Destructive Periodontal Disease and Tobacco and Cannabis Smoking

Destructive periodontal disease consists of loss of the supporting tissues of the teeth and can lead to tooth mobility, tooth migration, and eventual tooth loss. Enjoyments in life such as eating; relaxing; going out; and being free of pain, discomfort, and self-consciousness are adversely affected by destructive periodontal disease in 20% of periodontal patients seeking specialist care.¹ In the United States, the prevalence of destructive periodontal disease decreased from 7% in 1988 to 4% in 1999 and 2000.² In 1999, about $14 billion was spent on treating and preventing destructive periodontal disease.³

For most of the latter half of the 20th century, destructive periodontal disease was considered a disease that occurred after the age of 35 years, caused primarily by dental plaque and largely unrelated to lifestyle choices. These hypotheses were mostly based on animal studies, gingivitis studies, and case series but not controlled epidemiological studies on destructive periodontal disease.

In this issue of JAMA, Thomson and colleagues⁴ present the findings of a cohort study that have the potential to help eliminate some established beliefs and bring a more evidence-based approach to an understanding of the etiology of destructive periodontal disease, including the role of cannabis smoking. The cohort study consisted of 903 participants with self-reported tobacco and cannabis smoking information collected at the ages of 18, 21, 26, and 32 years and with half- and full-mouth dental examinations at the ages of 26 and 32 years, respectively. An average frequency measure of cannabis smoking at each of the 4 examinations was related to attachment loss (a linear measure of periodontal support destruction), which is a surrogate measure of destructive periodontal disease. Using this surrogate measure, the authors found that tobacco and cannabis smoking was associated with an increased incidence of destructive periodontal disease before the age of 32 years, whereas dental plaque was not.

Strengths of this study include the representative birth cohort, the high proportion of participants with dental follow-up (88%), the dose-response relationships between cannabis use and destructive periodontal disease, and the significant association between cannabis smoking and destructive periodontal disease among those who never smoked tobacco. Because the lower confidence limit of the relative risk is close to a null finding, biases due to residual confounding by lifestyle factors associated with cannabis use and reverse causality should be considered. Dental plaque and socioeconomic status were measured after baseline and after the periodontal destruction occurred, not at baseline or before incident disease as is usual in cohort studies. Because periodontal examinations occurred 8 years after baseline, the cohort at baseline may have been a mixture of individuals with and without signs of destructive periodontal disease, rather than a cohort of disease-free individuals at the start of follow-up.

Dental care and attachment loss were both ascertained between the ages of 26 and 32 years, making it difficult to determine which occurred first. Tooth loss at baseline or during follow-up (the ultimate dental outcome) and its potential relationship to cannabis smoking were not reported. As a result of these factors, the temporal sequence of cause and effect was difficult to disentangle and may have contributed to biases. As the authors indicate, it will be important to replicate the novel findings on cannabis smoking in other populations. If further studies confirm cannabis smoking as a potential factor contributing to destructive periodontal disease, it may offer opportunities to narrow which common elements of tobacco and cannabis smoke are related to the periodontal damage.

The study by Thomson et al adds to growing evidence that destructive periodontal disease occurs at a much younger age than previously believed. Obesity has been associated with signs of destructive periodontal disease in persons as young as 17 to 21 years.⁵ Impaired glucose metabolism has been associated with destructive periodontal disease in 12- to 18-year-olds.⁶ The study by Thomson et al confirms that tobacco smoking is associated with onset of destructive periodontal disease before the age of 35 years^{4 ,7} and moreover may be “the primary behavioral risk factor”⁴ for destructive periodontal disease.⁸ However, in the study by Thomson et al, dental plaque was—to paraphrase Sir Arthur Conan Doyle—the dog that did not bark, or at least not very loudly. Incident destructive periodontal disease was unrelated to dental plaque, whereas prevalent destructive periodontal disease was inconsistently related to dental plaque (Table 5 in the article). The lack of a strong association between dental plaque and destructive periodontal disease is consistent with a systematic review on this topic.⁹ Although dental plaque may play a role in the secondary prevention of destructive periodontal disease, it is becoming increasingly apparent that an evidence-based approach to the primary prevention of destructive periodontal disease should include smoking prevention and cessation and the adoption of healthy eating habits.

Destructive periodontal disease may well be the canary in the coal mine for chronic noncommunicable diseases (CNCDs), as was suggested 34 years ago.^{10 - 11} Smoking and unhealthy eating habits lead to destructive periodontal disease as well as to CNCDs such as diabetes, cardiovascular disease, and certain cancers in late adulthood. The presence of strong common causal factors suggests the need for a synergistic approach to preventing a substantial proportion of both destructive periodontal disease and CNCD cases; primary prevention of destructive periodontal disease should help reduce CNCDs, and primary prevention of CNCDs should help reduce destructive periodontal disease. The latter may already have occurred; successful smoking prevention and cessation programs aimed at reducing cancer and cardiovascular mortality may have inadvertently reduced the incidence of destructive periodontal disease, even before tobacco use became widely recognized as a cause of destructive periodontal disease.

Analogously, dental policy and research priorities aimed at the primary prevention of destructive periodontal disease can help reduce the occurrence of CNCDs. Professional dental organizations have been involved in policies or programs such as raising public awareness about issues such as sugar-laden junk food and dental health, in promoting smoking cessation programs in dental offices, in changing health behaviors, in increasing “the availability and consumption of healthy foods”¹¹ in school programs, and in providing appropriate physician referral when suspecting dental signs of potential drug abuse such as methamphetamine-associated caries. The findings reported by Thomson et al suggest that cannabis smoking could be added to the list of recreational drugs with potential dental consequences. Primary prevention of destructive periodontal disease (as well as dental caries) may lead to benefits beyond dental health and may have greater implications for general health than realized so far.

In summary, Thomson and colleagues have reported findings indicating that smoking of tobacco and potentially cannabis are associated with evidence of destructive periodontal disease that can be detected in early adulthood, long before other smoking-related diseases such as diabetes, cardiovascular disease, and certain cancers become apparent. Given the high prevalence of dental care in the young population in the United States, the dental profession has an opportunity to detect the early clinical signs of unhealthy lifestyles, including potential drug abuse, and could play a role with physicians in addressing the challenges of reducing CNCDs.^{11 - 12}