 Welcome to a new session of oral medicine and radiology series. Today, we will be dealing with oral submucous fibrosis. Oral submucous fibrosis was earlier considered to be a part of pre-malignant conditions. And by that term, it means that the generalized state of the body where there is more tendency for malignant to occur. So this term has now been discarded and another term has been used. That term is called as potentially malignant ketone. So both pre-malignant condition as well as pre-malignant lesion come under the same terminology. So these terms have been removed. So oral submucous fibrosis is a disease which is easy to diagnose but extremely difficult to manage. So what was the person who first discovered it in 1951? He named this entity as tropica, idiopathica, mucosa, oris. Maybe because by that time, xctiology was not found. So as we go through the historical reviews, we find that the term oral submucous fibrosis was suggested by an Indian, Joshi in 1952. And it's surprising that even though so many other terminologies have been suggested, we still stick on to use this particular term, that is oral submucous fibrosis. Coming to the definition. The definition was suggested by Pinburg and Sirasit. It's a very long definition. Oral submucous fibrosis is an insidious chronic disease affecting any part of the oral cavity and sometimes the pharynx. Although occasionally preceded by recycle formation, it is always associated with texture epithelial inflammatory reaction followed by a fibroelastic change of the lamina propria with epithelial apropia leading to stiffness of mucosa and causing chismis and inability to eat. So by the definition, we understand that it's an insidious disease, which means that it is very gradual in formation. So since it's very gradual, we won't discover it until it's too late. And then this could be perceived by recycle formation. But it's always associated with inflammatory reaction just beneath the epithelium. It is into the connective tissue. So there is deposition of collagen, which later leads to stiffness from mucosa and inability to eat. There is limited mouth opening. So coming to epidemology, Southeast Asian countries are mostly affected by this particular disease. And India is one of those countries apart from Bangladesh, Pakistan, etc. And it affects almost 0.2 to 0.5% of Indian population. The incidence is rising, especially among the younger population, around 20 to 40 years. The etiology is multifactorial. There are certain local factors and systemic factors. However, arachnid has been considered to be the most potent cause for there are certain reasons I'll be taking that. Apart from arachnid, capsicin, which is a component of chili, then there's tobacco and alcohol, and systemic factors which include nutritional deficiencies, infections, autoimmunity and genetic susceptibility. This nutritional deficiency has been controversial because some say that the nutritional deficiency is the cause for OSMF, whereas another school of thought suggests that it's because of OSMF that there is resulting nutritional deficiency. So this part is again conflicting, but still it has been considered to be an etiology factor. Coming to the components of arachnid, which actually take part in OSMF photogenesis. Arachnid consists of certain components, known as alkaloids, flavonoids, and others like minerals, especially copper. Alkaloids, they consist of arachnidine, govacin, isogovacin, arachnidine, and govacolin. And then there are flavonoids like tannins and cappagins, apart from other components. So the first two, that is alkaloids and flavonoids are the components which are notorious, which are known to cause OSMF. So I'll be dealing with that. So as I told you before, this particular component, this capsaicin, it is found in chili and peppers. This has also been considered to be a cause for OSMF, a particular etiology factor for OSMF, because people who actually consume a lot of chilies, a lot of spicy food have OSMF. But still, this is still controversial. A lot of states like Andhra Pradesh and Kannada, where chilies have been used more, more spicy food have been used. Those places have people more affected by OSMF, so that's why this is also considered. Coming to tobacco and alcohol, again, apart from other conditions like cancer or leukoplasty, this has also been attributed to OSMF formation. However, it is less potent than arachnidine. Arachnidine is more of the most potent of etiology factor. The systemic factors include nutrition deficiency, infections, autoimmunity, and genetic predispositions. Even certain articles point out, even five-year-old children have been affected by OSMF. So that actually points towards autoimmunity and genetic predispositions. Nutrition deficiency, especially depletion of iron stores and vitamin B complex, have been attributed to OSMF formation, especially the vitamin B complex deficiency that really promotes malignant. So that is more towards malignant transformation of OSMF. Coming to the pathogenesis of OSMF, as I told you before, arachnidine contains basically alkaloids, flavonoids in copper, alkaloids, which I had named earlier. They stimulate fibroblast formation. By fibroblast, I mean abnormal fibroblast, and they actually express genes. Gene expression is stimulated, and then there is increased production of collagen than the normal rate. There is more production of collagen. Then there are flavonoids, which cause increased cross-linkage of collagen. So what happens by that is that the collagen becomes more resistant, and it doesn't actually dissolve, or it doesn't get broken down, and it becomes more resistant to an enzyme, which is known as collagenis, which actually is an enzyme which causes lysis of the collagen. So lysis of collagen is required so that these bands can be removed. So during a normal process, there should be deposition as well as breakdown of collagen. However, in OSMF what happens is there is increased production of collagen, and the removal of collagen is hampered. So ultimately, you will have more and more of collagen deposition, and no removal of collagen. Then as I told you, there are minerals like copper in arachnidine, which upregulates an enzyme, which is called as lysyloxidase. So when you do that, there is more fibrinogenesis. Again, there is more deposition and formation of collagen. So together, they produce this particular tissue, that is OSMF. After OSMF begins to form or form, there is texta epithelium hyalinization, which will happen. That means there is deposition of collagen beneath the epithelium. That is just believe the epithelium into the connective tissue, the lamina property level of the connective tissue. So what happens is there are small tiny blood vessels, which actually supply nutrients and other important factors to the epithelium. So these blood vessels get obliterated because of excessive deposition of collagen. So by that, the blood supply is slowly, slowly getting cut off. And then due to continued showing or over activity, there is muscle contracture. And both of these together, they deplete the glycogen stores and which causes muscle fatigue and degeneration and which leads to fibrosis and scarring of muscle. So what happens is the particular person becomes a fully fleshed oral submucous fibrosis patient. So when there is vaso obliteration, what happens is that the nutrition is also cut out and whatever byproducts or whatever things need to be removed from there, that also isn't getting removed. Coming to the clinical pictures, as I told you, the anger age is mostly affected because they tend to use putka mode, putka or reconnect mode. This particular thing, that is the sex is controversial again because earlier females were considered to be more affected by or some of Dan males, but there are conflicting evidences too because it occurs in both ages, sorry, occurs in both sexes. Our recent article suggests that there is a male dominance in compared to female. So again, there's conflicting evidence. Coming to the site, again, the batil mucosa, the vichamola, trigone region, soft palate and the palate forces, the uvula and the labial mucosa are involved. So this particular predilection for site depends on how you tend to use the arachnid, whether it is just chewed as arachnid pieces or is it used as a powder or a paste or you know, in combination with any other thing, tamibutka, mawa, misery, whatever, you know. You tend to chew that and place it against some particular area. So if it is towards the mucal mucosa that you place it, then that area will be most affected. If you tend to keep it really more back, then that particular area will be most affected. And some people tend to keep it in the labial mucosa between the teeth and the lips. So that particular area will be more affected. So it all depends on what particular area you use. But usually what happens is the patient keeps on chewing the arachnid pieces. So, you know, most of the areas will be affected. It can even be, you know, affecting the areas near the pharyngeal region can also be affected. There are articles which suggest that, you know, people even swallow the juice, the arachnid, you know, after chewing. So that means even though the pharyngeal is also involved. The symptoms can be classified as early symptoms and late symptoms. Early signs include blanching of the mucosa, especially the butyl mucosa, soft palate region as well as the labial mucosa. And gradually it becomes white marbled appearance which can be seen in the later stages where you can see it is deposition of collagen fibers. So this particular appearance is called as white marbled appearance. You can see that the tongue is involved as well as the uvula, the soft palate region, all these regions are involved. So what happens here is that the uvula becomes a characteristic shape like this. It is called as a pocky stick appearance. It is also called as a J-shaped appearance. The uvula becomes shrunken and that region becomes very stiff when your cheek flexibility is lost. And then gradually your tongue movements are also restricted and then you will find vertical bands on the pocky mucosa. Coming to the various stages as described by Ballour in 1993. Stage 1, early OSMF, you find mild blanching. There is no restriction in mouth opening, no restriction in tongue protrusion and not much of effect on cheek flexibility. Burning sensation might be there but it only occurs on taking spicy food or hot liquids. Coming to the moderate stage, stage 2, there is a reduced mouth opening, setting of burning sensation. There are formation of palpable bands which can be restricted on the pocky mucosa, especially the partial area. Then there is lancotinopathy and anemia because there is less of nutrition. And then the restriction of soloing, this causes less intake of nutrients. And then anemia can be recited. Then coming to the severe OSMF stage, there is a stage 3, there is severe burning sensation, reduction in mouth opening, cheek flexibility and tongue becomes gradually fixed. There could be ulcerative visions and the bands which I had mentioned earlier, they become very thick and very evident. There is bilateral lancotinopathy. There is another staging by Hyder et al who actually gave two pronged staging. There is clinical staging and functional staging. Clinical staging can be classified as grade 1, grade 2 and grade 3 by the formation of bands. That is, in grade 1 you find only partial bands. In grade 2 only partial and butyl bands whereas in grade 3 you find partial as well as labial bands. These are vertical bands due to collagen deposition which you can be, sorry which you can elicit on the pocky mucosa by palpating. Then there is the functional stage which can be divided as stage A, stage B and stage C that is stage A, we have a mouth opening of more than or equal to 20 millimeter whereas in stage B you have a mouth opening of 11 to 19 millimeter and stage 3 for stage C we have a mouth opening of less than or equal to 10 millimeter. So, both these stages are almost related to each other. So, when there are bands there is restriction. So, when there are more bands there is more restriction. Coming to the investigations, you can find that the ESR levels are elevated. The serum ion stores are depleted. There is increased eosmophil count immunoglobin G. So, IgG is increased, pH in saliva is increased, salivary amylase is increased, alkaline phosphatase is also elevated as well as potassium but the calcium levels are decreased. You can find hyperglobinemia decreased vitamin B complex levels and decreased protein levels. Coming to the management stage. So, as I told you this is the stage you know which is a little bit difficult. All the other stages is easy, where is the identification of the signs and symptoms as well as associating the particular meteorology with the disease. However, management is a little bit difficult actually because you know patients come to you only after there is severe limitation of mouth opening or you know the stage has become severe. So, when that has occurred you cannot actually you know do justice to the treatment aspect because you can only reduce the symptoms or you know you can only give a comfort and help to the patient or you cannot completely eliminate it. So, I will be discussing the management steps. The first step includes preventive measures that is if a patient comes to you with a habit of arrogant chewing and use of tobacco and all those things you should tell him completely abstain from all that. You should also motivate the patient and inform about probable malignant transformation that itself will actually prevent the patient from further intake of all these harmful substances. Coming to the nutrition support part. So, you have to supplement the patient with iron, vitamins, minerals especially vitamin B and then antioxidants. So, regular hemoglobin analysis should be done. Vitamin B deficiency as I told you could lead to degenerative changes in the mucosa and lead to malignant transformation that is why vitamin B should be replenished. Antioxidants like lycopene it inhibits the abnormal fibroblast production and stimulates the immune system. So, that also should be given. Coming to physiotherapy muscle stretching exercises should be increased. So, these include forceful stretching of your muscles. You can also ask the patient to blow balloons and hold it like that for some time. So, this actually helps to improve the cheek flexibility. Then you can ask the patient to use tongue blades that is you know you can stack tongue blades one upon the other so that the patient himself can analyze how much this is mouth open. So, he should be encouraged to increase the number of tongue blades which we stack one upon the other. So, you know as the treatment progresses the patient can self monitor his improvement. That will be an encouragement for them. Then there is heat that is diatomy, microwave diatomy and shortwave diatomy that it is a selective heating of the extra epithelial connective tissue. So, by doing that you actually help to lyse the fibrous bands. So, this process is called a specieofidronolysis of fibrous bands. Selectively heat the extra epithelial connective tissue. Then coming to the immunomollated drugs the first you know line of immunomollated drugs is obviously steroids because you know it has a lot of beneficial effects. The first is obviously reduction in inflammatory response. So, you can use it topically, systemically or intellectually depending upon the severity. It also decreases the proliferation of fibroblasts and thus reducing the collagen fibres and helps to ingest the immovable collagen fibres. So, topically can be in the form of gels or appointments which can be applied to the particular lyse inside systemic you know it can be taken in and then it could be tapered down depending on the severity. And the solution is injecting steroids into that particular patient especially near the band area. This could be done alone or in combination with other drugs like you know maybe hyaluronadase which is collagenous which helps in lysis of the fibrous bands. Even placental extract can also be used along with. Okay so told you placental extract okay it comes by the brand name placentrix. It is an extract of human placenta which contains nucleotides, enzymes, steroids, vitamins and amino acids. It actually stimulates metabolic and vaginal activity. Okay. Coming to liver muscle it is an immunomodulated drug which is you know originally an anti-helmandic drug but you know it is used in a different dosage it acts as an immunomodulated drug. Then there is a interferon gamma which is known as anti-fibrotic cytokine. Okay it can also be given intralysmally and it improves the symptoms of poison. Okay then there is something which is called as an immune milk which contains anti-inflammatory components. It suppresses the inflammatory process and stimulates cytokine production. And this is also used in poison treatment. Okay and there are others like hyaluronadase. As I told you before this is a collagenous which actually helps to lyse or break down the collagen fibers. Okay break down the hyaluronic acid in collagen fibers and this. And there's something which is called as chymotrupsin which is an endopeptidase enzyme. It's a proteolytic agent and which helps in preventing inflammation of reducing inflammation. Then there are peripheral vasodilators. As I told you there is obliteration of blood vessels. So there are peripheral vasodilators which actually help dilate the blood vessels and improve the micro circulation. An example for this is pentoxypil. Okay so they are also called as rheologic modifiers. Okay then there are other products like turmeric which contains peppermint and aloe vera, green tea etc. Which has been really useful and experimented a lot these days. Which has been having very promising results. It has been used a lot now. When you know it is available in combination with strival finna comes by the name cure next. Then there is another called as turbo cord. It's a combination of both trimesin alone and curcumin. So as I told you this is a particular disease where you know one size doesn't fit all. So you need to combine several modalities. So you should combine medicinal management along with surgery. Sometimes you need to inject and then you need to physiologically stimulate certain exercises. So you know if all this doesn't work you need to go for the final part that is surgical management. So which includes you know minor breakage of fibrous bands work. If it's very severe then you know you need to replace it with buckle pad or patch or something after remaining all the fibrous and scar tissue. All those will be needed. So that comes on the surgical management that is actually beyond our domain. It's oral submersible fibrous is extreme states that will be managed by surgery department. Coming to the malignant potential it has been noted that almost you know 4.5 to 7.6 percent of OSM of turns into malignments. As I told you before prognosis is questionable. It's because you actually get these patients only after the disease has progressed a lot. So you only tend to reduce or alleviate the condition. You don't actually completely remove the problem. So the malignant potential as I told you it is because of the arachnol. It is an alkaloid. It undergoes nitrosation and then it produces certain nitro summons which damage the DMA. And this continuous damage of the DMA is the cause for malignant transfer. The patient should be avoided. So the patient should be advised to avoid taking of arachnol as soon as you sign it. Use all these things. So coming to the conclusion again once again I would like to stress on the point this particular disease is very easy to diagnose but extremely difficult to manage. It needs long-term follow-up and it is essential to detect these plastic changes and malignments. So you need to have this patient come to you for a long long time. So if you need to be motivated and encouraged on a regular basis. So with that I would like to wind up this session on OSMR. Thank you. Stay safe and stay enlightened.