Role of Poor Oral Hygiene in Causation of Oral Cancer—a Review of Literature

Abstract

Oral squamous cell carcinomas (OSCC) are among the commonest cancers in South East Asia and more so in the Indian subcontinent. The role of tobacco and alcohol in the causation of these cancers is well-documented. Poor oral hygiene (POH) is often seen to co-exist in patients with OSCC. However, the role of poor oral hygiene in the etio-pathogenesis of these cancers is controversial. We decided to evaluate the available literature for evaluating the association of POH with OSCC. A thorough literature search of English-language articles in MEDLINE, PubMed, Cochrane Database of Systematic Reviews, and Web of Science databases was conducted, and 93 relevant articles were short-listed. We found that POH was strongly associated with oral cancers. It aids the carcinogenic potential of other known carcinogens like tobacco and alcohol. Even on adjusting for known confounding factors like tobacco, alcohol use, education, and socio-economic strata, presence of POH exhibits higher odds of developing oral cancer.

Introduction

Oral squamous cell carcinomas (OSCC) are one of the most common cancers in the Indian subcontinent. India has the highest incidence of OSCC patients in the world. In 2015, approximately 80,000 new cases of OSCC were reported in the country and approximately 50,000 died of it [1]. This is a matter of grave concern not only for the health care professionals but also for the public at large.

Tobacco and alcohol consumption have been thought to be the major culprits for causing OSCC. OSCC prevalence is higher in areas where tobacco is used in smokeless forms. It is believed that apart from established etiological factors like tobacco, alcohol, and areca nut, other factors like chronic mucosal trauma [2, 3, 4], poor nutrition [5, 6], and poor oral hygiene (POH) may contribute to oral carcinogenesis [7].

POH has been considered as a risk factor for causing OSCC in several studies [8–10, 11]. Still, there is a definite lacuna in the knowledge about oral hygiene as a cause for OSCC and its etio-pathogenic mechanism. Therefore, through this review of literature, we have tried to shed light on the impact of POH on oral carcinogenesis.

Methodology

We searched the databases MEDLINE, PubMed, Cochrane Database of Systematic Reviews, and Web of Science through November 2017. The search terms used were “oral cancer,” “mouth neoplasm” (which is a mesh term for oral cancer), “oral hygiene,” “missing teeth,” “halitosis,” “bad odor,” and “teeth brushing.” These were searched as text word and as subject headings individually as well as in different combination which accounted for a total of 523 articles. While searching for “mouth neoplasm” and “oral cancer” with “bad odor,” we could not get any results. Abstracts, headings, and titles of all the results were studied, and we excluded repetitions and those which failed to describe the factors of interest for the study. We short-listed 93 relevant articles, including retrospective studies, review articles, case-control studies, questionnaire-based surveys, cohorts, and randomized control trials. Some cross-references from these articles, which were found to be relevant for the topic, were also included.

Quantification of Poor Oral Hygiene

The assessment of oral hygiene is mostly done subjectively. There have been efforts to quantify it or objectively assess it. It has been quantified using various indices, like the Oral Hygiene Index—Simplified (OHI-S), Community Periodontal Index and Treatment Needs (CPITN), Plaque Index (PI), Gingival Index (GI), and Decayed Missing Filled Teeth Index (DMFT). Although they bring uniformity, most of the indices are highly complicated and can be used only by trained dental professionals. During our review of literature, we found that the majority of studies, instead of using these indices, utilized various other parameters as a measure of POH, like tooth brushing frequency, regular dental visit, number of missing teeth in oral cavity, and use of mouthwash/dental floss.

Causative Factors of Poor Oral Hygiene

Factors contributing to POH include irregular teeth brushing habits, less number of dental visits, poor socioeconomic status, lower level of education, tobacco, and alcohol consumption (Fig. 1)

Fig. 1.

Factors and mechanisms by which poor oral hygiene can cause oral carcinogenesis

Tooth Cleaning Habits

In the Indian subcontinent, a large number of people still do not use tooth brush and paste to clean their teeth. A case-control study in southern India assessed the influence of smoking, alcohol, paan (betel quid) chewing, and oral hygiene in causation of OSCC in 591 cases and 582 controls [12]. They found that majority of participants, both cases and controls, (80.73%) did not brush teeth more than once daily. Females who brushed their teeth once or even less daily had significantly increased risk of OSCC (OR 3.39). Even individuals who used their fingers for cleaning of teeth had significantly higher chances of oral malignancy irrespective of gender (males OR = 1.75; females OR = 3.40) compared to those who used tooth brush. A large number of males diagnosed with OSCC in this study were found to use various teeth cleaning aids other than tooth brush and fingers (OR = 3.65, 95% CI 1.50–8.84). People still use plant sticks [9, 12], salt [13], ash [14], charcoal [15], and even brick powder to clean their teeth [13, 14]. Even tobacco is used as a tooth cleaning agent in certain parts of India [15], available by various names viz. Gul-manjan, Masheri, and gadakhu. In another case-control study assessing dental and periodontal status in patients with OSCC, it was found that 93.4% of cancer cases reported to have brushed their teeth less than once daily as compared to 81.1% controls [9]. In an analysis of two multi-center case-control studies held in Central Europe and Latin America, it was found that lack of tooth brush use-causing POH were risk factor for HNC (independent of tobacco and alcohol use) [8]. A meta-analysis assessing 18 case-control studies has highlighted the advantageous role of brushing teeth twice daily in reducing the risk of HNC to half (OR = 2.08, 95% CI = 1.65–2.62) [16] (Table 1).

Table 1.

Association of frequency of teeth brushing (fully adjusted for confounding factors) as a causative factor of Oral Squamous Cell Carcinoma (OSCC)/ Head and Neck Cancer (HNC)/ Carcinoma of Oral Cavity and Oropharynx (OCP)/ Upper Airway and Digestive Tract (UADT)Cancers

STUDY	COHORT	FREQUENCY	OR	CI
Chen [15]	OSCC	>=2	0.88	0.46-1.68
Chang [16]	OSCC	>=2 <2	1 1.45	- 0.92-2.27
Guneri [17]	OSCC	<1	0.170	-
Balaram [10]	OSCC	<=1	M= 0.96 F = 3.39	0.59–1.59 1.65–6.98
Talamini [18]	OSCC	>=2 1 <1	1 1.1 1.4	- 0.5-2.4 0.6-3.3
Zheng [19]	OSCC	Never	M= 6.9 F = 2.5	2.5 - 19.4 0.9 - 7.50
Franco [20]	OSCC	Infrequent	2.3	1.4-3.7
Kawakita [21]	HNC	<=1	1.13	0.89-1.44
Hashim [22]	HNC	1/Day	0.83	0.79-0.88
Tsai [23]	HNC	<2	1.40	1.02–1.91
Guha [7] (Central Europe)	HNC	>=2 1 <1 Never	1 1.38 1.00 1.37	- 0.79-2.41 0.51-1.95 0.65-2.88
Guha [7] (Latin America)	HNC	>=2 1 <1 Never	1 0.94 0.74 1.20	- 0.67-1.32 0.44-1.23 0.30-4.79
Marques [24]	OCP	1-2 <1 Never	0.7 0.7 1.3	0.5-1.2 0.3-1.5 0.4-4.5
Garrote [25]	OCP	>=2 1 <1	1 1.17 1.94	- 0.52-2.66 0.83-4.50
Ahrens [26]	UADT	2/Day 1/Day 1-4x / Week <1/WeekORNever	1 1.25 1.39 1.37	- 1.03-1.53 1.03-1.87 0.95-1.99
Sato [27]	UADT	Not brushing Once daily Brushing>1/ day	6.11 1 0.81	1.35-27.6 - 0.57 -1.14

Surprisingly, there have been a couple of studies which have failed to find any correlation between tooth cleaning habits, POH, and OSCC. A case-control study could not find any association between the frequency of tooth brushing in causing cancers of upper airway and digestive tract (UADT) [8, 30, 31].

Frequency of Dental Visits

Due to the symptomatology associated with oral cancers, dentists are often the first contact person for oral cancer detection [32]. Thus, higher frequency of their consultation would certainly help in maintaining oral hygiene and allow early detection of cancer or precancerous lesions [33–35]. A pooled analysis of 13 case-control studies with a large sample size assessed the association of POH and head and neck cancers (HNC). They hypothesized that annual dental visits were associated with more than 25% reduction in HNC for patients with gingivitis/periodontitis (OR = 0.82; 95% CI 0.78, 0.87) [24]. A case-control study in an Indian tertiary care center pointed that all of the OSCC patients evaluated in the study for oral hygiene status used to visit dentist less than once a year [36]. These results were quiet similar to that of Laprise et al. who found that 93% of the oral cancer cases did not visit a dentist on regular terms [37]. Narayan et al. in their study found that more than half of the cases (57.85%) never had a dental visit when compared to controls (46.06%) [9]. Balaram et al. found dental check-up gives significant protection from cancers of oral cavity in females (OR 0.4 with 95% CI of 0.19–0.87), but it was not found to be significant in males (OR = 0.89 with 95% CI 0.56–1.42) [12] (Table 2).

Table 2.

Association of Number of dental visits (fully adjusted for confounding factors) as a causative factor of Oral Squamous Cell Carcinoma (OSCC)/ Head and Neck Cancer (HNC)/ Carcinoma of Oral Cavity and Oropharynx (OCP)/ Upper Airway and Digestive Tract Cancers (UADT)

STUDY	COHORT	FREQUENCY	OR	CI
Chen [15]	OSCC	0/Year <1 >=1	1 0.92 0.39	1 0.35-2.38 0.08-1.85
Chang [16]	OSCC	Every 6 months or less 6-12 No	1 0.81 3.73	1 0.13-4.96 1.60-8.72
Guneri [17]	OSCC	Infrequent	0.171	-
Rosenquist [36]	OSCC	Regular	0.4	0.2-0.6
Balaram [10]	OSCC	Yes	M= 0.89 F= 0.41	0.56–1.42 0.19–0.87
Talamini [18]	OSCC	>=1 in 5 years <1 in 5 years	0.8 1.1	0.4-1.6 0.5-2.6
Franco [20]	OSCC	<1/ year >=1/ year	0.6 0.6	0.3-1.3 0.1-2.3
Kawakita [21]	HNC	>=1 /year 1/ 2-4 years 1/>=5 years never	1 1.72 2.09 3.70	1 1.10-2.67 1.40-3.14 2.51-5.45
Hashim [22]	HNC	>=1/ year	0.82	0.78-0.87
Tsai [23]	HNC	<=6 months 6-12 months No	1 0.78 2.19	- 0.30-2.04 1.30-3.70
Divaris [37]	HNC	Routine visit	0.68	0.53-0.87
Marques [24]	OCP	Occasional Never	1.5 2.25	0.8-2.8 1.3-4.8
Garrote [25]	OCP	>=1 in 5 years <1 in 5 years	1.61 0.71	0.83-3.07 0.64-1.86
Ahrens [26]	UADT	Every year 2-5 years <5 years never	1 1.25 1.52 1.93	1 1.02-1.53 1.23-1.87 1.48-2.51

Education Level

A questionnaire-based survey among Brazilian population found that the education level among the subjects had a direct influence on the knowledge about main oral diseases [40]. An Indian study categorized the participants in the study by their level of education as no education, basic education (up to 6 years), and higher education and found that OSCC cases were significantly lesser educated as compared to control subjects. This study also showed direct association between the level of education of spouse and risk of cancer [12]. A Chinese study assessing the influence of oral hygiene and its interaction with standard of education on the risk of oral cancer in women (adjusted for smoking and alcohol use) found that protection assumed due to tooth brushing twice a day was negated if the education of the subject was below high school. Only females with no habit abuse were included in this study; thus, there were no other confounding factors [17].

Arecanut, Tobacco, and Alcohol

Arecanut, tobacco, and alcohol habits may result in POH. These habits are an independent etiological factor for oral cancer [40–42]. They also promote POH which in turn may act as contributory factor for oral cancer [43]. Arecanut has been proven to cause POH, periodontal diseases, and precancerous conditions, which further deteriorates oral hygiene. Maier et al., in a Germany-based case-control study, have described chronic alcoholism to be a causative factor for neglecting oral health, leading to POH [33, 44, 45]. Tobacco use deteriorates oral hygiene represented by various indicators like tooth loss, dental caries, and periodontal diseases [46, 47].

Poor Oral Hygiene—an Additive Factor for Oral Carcinogenesis

1. Poor oral hygiene and areca nut: Areca nut usage is associated with oral pre-malignant conditions, such as oral submucous fibrosis, as well as OSCC. The particles of areca nut itself along with the oral submocous fibrosis being a resultant of areca nut chewing cause POH in quid chewers. This has predominantly been seen in South-Central and South-East Asia, where areca nut usage is very common not only as a habit but also as a part of culture and religious customs. Moreover, the individuals consuming it, especially without tobacco, are not even aware of its adverse effects. The OSCC which develops in the presence of oral sub-mucous fibrosis is believed to be a clinico-pathologically distinct entity.

2. Poor oral hygiene and tobacco: The role of POH in the formation of N-nitroso compounds was investigated by means of the NPRO assay. Endogenous nitrosation was significantly higher in tobacco chewers with POH (having greater plaque levels) compared to those who had good oral hygiene [48, 49]. NPRO levels in saliva of subjects with POH were found to be higher (190 μg NPRO/L) compared to those with good oral hygiene (24 μg NPRO/L) [50]. A case-control study assessing the oral conditions as risk factors for oral cancers found that the participants who smoked tobacco had greater missing teeth, representing POH were at greater risk of having oral cancer (OR = 7.3) than those who had a maintained oral hygiene and smoked tobacco (OR = 2.0) [21]. Thus, formation of nitrosamines is more extensive in tobacco users who have POH than those with better oral hygiene, thereby increasing the carcinogenic potential of tobacco.

3. Poor oral hygiene and alcohol: Alcohol is a known carcinogen involved in causation of oral cancer [51, 52]. A Chinese case-control study found that subjects who consumed alcohol and had POH (represented by inadequate dentition) had 5 times more risk of having oral cancer (OR = 9.1, 95% CI = 4.4–19) than those who just consumed alcohol but maintained a good oral hygiene (OR = 1.8, 95% CI = 0.7–4.7) [21]. According to a case-control study, the attributable risk percentage for causing OSCC due to alcohol consumption was 26% while that due to POH was 32%. This clearly shows that the effect of POH in causing OSCC was more significant as compared to that of alcohol in this particular study [12].

4. Periodontitis and tooth loss: POH is the main etiological factor for periodontitis [53], a plaque-induced chronic inflammatory disease. Tooth loss is an end result of POH [18] and is reported to be associated with oral cancer [54]. According to a meta-analysis studying relationship of tooth loss and HNC, tooth loss was found to be a significant risk factor for developing HNC. In fact, it was noted to have a dose-response effect too (> 5 vs. ≤ 5 OR 2.00, 95% CI 1.28–3.14; p =  0.002) [55]. However, this meta-analysis had substantial heterogeneity in the included studies (I²  =  82.9%; P  =  0.000). People who lost six or more teeth are at a higher risk of HNC, and losing 11–15 teeth may be the threshold. Out of twelve studies included in this meta-analysis, seven were related to cancer of oral cavity and pharynx. A Chinese hospital-based case-control study aimed to assess the role of oral hygiene and dental conditions in the genesis of oral cancer. They found a strong correlation of missing teeth, which reflected POH, as a strong risk factor for oral cancer after adjustment for tobacco smoking and drinking habits. They found that adjusted ORs in males for missing 3–6 teeth were 4.9 with 95% CI (2.4–10) and for 7–14 teeth were 5.9 with 95% CI (2.8–12.2) [21, 56–58]. A questionnaire-based European case-control study with 8925 HNC cases and 12,527 controls found that HNC were inversely associated with < 5 missing teeth (OR = 0.78; 95% CI 0.74–0.82) [24] (Table 3).

Table 3.

Association of number of missing teeth (fully adjusted for confounding factors) as a causative factor of Oral Squamous Cell Carcinoma (OSCC)/ Head and Neck Cancer (HNC)/ Carcinoma of Oral Cavity and Oropharynx (OCP)/ Upper Airway and Digestive Tract Cancers (UADT)

STUDY	COHORT	FREQUENCY	OR	CI
Chen [15]	OSCC	<=5 >5	2.53 2.84	0.99-6.48 1.10- 7.34
Chang [16]	OSCC	1-10 10-20 >20	1.15 1.34 2.40	0.61-2.20 0.58-3.07 0.97-5.97
Guneri [17]	OSCC	More natural teeth (case, control)	Mean Cases= 12.04 Controls= 19.3	- - -
Rosenquist [36]	OSCC	>20	3.4	1.4-8.5
Balaram [10]	OSCC	>5	M=3.89 F= 7.61	2.46–6.17 3.89–14.88
Talamini [18]	OSCC	<5 6-15 >= 16	1 1.1 1.4	1 0.5-2.6 0.6-3.1
Zheng [19]	OSCC	Inadequate dentition	3.9	2.1-7.4
Kawakita [21]	HNC	<5 >=5	1 1.49	1 1.08-2.04
Hashim [22]	HNC	<5	0.78	0.74-0.82
Divaris [37]	HNC	0-5 6-15 16-28	1 1.07 1.21	1 0.81-1.42 0.94-1.56
Guha [7] Central Europe	HNC	6-15	2.84	1.26-6.41
Guha [7] Latin America	HNC	6-15 >=16	0.87 1.21	0.56-1.35 0.77-1.90
Garrote [25]	OCP	<=5 6-15 >=16	1 1.82 2.74	1 0.76-4.35 1.23-6.12

Mechanism of Action

POH may not be a direct causative agent for oral carcinogenesis, but it certainly catalyzes the process by increasing the carcinogenicity of known carcinogens.

1. Tobacco: Formation of nitrite and nitric oxide in the presence of POH status occurs [8]. Increased formation of nitrite and nitric oxide in the mouth was found in people with dental plaque [48], and bacterial enzyme-mediated formation of nitrosamines has been reported [59]. Nitrate, after its absorption in the upper gastrointestinal tract, reaches the salivary glands via the blood circulation where it is secreted into the oral cavity and partially reduced to nitrite by the oral microflora [60]. Conventional smoking has been found to be the strongest signal of subsequent smoking, e-cigarette use, and nicotine dependence [61]. At least 36 carcinogens have been documented in smokeless tobacco, whereas the International Agency for Research on Cancer has found over 60 carcinogens in cigarette smoke for which there is “sufficient evidence for carcinogenicity” in either laboratory animals or humans [62].

2. Alcohol: Alcohol is a known carcinogen. Induction of cytochrome P-4502E1-producing free radicals, alterations in normal cell cycle causing hyperproliferation, alterations of the immune system, etc. are various mechanisms by which alcohol causes carcinogenesis [63]. The main carcinogen in alcohol is acetaldehyde which is a group 1 carcinogen. The bacteria prevalent in oral cavity have been hypothesized to convert ethanol in alcohol to aldehyde [64–66]. Tsai et al. in a Taiwanese case-control study found that POH and genetic polymorphisms of alcohol-metabolizing genes (ADH1B and ALDH2) modify the process of carcinogenesis in chronic alcoholics. Although complete abstinence or reduction in alcohol consumption will definitely decrease the occurrence of HNC, a good oral hygiene is supposed to provide additional benefits [25].

3. Areca nut: Areca nut (a group 1 carcinogen) usage is associated with oral pre-malignant conditions, such as oral submucous fibrosis, as well as OSCC which is believed to be a clinico-pathologically distinct entity [67]. Areca nut extracts cause inhibition of growth, attachment loss, and cessation of matrix protein synthesis of cultured gingival fibroblasts; hence, betel nut chewing affects periodontal health and predisposes to colonization and periodontal disease [68]. Also, the particles of areca nut are hard, which causes abrasion of tooth surfaces. These sharp teeth surfaces cause chronic mucosal trauma which is associated with the development of carcinogenesis [69]. A non-interventional case-control study found significant levels of IL-6 (p < 0.001) and IL-8 (p < 0.0001) in salivary samples of areca nut chewers [68, 70].

4. C. albicans: Though not very well proven, few retrospective studies have found correlation between C. albicans and oral cancer. Oral cavities with POH may develop opportunistic infections. Candidiasis is one of the commonest lesions in immunocompromised individuals [71]. C. albicans invades keratinocytes either by digestion of surface components of epithelial cells or by surrounding itself by pseudopod-like structures. C. albicans present in oral cavity of an immunocompromised individual can form nitrosamines from their precursors, thereby leading to oral cancer [72]. A case-control study also found a significant association between oral colonization of Candida and oral cancer occurrence (OR = 3.242; 95% CI = 1.505–6.984) [73].

5. Porphyromonas gingivalis: P. gingivalis, one of the chief pathogens to cause acute periodontitis, has been reported to promote the invasion and metastasis of highly invasive oral cavity cancers [74]. In individuals with POH/periodontitis, infection with P. gingivalis is very common. A case-control study reported P. gingivalis infection in 79% of patients with periodontitis, which was statistically significant (p < 0.0001) [75, 76]. P. gingivalis aids in cancer formation and its metastasis by activation of promatrix metalloproteinase [74, 77] and also by anergy and apoptosis of activated T cells [77, 78] as explained in Fig. 2.

Fig. 2.

Mechanisms of carcinogenesis by Porphyromonas gingivalis in the presence of poor oral hygiene

Oral Hygiene and Oral Cancer

Though most of the studies found POH as an additive factor in causation of oral cancer [79–83], some studies have reported a stronger correlation between the two [84]. A case-control questionnaire-based study adjusted for tobacco and alcohol habit proposed that POH may be a sole causative factor of OSCC. Inclusion criterion for the study was absence of habit abuse among the oral cancer patients; thus, confounding factor in the form of tobacco (smokeless or smoked) and alcohol was said to be negated [85]. However, the study was confined to two specialist hospitals, with low sample size (= 60). The content of the material used for tooth brushing was not mentioned. Oral cavity cancers show ethnic variation, which has also been missed out in the study [86]. An Indian retrospective tertiary hospital-based case-control study found that 79% of the cases of SCC of the oral cavity and oropharynx failed to have a good oral hygiene, compared to the 36% of controls [36]. Similarly, another Indian retrospective study evaluating etiological factors and patient characteristics in oral cancer on 337 patients found that 71% of the cases had poor to very POH [87]. A European case-control study assessed the association of oral health (OH), dental care (DC), and mouthwash use with upper-aerodigestive tract (UADT) cancer risk [28]. They have hypothesized POH as an independent risk factor for UADT cancers. Though almost half of the cases included in the study were oral cavity and oropharynx, the cases with poor oral health (having OH score > 6) were at double the risk of developing oral cavity and oropharyngeal cancers (OR = 2.00, 95% CI = 1.21–3.31) as compared to those with better oral hygiene (having OH score = < 6) (Table 4).

Table 4.

Association of Poor Oral Hygiene (fully adjusted for confounding factors) as a causative factor of Oral Squamous Cell Carcinoma (OSCC)/ Head and Neck Cancer (HNC)/ Carcinoma of Oral Cavity and Oropharynx (OCP)/ Upper Airway and Digestive Tract Cancers (UADT)

STUDY	COHORT	FREQUENCY	OR	CI
Hashim [22]	OSCC	>=4 3 2 <=1 Worst	1 2.45 2.42 3.12	- 1.93-3.12 1.87-3.15 2.08-4.68
Subapriya [86]	OSCC	Poor	9.63	-
Balaram [10]	OSCC	Poor	M=4.90 F= 5.99	3.09–7.78 3.00–11.96
Talamini [18]	OSCC	Good Average poor	1 1.8 4.5	- 0.9-3.6 1.8-10.9
Kawakita [21]	HNC	0 (Best) 1 2 >=3 (Worst)	1 1.99 1.88 4.76	- 1.41-2.82 1.30-2.71 2.88-7.85
Tsai [23]	HNC	1 (Good) 2 3 4 (Poor)	1 3.50 3.40 5.64	- 1.56-7.87 1.54-7.47 2.48-12.83
Guha (2007) [7] Central Europe	HNC	Poor Average	4.51 2.24	1.95-10.44 1.19- 4.21
Guha (2007) [7] Latin America	HNC	Poor Average	2.91 1.28	1.87-4.52 0.84-1.96
Dholam [34]	OCP	OHI-S score= 0-2 (Good) OHI-S score= 3-4 OHI-S score= 5-6 (Poor)	1 4.385 17.4000	- 2.112–9.101 5.858–51.686
Rosenquist [36]	OCP	Good Average Poor	1 2.0 5.3	- 1.1-3.6 2.5-11.3
Garrote [25]	OCP	Good Average Poor	1 1.82 2.55	- 0.94-3.53 1.24-5.24
Ahrens [26]	UADT	Low vs High	2.22	1.45-3.41

Poor oral hygiene has been hypothesized to contribute to causing oral cancer. However, it may be stated that good oral hygiene may act as a protective barrier against oral cancer [28, 45, 89]. Though many studies from around the world have found a significant or strong correlation between the POH and OSCC/HNC, many still did not find any correlation between the two [8, 27, 90, 91]. Among the Indian population, buccal mucosa forms the commonest site involved in OSCC [9, 36, 37, 88]. If oral hygiene would have been responsible for oral cancer, then we would expect cancer to occur at sites which are more prone to have poor hygiene. Lingual surface of lower incisors have maximum plaque accumulation [92] resulting POH due to lack of maintenance in that particular region, but anterior floor of mouth and anterior lower alveolus are not the most common sites of oral cancers. Thus, reason for buccal mucosa involvement more convincingly appears to be placement of quid among tobacco chewers or chronic mucosal trauma from sharp cusped teeth in others [69].

Studies with Adjustment of Confounding Factors

INHANCE consortium conducted a multi-centric case-control study to evaluate the role of POH as a causative factor for HNC [24]. The study included 8925 patients of HNC and had adjustments done for the use of alcohol, tobacco, smoking, age, sex, race, and educational level. They found that among all HNC, oral cancers had strongest association with POH and that good oral habits decreased the odds of developing oral/HNC—< 5 missing teeth (OR = 0.78; CI 0.74–0.82), annual dentist visit (OR = 0.82; CI 0.78–0.87), and daily tooth brushing (OR = 0.83; CI 0.79–0.88).

Another multi-centric study where adjustment was done for smoking, alcohol, and socio-economic strata included 1963 patients of UADT tumors and 1993 controls [28]. They found that patients with POH had higher odds of developing UADT cancers (OR = 2.22; CI 1.45–3.41). Habits suggestive of POH were involved with higher odds of developing cancer like those who had never visited a dentist were noted to have an OR of 2.22 (CI 1.45–3.41) for developing UADT cancers.

There was a hospital based case-control study where they had adjustment done for ethnicity, education level, tobacco smoking, betel quid chewing, alcohol drinking, etc. [23]. They compared 921 cases of HNC and 806 controls. They also found that lesser dental visits and greater numbers of missing teeth were significantly associated with an increased HNC risk. Poorer oral hygiene was associated with greater odds of developing cancer.

Another study had data included from two centers—one in Central Europe and other in Latin America [8]. They had also done adjustment for education, tobacco pack-years, and cumulative alcohol consumption. They also found that POH had higher odd of developing HNC (OR in Central Europe 4.51; CI 1.95–10.44; in Latin America 2.91; CI 1.87–4.52). In a recent study, on adjusting for tobacco usage, POH was found to be an important factor for causing OSCC, only in tobacco chewers [93].

Indian Scenario

Poor general oral hygiene is observed in the Indian population. This may be due to lack of awareness and low socio-economic conditions. People generally do not brush teeth more than once a day, while some do not even brush daily. Regular dental checkups are not observed by a large population. Due to lack of awareness, a large percentage of cases of dental caries and periodontal diseases use tobacco for local application. Rampant tobacco and gutkha usage with/without alcohol make the condition worse. The Global Adult Tobacco Survey (GATS) recorded a fall in tobacco prevalence in the Indian population from 35% in 2009–10 (GATS-1) to 28% in 2016–17 (GATS-2) [94].

National Oral Health Program

The National Oral Health Program (NOHP) was drafted by the Indian Dental Association (IDA) to address the burden of oral diseases in an effective manner for bringing about “optimal oral health” for all by 2020. It aims to improve total health for all Indians by oral health promotion and disease prevention and to improve knowledge, tools, and networks enabling effective dental practices and programs. It provides information regarding common oral health concerns and creates awareness about importance of oral health which is a better way of early detection of OSCC [95].

Oral cavity screening is a simple and effective tool which may help in detection of oral cancer cases at early stages. A Cochrane’s systematic review suggests that if the disease is treated in early stages, the survival rates are improved. Thus, a systematic examination of the oral cavity by a dental hygienist, dentist, or a general physician should be an integral part of routine check-up, especially in high-risk individuals [96–98]. Oral hygiene can be maintained by regular oral cavity check-up. Beneficial effects of oral cancer screening are well-established by cluster-randomized control trial done in Kerala. Results of this study have shown that oral cancer screening can help in reducing the mortality in high-risk individuals and has the potential in saving at least 37,000 lives worldwide. Thus, oral screening will not only reduce potential carcinogenic effects of POH but also help in diagnosing oral cancer at nascent stages and reducing mortality in high-risk individuals [99–101].

Conclusion

Poor oral hygiene is strongly associated with oral cancers. It aids the carcinogenic potential of other known carcinogens, like tobacco and alcohol. Even on adjusting for known confounding factors, like tobacco, alcohol use, education, and socio-economic strata, presence of POH exhibits higher odds of developing oral cancer.

Compliance with Ethical Standards

Conflicts of Interest

The authors declare that they have no any conflict of interest.