income and education, current smokers, obese, and consuming 8 or more drinks a week. However, multivariable linear regression analyses when adjusting for confounding variables showed that participants who consumed 1– < 8, and ≥8 drinks per week had statistically significant higher mean PD, extent PD ≥4 mm, mean CAL, and extent CAL ≥3 mm scores compared to those who consumed < 1 drink per week. The study additionally found that there was a greater odds ratio of having severe periodontitis for participants who had ≥8 drinks compared to the consumption of some alcohol but < 1 drink per week. Results also showed that there were, however, no statistically significant differences in the odds of having periodontitis, mean PD, extent PD ≥4 mm, mean CAL, and extent CAL ≥3 mm between nondrinkers and participants that consumed < 1 drink per week. This study came to the conclusion that a potential biological reason in its results may be related to the amount of lipopolysaccharide (LPS) traveling to the blood vessels from the intestine due to bacterial translocation. This leads to the activation of TLRs on cells such as macrophages and monocytes which further induce the activation of proinflammatory cytokines.^26,27

Research on the relationship between alcohol consumption and periodontitis has often been restricted to cross-sectional observational studies, which were often at times underpowered with no definitive results.²⁶ Future research consisting of larger samples are necessary to help identify and understand the mechanisms involving the negative effects of alcohol on periodontitis and the possible explanation of the translocation of oral pathogen LPS to the bloodstream and proinflammatory cytokine production. However, such studies must be carefully executed when exploring their external validity, as well as the potential for issues to arise in participants exhibiting poor social behavior, emotional stability, and willingness to participate in such studies.

Dental management

The primary goal of dental management is to arrest, prevent progression, and prevent the re-occurrence of active disease and to resolve inflammation.²⁸ As periodontal disease varies in severity, it also varies in its dental management. Depending on factors such as the periodontal diagnosis and compliance level of the patient, there are different levels of dental management that include at-home care, non-surgical and surgical techniques.²⁸

All patients should be given oral hygiene instructions to follow for periodontal care at home, as a proper at-home regimen is essential to the resolution of periodontal disease at all levels of severity.²⁸ It is important to reinforce the importance of home care to patients as this will help to eliminate active disease, as well as prevent its recurrence after therapy.²⁸ It should be explained to the patient that although periodontal disease is multifactorial, proper periodontal care at home aims to eliminate biofilm and thus eliminate one of the primary factors responsible for producing inflammation and active disease.²⁸ Additionally, it is important that patients continue with proper home care regimens even after resolution of periodontal disease, due to possibility of recurrence.²⁸

While at-home care regimens carried out by the patient are essential to the management of periodontal disease, these regimens should be done in conjunction with periodic scaling and root planing of the crown and root surfaces by a dental professional.²⁸ For patients with more advanced stages of periodontitis that may not be responding to previous disease control attempts, there are various chemotherapeutic and host-modulating agents that have been found to be successful at controlling active disease.²⁸ Randomized clinical trials, systematic reviews, and meta-analysis found that the use of systemic antibiotics as an adjunct to scaling and root planing for patients with moderate to severe periodontal disease showed significant improvements in probing depth and clinical attachment gain, as well as a reduction in bleeding on probing and residual periodontal pockets.²⁸ These improvements were primarily observed with adjunctive use of amoxicillin and metronidazole.²⁸ Although more research is required, it has been found that host-modulating agents have been found to show significant improvement as an adjunct to scaling and root planing include doxycycline, omega-3 fatty acids and 81 mg acetylsalicylic acid.²⁸

After scaling and root planing is performed, patients should be scheduled for a periodontal re-evaluation four to six weeks later. It is at this re-evaluation appointment where a comprehensive periodontal exam is performed.²⁸ The periodontal charting from the re-evaluation appointment should be compared to the initial periodontal charting to determine whether the previous attempts at disease control have been successful, and whether the etiologic factors have been controlled.²⁸ If it is determined that the patient no longer has active periodontal disease, the patient can be placed on a two-to-six month recall schedule for periodontal maintenance therapy.²⁸ However, if it is determined at this re-evaluation that there is still active periodontal disease, scaling and root planing should be performed once again.²⁸ It is important to continue to emphasize the importance of maintaining the at-home periodontal care regimen and ensure that the patient is compliant.²⁸

If the patient is compliant with the at-home periodontal care regimens and periodic scaling and root planing are not showing clinical improvement at periodontal re-evaluations, there are surgical therapies that have been found to be effective.²⁸ However, if it is determined that the patient is not compliant with the at-home periodontal care regimen, surgical therapy should not be performed. This is due to the possibility of recurrence of periodontal disease, and if the patient is not vigilant with maintaining their periodontal health and control of biofilm, surgical therapy will not be effective.²⁸ The two primary surgical options include resective and regenerative periodontal surgery.²⁸ Resective surgery aims to reduce pocket depths by reducing or eliminating osseous defects (e.g. osteotomy or osteoplasty) or soft tissue resection, and regenerative surgery aims to increase periodontal attachment by re-establishing lost periodontal tissue (e.g. Guided tissue regeneration, enamel matrix derivative).²⁸

The role of the dentist

According to the Canadian Dental Association, approximately 75% of Canadians will visit a dentist once a year, and 86% of Canadians will visit a dentist at least one time every 2 years.²⁹ Additionally, dentists will see patients that may not be routinely visiting other healthcare professionals.³⁰ It is for this reason that dentists can have the opportunity to play a key preventative role to inform their patients about alcohol consumption.³⁰ However, although dentists have this unique opportunity, this information as well as any form of intervention are not routinely being provided due to barriers including lack of training, funding, time, and available resources.³⁰ One study reported that only 11.6% of practitioners were providing information to their patients about alcohol consumption on a regular basis, indicating that dentists need to better utilize their unique role as healthcare professionals by providing information and education about alcohol consumption, as well as any interventions to their patients.³⁰ Everyday, dentists will see patients who consume a variety of different levels of alcohol, and there are different levels of intervention, primarily centered around education, that dentists should be providing to their patients depending on that level of alcohol consumption.³⁰

For every patient, new or existing, the dentist should record the patient’s total alcohol consumption per week when they are taking or updating the patient’s medical history.³⁰ Based on the level of alcohol consumption, the dentist can then determine what level of preventive advice to provide the patient.³⁰ Table 2 includes information about units of alcohol, and Table 3 includes information about the different levels of risk.³⁰ Patients who are classified in the lower-risk category should be educated about the guidelines for lower risk individuals, whereas the patients who are classified in the increasingly higher risk categories should be educated about the guidelines for lower-risk individuals, as well as about their increased level of risk for alcohol-related sequelae.³⁰ This education includes information about the negative health effects of alcohol as well as the health benefits of reducing consumption and should be tailored specifically to each patient. Patients classified in the high-risk categories should also be referred to their medical doctor as well as alcohol support services in the community, as interprofessional care and support is crucial in these cases.³⁰ Although one of the reported barriers to educating patients about alcohol consumption may be time constraints, it has been found that screening patients for alcohol consumption as well as short interventions have proven to be very effective in reducing alcohol consumption.³⁰ Additionally, it was found that longer interventions did not significantly reduce patient alcohol consumption over the shorter interventions.³⁰

Table 2: Units of alcohol per drink type (Grocock R., 2018)

Drink type	Units of alcohol
Small glass of wine	1.6
Medium glass of wine	2.3
Large glass of wine	3.3
Bottle of wine	10
Pint of beer	2.3
Shot of spirits	1
Bottle of alcopop	1.5

Table 3: Risk category based upon alcohol consumption (Grocock R., 2018)

Category of risk	Woman	Men
Higher risk	35 units or more per week	50 units or more per week
Increased risk	14 to 35 units per week	14 to 50 units per week
Lower risk	2 to 3 units per day regularly, with a weekly maximum of 14 units	2 to 3 units per day regularly, with a weekly maximum of 14 units

Dentists can use motivational interviewing as an intervention strategy for patients’ alcohol consumption.³¹ Motivational interviewing is a patient-centered strategy with the purpose of motivating patients towards healthy behavior changes.³¹ The role of the dentist is to guide and support the patient towards a goal, rather than simply giving them instructions to follow. Motivational interviewing has been found to be a successful intervention strategy in practice, and particularly effective for alcohol consumption.³¹ Its effectiveness as an intervention strategy is supported by both randomized controlled trials and systematic reviews.³¹ Of the extensive research on the effectiveness of motivational interviewing, one meta-analysis that includes 72 randomized controlled trials investigated its effectiveness on substance abuse.³¹ This study demonstrated that motivational interviewing was effective for these patients.³¹ Another review of four meta-analyses also showed a significant reduction of 10%–20% in negative health behaviours such as substance abuse in those patients that received motivational interviewing, compared to the patients that did not.³¹ An additional advantage of motivational interviewing by dentists is the short amount of time that this intervention requires. As discussed previously, it was found that one of the reported barriers to educating patients about alcohol consumption may be time constraints, and that it has been found that short interventions have proven to be very effective in reducing alcohol consumption.³⁰ There are brief forms of motivational interviewing to provide shorter interventions in the range of 5 to 20 minutes, including forms that exist specifically targeted towards those patients in the high-risk categories.³¹

In addition to behavioral counseling, dentists should be aware of the psychological treatments, or psychotherapy, available to assist patients in reducing their alcohol consumption. Of these psychological treatments, the most common one is cognitive behavioral therapy, which involves both behavioral and cognitive behavioral interventions targeted to assist patients in achieving positive changes.³² Cognitive behavioral therapy has proven to be successful when used for alcohol use disorders, and this is supported by a meta-analysis that includes 34 randomized controlled trials that reported an overall moderate effect.³² In addition to psychotherapy, dentists should also be aware of the other various referral pathways and help services that exist in their community that are available to assist and support patients, including programs and services such as alcoholics anonymous or SMART recovery.³³

While behavioral counseling and psychological treatment can be very effective for some patients, it may not be as successful for others. The current three Health Canada approved medications for alcohol use disorder include Disulfiram, Naltrexone, and Acamprosate.³⁴ It is important to note that pharmacotherapy should be used alongside behavioral counseling and psychotherapy, as this has been found to be more successful.³²

There are existing intervention strategies or frameworks that can be used to assist patients with smoking cessation, that could also be applicable or adapted to assist patients with reduction or cessation of alcohol consumption. An effective framework that is used in the dental setting to provide tobacco cessation intervention is the 5As approach.³⁵ The 5As are ask, advise, assess, assist and arrange, with more information found in Table 4.³⁵ This framework is used to assist patients with individual treatments and potential referrals, and arrange follow-up visits to support cessation.³⁶ The 5A model guides the healthcare practitioner through the correct process to talk to patients who are ready to quit tobacco use to deliver personalized advice, develop a cessation plan and connect them to referral services if need be.³⁵

Table 4: The 5As Framework for assisting patients with cessation (Cadet, 2018).

Ask	Ask all patients over 18 years of age about their tobacco usage. Document patients smoking status in their chart.
Advice	Advise those patients who are current smokers to quit smoking. Advice should be personalized to the patient based on their reason for wanting to quit smoking.
Assess	Assess the patient’s willingness and readiness to quit. Assess the patients smoking history, possible barriers to quitting, as well as past quit attempts and perhaps why those quit attempts were unsuccessful
Assist	Assist the patient’s quit attempt. This includes assisting with their quit plan and providing them with resources such as pharmacotherapy.
Arrange	Arrange for future follow-up appointments with the patient, as well as counseling therapy appointments.

Conclusion

Although both alcohol and periodontal disease have been researched extensively, the impact of alcohol consumption on our oral cavity, specifically how it can contribute to the multifactorial destruction of periodontal disease is an understudied area in the dental field. It has been found that the severity of periodontitis is proportional to the frequency of alcohol consumption, as well as causing an increase in plaque index. However, future research with larger sample sizes are necessary to better understand the mechanisms involving alcohol’s deleterious effects on the periodontium. It is important that dental professionals understand their role in recognizing alcohol abuse, assisting patients who abuse alcohol, as well as educating about alcohol consumption, specifically emphasizing the negative health effects that alcohol consumption can have on the oral cavity, and the intimate connection that the oral cavity has with the rest of our body. It is also because of this intimate connection that interprofessional collaboration is important when assisting patients to reduce their alcohol consumption. Dentists should communicate and work together with family physicians, as well as be aware of the various referral pathways available to patients in the community that can provide support and further education to patients. 

Oral Health welcomes this original article.

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About the author

Mr. Stefan Radovic is a 4th year dental student at the faculty of Dentistry, University of Toronto.

Mr. William Irwin is a 4th year dental student at the faculty of Dentistry, University of Toronto. 

Dr. Aviv Ouanounou is an associate professor of Pharmacology & Preventive Dentistry at the Faculty of Dentistry, University of Toronto, and a clinical instructor and Treatment Plan Coordinator in the university clinics. He is the recipient of the 2014-2015 Dr. Bruce Hord Master Teacher Award for excellence in teaching and the 2018-2019 National W.W. Wood Teaching Award for Excellence in Dental Education. He is a Fellow of the International College of Dentists, American College of Dentists and Pierre Fouchard Academy. Dr. Ouanounou maintains a private practice in Toronto and is the corresponding author for this article. Reach him at aviv.ouanounou@dentistry.utoronto.ca.