dr suneel kumar fcps assistant professor omfs department lumhs [email protected]
TRANSCRIPT
DENTAL CARIES Baby Bottle Syndrome
Mother feed Milk Bottles Pacifier
SWEET SUPARI (BETEL NUT)
BETEL NUT (TREE)
PRODUCTION COUNTRIES Indonesia Malaysia Philippines India Bangladesh Pakistan (Less)
ORAL SUBMUCOUS FIBROSIS High risk precancerous condition which
was first described in the early 1950s Described by Schwartz in1952 among
five Indian females living in Kenya and he coined the term atrophia idiopathica (trophica) mucosaeoris.
It is characterized by changes in the connective tissue fibers of the lamina propria and deeper parts leading to stiffness of the mucosa and limited mouth opening.
Oral Diseases (2011) 17 (Suppl. 1), 42–57
CLINICAL PICTURES
CLINICAL PICTURES
CLINICAL PICTURES
IARC & WHO The International Agency for Research on
Cancer (IARC) and the World Health Organization (WHO) accept the scientific evidence that chewing betel quids and areca nut is carcinogenic to humans.
The main carcinogenic factor is believed to be areca nut. A recent study found that areca-nut paan with and without tobacco increased oral cancer risk by 9.9 and 8.4 times, respectively.
IARC 2010
ETIOLOGY
GUTKA
Collagen synthesis
Reactive oxygen species
DNA & Fibroblast damage
DNA damage
Fibroblast damage
Gingival blood flow
Cell turnover (By killing cells)
Reactive oxygen species
DNA Damage &Chromosomal abnormalites
nm
Areca nut TobaccoSlaked lime
ORAL MUCOUS FIBROSIS ORAL CANCER PERIODONTAL DISEASE
Oral Surg Oral Med Oral Pathol oral radiol 2010 :109:857-864
ARECA NUT CONSUMPTION PATTERNS AMONG PRIMARY SCHOOL CHILDREN OF KARACHI
50% to 60% school going children's using sweet supari
Males (64)
Females (227)
Education status of Parents (Intermediate)
JDUHS 2013, Vol. 7 (1): 25-29
SMOKING
SMOKING Lung Cancer Oral Cavity Cancer
CANCER REGISTRY DATA Karachi Cancer Registry (KCR) Different cancer types in Pakistan during
the period of 2000-2008 Female 51.8% Male 48.1 %. In Males head and neck cancer 32.6 %
of total cancer cases lung was 15 % of cancer cases
SMOKING EFFECTS ON BODY
PAKISTAN TODAY 18-1-14
NASWAR
PAAN CHALIA
PAAN
REPORT BY KARACHI UNIVERSITY
A major reason of death in underdeveloped countries including Pakistan is mouth cancer which occurs as a result of genetic changes that take place due to the chewing habits of tobacco, paan, chhaliya, gutka, niswar and manpuri.
http://www.nays.com.pk/nays-survey/
ORAL CANCER Oral cancer accounts for about 3-4% of
all cancers The most common type of oral cancer is
squamous-cell carcinoma, constituting about 90% of oral malignancies.
FRQUENCY Fourth commonest in Men Sixth commonest in women
More common in men Age above 40 years
COMMON SITES Tongue 35% Buccal Mucosa 10% Lower Alveolus 15% Upper alveolus, hard palate 08% Floor of mouth 30% Retro-molar area 02%
CLINICAL PICTURE
CLINICAL PICTURE
CLINICAL PICTURE
CLINICAL PICTURE
CLINCAL PICTURE
COMMISSIONER, ROSHAN ALI SHEIKH BURNS CONFISCATED TOBACCOS, GUTKA AND MAINPURI
DURING CEREMONY TO MARK THE WORLD CANCER DAY (2012)
http://pakistan.onepakistan.com.pk/photogallery/news-politics/day-in-pics-4th-February/pakistan/120204-19
BRUXISM Bruxism is the habitual grinding of
teeth. It most often occurs at night but can occur when awake or asleep.
The etiology of bruxism includes habit, emotional stress (response to anxiety, tension, anger, or pain), neurologic abnormalities
BRUXISM
NIGHT GUARD
USING OF TEETH AS SCISSORS
PENCIL BITING HABIT
THUMB SUCKING
http://www.aap.org/oralhealth/pact
The International Agency for Research on Cancer (IARC) and the World Health Organization (WHO) accept the scientific evidence that chewing betel quids and areca nut is carcinogenic to humans.[5][7][8][9] The main carcinogenic factor is believed to be areca nut. A recent study found that areca-nut paan with and without tobacco increased oral cancer risk by 9.9 and 8.4 times, respectively.[10]
In one study (c. 1985),[4] scientists linked malignant tumours to the site of skin or subcutaneous administration of aqueous extracts of paan in mice. In hamsters, forestomach carcinomas occurred after painting the cheek-pouch mucosa with aqueous extracts or implantation of a wax pellet containing powdered paan with tobacco into the cheek pouch; carcinomas occurred in the cheek pouch following implantation of the wax pellets. In human populations, they reported observing elevated frequencies of micronucleated cells in buccal mucosa of people who chew betel quid in the Philippines and India. The scientists also found that the proportion of micronucleated exfoliated cells is related to the site within the oral cavity where the paan is kept habitually and to the number of betel quids chewed per day. In related studies,[4] the scientists reported that oral leukoplakia shows a strong association with habits of paan chewing in India. Some follow-up studies have shown malignant transformation of a proportion of leukoplakias. Oral submucous fibrosis and lichen planus, which are generally accepted to be precancerous conditions, appear to be related to the habit of chewing paan.
In a study conducted in Taiwan,[11] scientists reported the extent of cancer risks of betel quid (paan) chewing beyond oral cancer, even when tobacco was absent. In addition to oral cancer, significant increases were seen among chewers for cancer of the oesophagus, liver, pancreas, larynx, lung, and all cancer. Chewing and smoking, as combined by most betel chewers, interacted synergistically and was responsible for half of all cancer deaths in this group. Chewing betel leaf quid and smoking, the scientists claimed, shortened the life span by nearly six years.
A Lancet Oncology publication claims that paan masala may cause tumours in different parts of the body and not just the oral cavity as previously thought.[12]
In a study conducted in Sri Lanka,[13] scientists found high prevalence of oral potentially malignant disorders in rural Sri Lankan populations. After screening for various causes, the scientists reported paan chewing to be the major risk factor, with or without tobacco.
In October 2009, 30 scientists from 10 countries met at the International Agency for Research on Cancer (IARC), a World Health Organization sponsored group, to reassess the carcinogenicity of various agents including areca nut, a common additive in paan. They reported there is sufficient evidence that paan chewing, even without tobacco, leads to tumours in the oral cavity and oesophagus, and that paan with added tobacco is a carcinogen to the oral cavity, pharynx and oesophagus.[14]
Effects of chewing paan during pregnancy
Scientific teams from Taiwan, Malaysia and Papua New Guinea have reported that women who chew areca nut formulations, such as paan, during pregnancy significantly increase adverse outcomes for the baby. The effects were similar to those reported for women who consume alcohol or tobacco during pregnancy. Lower birth weights, reduced birth length and early term were found to be significantly higher.[15][16]
Oral leukoplakia more commonly occurs in those who smoke,[5] but often the cause is unknown (hence the synonym idiopathic leukoplakia).[6] Chewing tobacco is also associated with this type of lesion.[9] Leukoplakia is a premalignant lesion, i.e. "a morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart".[6] The chance of transformation into oral squamous cell carcinoma (OSCC, a type of oral cancer) varies from almost 0% to about 20%, and this may occur over 1 – 30 years.[6] The vast majority of oral leukoplakias will not turn malignant,[10] however some subtypes hold greater risk than others. No interventions have been proven to reduce the risk of cancer developing in an area of leukoplakia,[6] but people are generally advised to stop smoking and limit alcohol consumption to reduce their risk.[3] Sometimes the white patch will shrink and eventually disappear after stopping smoking,[11] but this may take up to a year.[7] In many cases, areas of leukoplakia will slowly expand, become more white and thicken if smoking is not stopped.[1] Management usually involves regular review of the lesion to detect any possible malignant change early, and thereby significantly improve the prognosis, which normally is relatively poor for OSCC.[6]
Chewing tobacco
Chewing tobacco has been known to cause cancer, particularly of the mouth and throat.[180] According to the International Agency for Research on Cancer, "Some health scientists have suggested that smokeless tobacco should be used in smoking cessation programmes and have made implicit or explicit claims that its use would partly reduce the exposure of smokers to carcinogens and the risk for cancer. These claims, however, are not supported by the available evidence."[180] Oral and spit tobacco increase the risk for leukoplakia a precursor to oral cancer.[181]
Reporting in the July 2008 issue of The Lancet Oncology, a team led by Dr. Paolo Boffeta, of the International Agency for Research on Cancer, wrote that "while they did not intend to address explicitly the use of smokeless tobacco to reduce the risk from tobacco smoking ... nevertheless, several conclusions can be reached based on the available data ... the risk of cancer, especially that of oral and lung cancer, is probably lower in smokeless tobacco users in the USA and northern Europe than in smokers, and the risk of cancer is higher in smokeless tobacco users than in non-users of any form of tobacco."
Cigars
Like other forms of tobacco use, cigar smoking poses a significant health risk depending on dosage: risks are greater for those who inhale more when they smoke, smoke more cigars, or smoke them longer.[182] The risk of dying from any cause is significantly greater for cigar smokers, with the risk particularly higher for smokers less than 65 years old, and with risk for moderate and deep inhalers reaching levels similar to cigarette smokers.[183][184] and are hard to measure; although it has been claimed that people who smoke few cigars have no increased risk, a more accurate statement is that their risks are proportionate to their exposure.[61] Health risks are similar to cigarette smoking in nicotine addiction, periodontal health, tooth loss, and many types of cancer, including cancers of the mouth, throat, and esophagus. Cigar smoking also can cause cancers of the lung and larynx, where the increased risk is less than that of cigarettes. Many of these cancers have extremely low cure rates. Cigar smoking also increases the risk of lung and heart diseases such as chronic obstructive pulmonary disease.[182]
Hookahs
A common belief among users is that the smoke of a hookah (waterpipe, narghile) is significantly less dangerous than that from cigarettes.[185] The water moisture induced by the hookah makes the smoke less irritating and may give a false sense of security and reduce concerns about true health effects.[186] Doctors at institutions including the Mayo Clinic have stated that use of hookah can be as detrimental to a person's health as smoking cigarettes,[187][188] and a study by the World Health Organization also confirmed these findings.[189]
Each hookah session typically lasts more than 40 minutes, and consists of 50 to 200 inhalations that each range from 0.15 to 0.50 liters of smoke.[190][191] In an hour-long smoking session of hookah, users consume about 100 to 200 times the smoke of a single cigarette;[190] in a 45-minute smoking session a typical smoker would inhale 1.7 times the nicotine [192] of a single cigarette. A study in the Journal of Periodontology found that water pipe smokers were five times more likely than non-smokers to show signs of gum disease.[citation needed] According to USA Today, people who smoked water pipes had five times the risk of lung cancer of non-smokers.[193]
A study on hookah smoking and cancer in Pakistan was published in 2008. Its objective was "to find serum CEA levels in ever/exclusive hookah smokers, i.e. those who smoked only hookah (no cigarettes, bidis, etc.), prepared between 1 and 4 times a day with a quantity of up to 120 g of a tobacco-molasses mixture each (i.e. the tobacco weight equivalent of up to 60 cigarettes of 1 g each) and consumed in 1 to 8 sessions". Carcinoembryonic antigen (CEA) is a marker found in several forms of cancer. Levels in exclusive hookah smokers were lower compared to cigarette smokers although the difference was not statistically significant between a hookah smoker and a non-smoker. Also the study concluded that heavy hookah smoking (2–4 daily preparations; 3–8 sessions a day ; >2 hrs to ≤ 6 hours) substantially raises CEA levels.[194] Hookah smokers were nearly 6-times at risk for development of lung cancer as compared to healthy non-smokers in Kashmir (India).[195]
Hookah in Kashmir has some peculiar features in having a direct contact of the live embers with the burning tobacco thus resulting in high temperatures that augments the production of carcinogenic products from tobacco burning. Additionally water in the hookah base is not changed after every session that renders the water contaminated to a greater degree and thus a possible source of dissolved carcinogens.
Snuff
Users of snuff are believed to face less risk of some cancers than smokers, but are still at greater risk than people who do not use any tobacco products.[196] They also have an equal risk of other health problems directly linked to nicotine such as increased rate of atherosclerosis
