 Hello everyone, welcome back to a new session on dentistry and more. So let's continue our epidemiological sessions that is epidemiology of dental caries we covered already and its prevention. Now we have epidemiology of periodontal diseases and its prevention. So the prevention is basically focusing on the plaque control that I will be doing in my next video. So let's see what is the epidemiology of periodontal diseases. So periodontal diseases like we can say that it is periodontitis is an inflammatory disease of the supporting tissue. So we know what are the supporting tissues like gums and other gingival elements. There will be inflammation which is caused by specific micro-organisms or a group of micro-organisms which results in progressive destruction of the periodontal ligament and alveolar bones. So these are the supporting structures which results in pocket formation and recession. So that is periodontal disease or periodontitis. So we have this epidemiological tract just like what we seen in our periodontal caries. So we have agent factors, four-stand environment factors. So those factors are race, age, sex, internal variations, habits, occupational habits, presence of concomitant diseases and other artificial habits. Agent factors are geographic area, nutrition, urbanization and educational background. In agent factors, material, alba, plaque, calculus and stains. So let's see a survey of India that is national oral health survey which was done in 2002-3. So that survey showed that it was around 57% of people in the age group of 12 on 68% in age group of 15, almost 90% in this age group that is 35 to 44 and 80% in this group are having periodontal diseases, that is periodontitis. So periodontitis usually increases with age. So let's see what are the host factors of this disease. Host factors, the first one is racial differences. So racial differences, if you see African and Latin American backgrounds suffer from highest risk of periodontal issue and the whites. But the main problem is there they belong to the low socioeconomic status. It is not the racial characteristics which causing this difference. It is why because these minorities are belong to low socioeconomic status. So it could be the affordability to maintain a good oral hygiene and other factors contributing to this difference, not the racial characteristics. Second one is age. We know periodontitis is a disease of old age but there are certain diseases which can seen in early age also like aggressive periodontitis. So commonly attachment loss and pocketing increases with age, older age have chronic periodontitis and like I said juvenile periodontitis are also there and very early age you may see pre-pivotal periodontitis. So depending upon age the various diseases are there but still it is a disease increases with age. So what happens is there are two mechanism with regard to age. It might increase by itself due to cumulative effect of risk factors over time. That is as the age increases there will be deterioration of host defense mechanism, there will be more susceptibility to infection and less salivary flow and it could be due to the cumulative effect over time like multiple illustrations, calculation, calculus, deep pockets, teeth and vocation involvement, fluid queries which increases more plaque accumulation, more plaque means more bacteria it causes periodontal lysis. So it could be one of these due to cumulative effect or due to the age itself. Regarding sex, gingivitis is more common in male than female and it has higher odds with studies have shown that males are having more periodontal problems compared to females. The dental caries was exactly opposite what we have seen and the reasons also we have seen like more hormone changes like fullness and early eruption of teeth. So it could be due to estrogen has an effect in protecting the supporting structures for especially in the females but what happens after the menopause? The studies have shown that there is no much difference between male and female since the estrogen effect is out of the context once the menopause starts. So estrogen effect can explain the better periodontal health in females and also there is a lot better oral hygiene practices by the females and better utilization by the females because they are more aesthetically concerned and tobacco usage is very common among men compared to females. So all these can contribute to the gender difference of periodontal lysis. Genetics like aggressive periodontitis can be explained by genetics it is an autosomal dominant disorder. So anatomical factors like pohocusp anatomy and even marginal reduced lack of contact between teeth and crowded which can lead to food impaction and accumulation thereby ginger irritation which ultimately leads to gingeritis and periodontitis. So the other systemic concomitant diseases is having a very significant effect on our periodontal structures which causes altering in the host tissue reducing the host defense mechanism. So there will be changes with related to HIV AIDS because it reduces immunity of a person and there will be oral hygiene status and they are very vulnerable to periodontal diseases. So in HIV patients commonly see an acrotizing periodontitis. So diabetes is like a very common cause for the periodontal problems in most of the people that is it is the sixth complication of diabetes militis. So there will be increased tendency of ginger enlargement, polyps, multiple abscess formation, bone loss and pockets with regard to uncontrolled diabetes. So it can cause periodontitis by altering the periodontal response to local factors. So there will be hyperglycemia causing protein molecules to undergo non enzymatic like oscillation, thereby forms glycation end products. So there will be cross linking of collagen affecting its renewal through which cellular migration is impeded. So actually it affects the collagen and there will be bone loss and tooth loss. So periodontitis is a biggest problem the most of the diabetic patients face because it affects all these products and causes it affects the collagen. Collagen is the main fiber which causes ankerage. So collagen is affected so there will be loss of ankerage and tooth might be loose and there will be other problems for the periodontal structures. So osteoporosis is also a risk factor for periodontitis. Disabled people why because they are having limited capacity to do a proper oral hygiene measures or personal hygiene so which can contribute to periodontal diseases. So stress like it causes behavioral change they'll be over eating and smoking at the same time they maintain very poor hygiene, poor compliance and bacterial infection like cortisol all leads to periodontal diseases. This is like a web of causation what we learned in concept of causation. So stress can cause periodontal disease. So habits like occupational habits we have holding of nails in mouth like for carpenters and tailors and other musical instruments which is detrimental to our periodontal structures. So nail biting, fingernails, toothpicks, lip biting all are periodontal structures, damaging or was structural damage to periodontia. Luckily written such as mechanically written faulty tooth brushing or faulty restorations and orthodontic treatment all can cause damages to our supporting structures. And locally written like if we have a mouth opening habit so there'll be dehydration of this mucus membrane decreased tissue resistance and ginger enlargement and there'll be inflammation. Smoking is one of the biggest factor which causes periodontal disease. It has proven in many of many of the researchers like one study has proven five times higher periodontal diseases and smokers compared to non smokers. So most of the studies has proven this smoking and periodontal disease and was a link. So alcohol consumption also has a bad effect on our periodontal structures because it impairs neutrophil, macrophage and other inflammatory functions and there'll be more chances for the infection. So we'll come to the agent factor of the most common is material and dental plaque. Material is nothing but the accumulation of bacteria discriminated epidural cells, leukocytes and salivary proteins. It lacks an organic structure that is a difference between dental plaque. There is no organic structure. But the dental plaque is a structured resilient yellow grade substance that adheres tenaciously to the intraoral heart surfaces. So there'll be a structured property in dental plaque which is lacking in material alpha. So plaque is composed of bacteria, leukocytes and extracellular polysacrates. It is because of this matrix the plaque cannot be removed by rinsing because it will be strongly, firmly adhered to the tooth surfaces. It has to be removed by proper brushing or scaling. Normal rinsing cannot remove the plaque. What it removes is oral debris. So we need to learn two hypotheses. The dysplac hypothesis, a non specific plaque hypothesis says the periodontal disease results from the noxious products of the entire plaque flora. They are not highlighting any specific bacteria. So it says that larger amount of plaque and its accumulation is necessary for onset of periodontal disease. The theory was discarded because some individuals with considerable amount of plaque calculus and gingivitis do not develop a destructive periodontitis. But individuals with periodontitis show site specifically with some areas unaffected and some site showing advanced disease. So this hypothesis are not able to prove or not able to explain these two scenarios. So specific plaque hypothesis by Lausche came into existence. This theory states that only certain plaque is pathogenic and its pathogenicity depends upon the presence or increase in the specific microorganism. Not all pathogens are dangerous, only few are dangerous and its presence or increase in specific microorganism can cause the disease. So March 1991 formed ecological plaque hypothesis and proposed that a change in key environmental factors will trigger a shift in the balance of the resident plaque microflora. So there will be always microflora in the mouth. Some are beneficial. Most of them are non beneficial. So if the balance is disrupted, the problem starts. So calculus we know the heart opposites formed by the mineralization of dental plaque. There is supragenjival and subgenjival calculus. So supragenjival is mostly collecting its minerals from saliva whereas subgenjival collecting it from the GCF. So etiological significance is there is a positive relation between the presence of calculus and prevalence of gingivitis. So dental stains we know extrinsic stain and intrinsic stain. Extrinsic stain is like tobacco stain and intrinsic stain like retrocycline and dental fluorescence. So agent factors like all these are the agent factors of various bacterias, actinomyces, leptococcus, tryponema, fuso bacterium and actinomyces, actinobacillus, actinomycetamcomitums is for the juvenile parameters. All these are the agent factors. Now let's see what are the environmental factors. So geographical areas. The scientist Russell summarized from his experience like which are high among countries like India, Thailand, Jordan, Lebanon and low among USA and Eskimos of Alaska. So nutrition if there is vitamin deficiency, protein starvation and calcium phosphorus magnesium deficiency and there will be more of paranormal diseases. So fluoride presences inversely proportional to diseases and degree of urbanization, education and income. Education is definitely will improve the patient's oral health and it is inversely proportional to the disease and deteriorating habit which is common among law, social, economic group. So that type of habits are predisposing to the paranormal disease which are common among law, social, economic strata and some cultural factors and beliefs are also important. Prevention of paranormal disease is by plaque control that I'll be explaining you in my next video. So let's see how do we prevent plaque control formation or paranormal disease under three levels because this is we already seen levels of prevention and modes of intervention. How do we apply this primary secondary tertiary primary we have health promotion, specific protection, early diagnosis and prompt treatment, disability limitation and rehabilitation levels of prevention we have at individual level, community level and dental professional level. So under primary we have to visit and education by the community and education by the professional. In specific protection we have to remove the avoidance or proper oral hygiene practices. By the community we have to conduct school brushing programs or oral hygiene aids distribution. By the dental professional they can help us by removing plaque control like scaling, correction of malilane teeth and prophylaxis. Under secondary the disease is just beginning. So self examination and visiting a dentist periodic screening by the community and by the professional what he can do is scaling, curatage, restorative and occlusion services. Tertiary is already caused the damage. So disability limitation but the dentist can give us deep curatage, root planning, periodontal surgery and splinting. Rehabilitation here just visiting a dentist that is under individual and community. But dental professional we can give removal or shield intervention. So that's all about periodontalysis epidemiology. So just like dental caries we have agent, host and environmental factors. The main thing is the hypothesis plaque hypothesis, non specific, specific and ecological hypothesis and various factors which are involved. So the next video I'll be explaining about the prevention. So prevention various levels we have seen. So under primary prevention we have this plaque control measures mechanical and chemical. So next video is of plaque control. Okay, thank you.