Periodontics

Periodontics # 4 Dr. Muhammad Hammad Tahboub

Done by: Kawkab Y.

= = = = = = = == = = = = = == = = = = = = = = = = = = = = = = = = = = = = ==== My colleagues, this lecture is easy , it's not as it seemed , there are some names repeating through out the lecture , not difficult to be memorized, so , prepare ur seat belt>> lets start!

Today we will talk about the main external etiologic factor of periodontal diseases "dental PLAQUE" ,which you have seen in the clinics . Plaque is defined as a host (which is human here-teeth) associated biofilm ( thin layer or a coat ), we say that because bacteria, which is the major component of dental plaque , behaves differently from bacteria that is present in the lab or in the culture . This host associated biofilm lives with us all the time , and as we will see it’s dynamic . the periodontal health and the good healthy mouth environment is established when there is a state of balance between the host ( the patient) and this biofilm or bacteria population ( i.e the bacterial component of the biofilm ) , if this balance is disturbed – particularly toward the biofilm side - we will get a disease . sterile mouth doesn’t exist . The Dr put a picture of a case from 10 years ago to a student from the faculty of engineering in our university , he had never brushed his teeth besides he was a smoker! so his mouth presented with plaque, calcified plaque, calculus and he has layers of plaque above that calculus . He had a lot of changes in his oral mucosa and inflammation , he was lucky not to have true periodontisis , 1 week after cleaning his mouth he come back very healthy.

::The structure and the composition of plaque:: Plaque is a very organized bacterial community or oral film ( especially the SUPRAgengival plaque)  another definition for plaque : the soft deposits that adhere to the tooth surface or other hard surfaces in the oral cavity that may include : complete\ partial dentures; you can find calcifications on the surfaces of these appliances and that means that these calcifications were plaque before they get calcified . Plaque is strongly adherent to the tooth surface . (that to differentiate if from a material called material alba ) . -1-

material alba :- material ( material ) , alba ( white) , which is a soft accumulation of bacteria plus desquamated cells and probably food debris, this material is NOT strongly adherent to the tooth surface ; it can be washed away easily just by a spray, while d ental plaque needs to be removed physically . plaque if left for a long time untouched will be calcified , calculus salts come from People howmore fast you did a job - but how well) aspects you did it of the saliva , that’s whyforget we find calcifications onthey theremember inner (lingual lower anterior teeth; because they are close to the sublingual salivary glands orifices where saliva is stagnate because of the gravity effect , also we can find them on the upper 6 molars near the orifice of Stenson's duct ( of the parotid glands ) . the major component of dental plaque is bacteria , and that’s the most harmful part . non- bacterial microorganisms also exist ; we can find : • mycoplasma ( remember from your microbiology it has no cell wall ) • yeasts ( such as candida ) • protozoa ( such as ameba ) • viruses. ( free viruses or phage viruses (infect bacteria within the plaque itself) ) intracellular matrix holds these components of the dental plaque together and it composes 30% of the wet mass of the plaque , the remaining 70% is composed of bacteria ( that was what the Dr said , but I think he meant bacteria and other microorganisms ~mainly bacteria ).

This matrix is composed from organic and inorganic materials : These are derived from saliva , crevicular fluid , bacterial products , and dead human cells … crevicular fluid: the fluid that oozes out from the gingival sulcus through the junctional epithelium ( it comes from the blood vessels and periodontal tissues ) .  periodontal area is unique because it’s provide a direct contact between the external and internal environment . The organic components of the intracellular matrix : 1- polysaccharides : molecules attached to each other , mainly it's DEXTRAN >>  dextran is produced by the 1st bacterial invader to our teeth i.e Streptococcus mutans , dextrose is another name for glucose so another name for dextran is GLUCAN . (( you can find dextrose written on Glucose drips in hospitals )) . - S. mutans has an array of enzymes collectively called Sucrase >>  sucrose is the regular daily sugar we consume and add for tea , it's composed of fructose + Glucose . S. mutans and the other streptococci in our mouths (( which known as Streptococcus Viridans )) are capable of producing dextran , but dextran's viscosity depends on it's forming bacteria ( different linkages , different viscosities and stickiness ) the stickiest one is the dextran produced by S. mutans , and it acts as a glue that sticks plaque to the tooth surface .  streptocoocus viridans : viridans is a word derived from a French word (vert) means green ( as I found it's from a Latin word ~viridis ), they are α-hemolytics ;causing partial hemolysis of blood agar and causing the greenish discoloration hence there name.

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( this name is not accurate because it's not a one species so now they are known as oral streptococci , and they include : S. mutans , S. sanguis , S. salivarius , S. milleri ).

But what is the fate of the other molecule of sucrose which is fructose?? it will be converted to another polysaccharide called furan , then it will be taken by the bacteria to be used inside it as an energy source . not to become a man of success but rather to become a man of value" ".Try 2- Glycoproteins : Means => sugar + protein .  the protein comes from saliva and it initially coats the clean tooth and participate in forming the pellicle as we will see. 3- Lipids : Fats come from the outer membranes of disrupted bacteria and host cells ( as you know, the membrane has is a phospholipid bi-layered structure ) The inorganic components of the intracellular matrix : Composed mainly of Calcium ( which is the most abundant salt in addition to Sodium ) , phosphorus , we have trace amounts of other minerals such as Sodium, Potassium and Fluoride . These materials give the hard structure of calculus later on . According to the location in relation to the gingival margin, plaque is divided into : supragingival plaque :if it's within the oral cavity . subgingival plaque : if it's within the pocket .

inorganic components of subgingival plaque are derived from the crevicular fluid which is originally derived from blood, that’s why you can see plaque in a black color ( bcz of the hemoglobin in the blood ).  there are 2 colors for plaque , a creamy or a yellowish one and a blackish one , the darker is harder to be removed , because it is attached to the root surface , which is more rough in comparison to the enamel . -

fluoride comes from diet and tooth pastes ..etc.(Dr

said that the Tea is a rich source of Fluoride!)

::the sequence of plaque formation: : 1dental pellicle: pellicle means an initial coat or a thin layer, ( ‫ )الغللة‬that coats the tooth surface and makes it smooth , ( if you passed your tongue against your teeth you will feel this smoothness as if they are lubricated because of the mucins in the sliva and the pellicle , when you drink lemon juice or anything sour for example it will disappear so you won't be able to feel smoothness in Arabic that feeling of the surfaces rubbing against each others is called (‫س‬ َ )) . ْ ‫ضَر‬

،‫وهي في البحر تظن أنها في كأس صغير‬..‫بعضنا كسمكة عمياء‬ ‫ وأحطنا أنفسنا بجبال الكره والخوف والعداوة والحزن‬..‫خلقنا في عالم اليمان‬ ُ

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pellicle is formed by a selective adsorption ( ‫ )التصاق‬of environmental macromolecules . Hydroxyapattite is the main salt or building unit in our teeth, the net charge of this compound is negative ( so if we have positive components they will stick to it )  if we don’t have this pellicle , probably bacteria won't be able to stick to the tooth surface because it's net charge is also negative ( repulsion ) , the pellicle provide the lubricated surface which bacteria can adhere using it to the tooth surface. 2pellicle is formed almost with no ( zero ) time , you do scaling and you have zero bacteria on the tooth surface , within few hours the bacteria will start accumulating on the tooth surface. ( particularly the initial microorganisms will be Gram +ve facultative ones ) like S.mutans and the other oral streptococci .  Gram +ve : absorbs the blue\violet stains , then forms links with the added Iodine , after destaning with alcohol , the stain which wasn’t retained by the bacteria will be washed away , then we add the red counter stain Safranin , because Gram +ve has Iodine the color stays blue , while it will be red in Gram –ve bacteria . ( Gram +ve bacteria has thicker wall of peptedoglycans )  theses information are important when prescribing antibiotics .  facultative : can live normally in the presence and absence of oxygen . *These bacteria include :(the Dr : remember the key-names only which are ) Streptococcus mutans ( the major one ) Actinomyces viscosus Streptococcus sanguis ( important because it causes bacterial endocarditis

>> )  if we have a patient with rheumatic heart disease we give an antibiotic prophylaxis to prevent bacterial endocarditis;, S. sanguis can go to the blood reaching the valve then causes problems ( the word sanguis means blood- it was the first organism isolated from blood ) so direct relation for plaque when reaching blood stream >> as another example in a patient having atherosclerosis , it was associated with low birth weight in pregnant women , some of dental plaque components were isolated from the amniotic fluid that surrounds the fetus .  some of dental plaque components are being studied for the relation with some pulmonary diseases.

3Gram +ve bacteria are dominant in health- sates , plaque will start growing in the 3 dimensions , the deeper inner parts will become far away from Oxygen and nutrients , here the environment will be more anaerobic facultative bacteria can survive as we said , but here we will have other anaerobes which only can survive in an anaerobic conditions >>  aerobic bacteria release CO2 while breathing , Gram –ve bacteria releases toxic materials because of fermentation products . -4-

**as plaque grows up , the RATIO of Gram –ve : Gram +ve bacteria will increase ( both will increase in number but G-ve ratio will increase ) 4Then we will have secondary colonization and maturation and we will start having bad bacteria ( associated with periodontal disease) , (you should remember these names ) : - -provotella intermedia ( formely known as Bacteroidis intermedius ) and it's associated with so many forms of destructive periodontal diseases in particular PERGNANCY ASSOCIATED PROBLEMS [ pregnancy gingivitis , pregnancy tumors ]  during pregnancy Progesterone hormone level increases ( which stabilizes the pregnancy) Set from the 3rd – 8th months of gestation , then it will decrease, your ambition to infinity, ..infinity = PARADISE It was found that periodontal problems occur during the period between 3rd th –8 months of pregnancy ( that was the subject of Dr. Rula's master thesis) progesterone blood  crevicular fluid  P. intermedia loves feeding on . -- Provotella loeschei ( not important) -- Capnocytophaga group ( capno = loves CO2 ) -- Fusobacterium nucleatum ( associated with certain periodontal diseases ANUG [acute necrotizing ulcerative gingivitis ] ) -- Porphyromonas gingivalis ( THE MOST DANGEROUS\VIRULENT ONE )  P . gingivalis is the only bacteria able to produce gelatinase enzyme , it was called previously bacteroidis gingivalis both Porphyromonas and provotella produces black colonies on blood agar , that’s why that’s why they were called black pigmented Gram –ve anaerobes . How much bacteria we have in this plaque ? there is 1.7 X 1011 microorganism in 1 gm of wet plaque , ( imagine 17 with 10 zeros next to it !) - interactions between these bacteria varies , some of them like each other and some hate each other , ( just like humans they are a large community ) and supragingival plaque is a well organized community . - so the relations can be either Symbiotic [ where you give me and I give you ,and both benefits from each other ‫ ] تبادل المنفعة‬, or it can be Antibiosis [ where some may kill the other – competitors ] , or they may be indifferent . - there is a unique phenomenon only found with oral bacteria called aggregation, where some bacteria stick to each other giving a unique form such as corn cobs ‫كوز‬ ‫ الذرة‬huge filaments fusiform or G +ve or small cocci stick to it , -also we have test tube brush appearance where there are filaments with small rods attached to it.

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::the chronological sequence of plaque formation :: 1after cleaning the teeth.

the acquired pellicle formed almost immediately

2the supragingival plaque : subgingival plaque is not formed without being preceded by supragingival plaque , although most of the damage occur because subgingival plaque because anaerobes mostly are in subgingival plaque , so one method for preventing the damage is by prevention of the supragingival plaque , and that’s what we do in our oral hygiene measures at home by tooth brushing . on Day 0  we have sparse ( little ) flora , 90% is Gram +ve cocci and rods , 10% only Gram –ve cocci and rods . 3between first few days ( 3-4 days ) fusobacteria start to show up , [fusoform= cigar shape] which are big bacteria , also filaments (threads) which are long bacteria will start to proliferate , here the percentage will be 20% of plaque Gram +ve cooci and rods still forms 55% , notice the drop from 90% to 55%. st 4- The true test of character is By week 5-7how ) , we Gram +ve not the how end much of we1know how (todays do, but behave " cocci and rods down to 34% , filaments are 15% , andtoGram –ve about 50% . ".when we don't know what do - we have something new here which is spirochetes , some people believe that there appearance indicates the beginning of disease.

5Between day 8-29 , there is no major shift in percentages , but the volume increases,

How did we know that plaque causes disease ? the Dr told us this story  Until the 60s of the last century there was a debate on what causing the periodontal disease, [ cariogenic theory by Miller was presented in the 19th century as you know ;) ] until the famous experiment of Loe and Sillness ( who put plaque and gingival indices ) proved that the etiological factor is plaque , Loe, Sillness and Thylade ( Scandinavian scientists) , did the following experiment on dental students, They got these healthy young volunteers of dental students, the performed prophylaxis for their teeth , where they got "0" gingival index , then the refrained them from all their oral hygiene measures : the asked them to stop brushing their teeth , after 3 weeks (day 21 ) all the students developed gingivitis , then they reinstate the oral hygiene measures and let them to clean their teeth again ,here gingivitis disappeared , that was the 1st experiment . Another proof , where germ free animals ( with zero bacteria in their mouths ) like mice and rats , then they started adding different types of bacteria and they started getting different periodontal diseases . -6-

also it was clinically shown that when you clean the mouth or give the patient a mouth wash gingivitis goes away . Plaque is associated with tooth surface and periodontal tissues , On the tooth surface : we have different types of bacteria attached to the tooth surface in comparison to these in the tissues . we have : S. mitis S. sanguis -

(( oral streptocooci )) + actinomyces

(( these? Are important in caries , I don’t want you to remember the name in particular )) dr said thE apical border of plaque is going down into the pocket , it's separated from the junctional epithelium by a layer of leukocytes ( PMNs in particular – they are the first cells to fight infections) they leak from blood vessels to the crevicular fluid in the sulcus area to fight invaders , in the apical tooth associated regions : we see an increase in Gram –ve rods because

the area is more anaerobic ( blood stagnation and Oxygen loss ) ,tissue associated plaque in not organized as supragingival plaque , we have : Provotella intermedia Porphyromonas gingivalis The Dr put a figure showing that: ‫ ويقيني بال يقيني‬..‫بال سأبلغ آمالي‬ * bacteria on the tooth surface is different from the ones ِ ‫مشحو‬ ‫ن‬ ٍ ‫سأطل كصب‬...‫فاق‬ ‫ح‬ ّ ‫كطيٍر خ‬ ‫سأجّد‬in the soft tissues , • bacteria can invade tissues even if they are immotile , the can reach the bone as well causing damage ,  in the past they thought that bacteria cant invade tissues because they are immotile (such as P. gingivalis ) so how it reached there? it was thought that it's an artifact comes when doing the biopsy , when you cut a cake that has a layer of chocolate on top of it , the knife will bring part of the chocolate underneath it's edge downward to the cake base , the same thought to be happening when you make biopsies and fix it with paraffin wax and stain it then when cutting it with the microtome , but tissue cultures showed that when we are growing epithelium for example on a dish in the lab , and put bacteria after washing out bacteria we will find that bacteria invaded the cells because the cells have the ability of phagocytosis . we know that each disease in caused by certain bacteria , Typhoid for example is causes by salmonella ,flue is caused by certain viruses == specific organism causes a specific disease, but in periodontal diseased it's not the case , we have 3 theories : 1the Non- specific hypothesis : it says all plaque is bad, although we said we have a balance , but it the plaque mass overwhelmed the host defenses we will have diseases . more plaque  more inflammation . 2the specific plaque hypothesis : we was battled that some clean mouths have severe forms of periodontitis , -7-

and certain bacteria were isolated from these cases , here we have the specific plaque theory . it assumes that only certain members of plaque is bad, like - provotella intermedia - Actinobacillus actinomycetemcomitans ( Aa ) - Porphyromonas gingivalis 3- however , the truth probably lies in between ( both hypothesis are true ) * more plaque  more disease * certain bacteria  more forms of disease .

in case of periodontal health you mainly find Gram +ve bacteria , ( oral streptococci ) and Actinomyces - rods ( viscosus & nuselandi ). [ that doesn’t mean that we don’t have Gram –ve bacteria , we have them but the ratio and the number is small  not enough to cause diseases ( P. intermedia , F.nucleatum just with flora) ]

** we have about 300-500 species of microorganisms in our oral cavities , some of them is not even identified yet ! so its very hard to prove the association of certain bacteria with certain plaque.

A truly rich man is one whose children run into his arms even .when his hands are empty

~~ very easy as u will see , same names repeating ;) ~~ - in pregnancy gingivitis : 1- Provotella intermedia ( strongly associated ) - Acute necrotizing ulcerative gingivitis: ANUG ( 4 associated bacteria at least ) 1- Provotella intermedia ( now considered a primary one ) 2- Treponema vencenti ( older books called it Borrelia vencenti but they are large spirochetes (treponemes not borrelia) )

3- unidentified small spirochetes 4- Fusobacterium nucleatum . - chronic periodontitis ( adult periodontitis ) 1- porphyromonas gingivalis ( top of the lest ) 2- Provotella intermedia 3- fusobacterium nucleatum 4- Actinobacillus acyinomycetemcomitans (Aa)  P. gingivalis and P. intermedia don’t like each others if they are present together , P. gingivalis prevails ( win ) , - rapidly progressive periodontitis ( aggressive ) in yonger patients : 1- Actinobacillus acyinomycetemcomitans ( on the top ) 2- P. gingivalis 3- P. intermedia

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- juvenile periodontitis : ( localized aggressive periodontitis ) 1- Actinobacillus acyinomycetemcomitans ( most important ) 2- Porphyromonas gingivalis 3- Provotella intermedia ( added recently ) (( nOte : in localized it's Aa , in Generalized it's P. Gingivalis )) - prepupertal periodontitis ( associated with hormonal changes ) same bacteria ( that what the dr said ) - HIV gingivitis cultures reveals that CULTURES ARE SIMILAR TO THOSE OF HEALTY PEOPLE not like gingivitis , the Dr said it may be a question in the EXAM! ( G+ve : strps +actinomyces )

================= the Dr put some slides to some bacterial colonies , P. intermedia  black colonies ( darker colors depend on blood type , darker with rabbit blood cultures ) , Aa , Bacteroides forsythus (Provotella), P. gingivalis on sheep blood doesn’t look dark in color here , but it will be darker with time and will be black also, F. nucleatum .

::Virulence factors ::( give the ability to the bacteria to cause damage ):they give it the ability either to colonize , invade or evade (‫ ) تتجنب‬and avoid the One generation plants the trees; another gets the shade host's defenses. This damage is either : direct damage , physical damage or indirect . - colonization and invasion of Periodontal tissues is a physical one . ( bacteria violates and disrupts the cell itself ) - most of the damage , however, occurs because of the host's immune system. how can bacteria cause damage? a- degradation of the host tissues .and releasing of biologically active substances from the tissues; for example the PMN's have many enzymes , if the cell bursts , these enzymes will damage the tissue itself . b- inhibit the growth or altering the metabolism of the host tissue cells .( cells become sick ) c- the enzymes produced by the periodontal pathogens also can destroy the host tissue , because these bacteria ( e.g P . gingivalis ) are very small , so when it release proteolytic enzymes in an area it breaks proteins ( as collagen ) into smaller particles that they can feed on . so bacterial enzymes facilitate destruction and invasion of the host tissues . ( it open the road ) the Dr put a picture from our book saying its very complicated , it shows how one step of bacterial invasion facilitate an other ,,, -9-

Defence mechanisms of the gingiva : - crevecular fluid continuously washes bacteria.(its activity decreases at night, not inflammatory exudate )

- electrolytes . - PMN's in the sulcular fluid . - saliva : it has antibodies , ( IgA ) The Dr put another picture , showing a rat mouth with bone resorption by only one organism Aa , The Dr then put another one and told us that an end product of one bacteria is used by another one . Menadione ( vitamin K ) for example , is needed by P. gingivalis , this will produce isobutyerate ( fatty acid ) will be used by treponema for example . the Dr said that there is a mistake in the figure in our books , Lactate increases the growth of Porhphyromonas gingivalis not the opposite ( the Dr's PhD thesis ). That was the end of the lecture …

... ‫تمت بحمد الله‬ : Done By ..KAYATA ® ‫وإني لرجو ال حتى كأنني أرى بجميل الصبر ما ال صانع‬ .

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