This lecture is include slides

Introduction
Today we start a new topic which is more related to the true periodontal disease in terms of clinical application we know that what etiology means ? " cause " and today's lecture is a fundamental one you will need this information for your course out until you graduate and maybe later on because we said maybe lecture that basically periodontal disease is an inflammation of the periodontal tissue (gingiva , PDL , and so on .. ) the cause of this inflammation multi factorial but it is related mainly to the present of microorganisms in the oral cavity , specific type of MO or specific percentage of it that induce bury-inner - reaction that cause PD destruction .

Health : is defined general as a state of well being physical, mental

,social so its normally a balance between the body ability to defend itself against the invading MO (mainly bacteria ,some viruses and some fungal species) . when we have this balance there is No PD destruction but once this balance is shifted to either right or left side we will have problem if the bacterial population is stronger than the host defense disease take place on the other hand if the body ability to fight bacteria is more than needed what happen is body destruction and this is very prominent in case of autoimmune disease or immune mediated disease .

NOTE
It was found that most of the destruction of PD tissue is not caused by bacteria ! it caused by the exaggerated response of the host against the bacteria "the pattern of body defense against bacteria dose a lot of collateral damage". Soo health : is balance between host defense and bacterial population , disease imbalance HD,PP .

Q:when we have theses microorganisms in our oral cavity?

**The human intrauterine fetus is sterile , but after passing through birth canal , the fetus acquires vaginal and fecal microorganisms some bacterial colonization maybe detected in the mouth of the fetus within first hours after birth . maybe you note from microbiology courses that some or most of the bacteria with in the oral cavity are microflora (good bacteria )they defend our selfs & defend the oral cavity against some worse bactaria .. **After tooth eruption , more complex micro flora is established , we found that > 500 species of bacteria that live in the oral cavity some researchers said than we have >1000 MO species including bacteria and other species. **After the age of 2 years , human micro flora is established which generally lives in harmony with the body (commensal or beneficial) .

Mechanisums that involoved in removal of bactria from the oro-pharyngeal area :

1- Swallowing, mastication and blowing the nose . 2- Flow of different fluids (saliva, nasal, GCF,..) . 3- Tongue and oral hygiene measures . 4- Movement of cilia in nose and sinuses . 5-High turnover of the oral epithelial cells ( to differentiate between soft and hard tissue u know that enamel is a hard tissue ; there is no turn over , this happens with the normal mucosa so that's why we have

dental caries , imagine that enamel can slough away the super facial layer that intact from bacteria will slough but fortunately this is not happen :P and this make dentistry in high value ) .

Old belief

Periodontal disease are caused by cumulative accumulation of all type of bacteria on tooth.

Current , understanding

A small group of bacteria are the initiators for the disease and most of tissue destruction caused by host defense reaction to bacteria

Therefore

The central role of microorganism has always been , and is still recognized

So although the belief have changed from all type of bacteria to the group of bacteria the role of bacteria is still the focus or intention and important

These microorganisms, mainly bacteria, populates the oral cavity in biofilms called: Dental Plaque . Dental plaque is defined clinically as structured , resilient yellow-grayish substance that adheres tenaciously to the intraoral hard surface . .

Soft deposits starts as Materia Alba that forms the dental pellicle immediately after tooth brush saliva covers newly clean teeth and we know saliva is composed of glycoproteins so this chemical which can be removed by just eating or mouthwash & if its lift for enough time what happens it becomes thicker & more deposits attached to this small layer to form what we call Materia Alba so these are basically soft deposits and they dont have ascertain organization or structure so that its easily removed by water spray and mouthwash they dont need toothbrush ,,, now if those deposits leave for enough period it start organize itself and form the Dental plaque which cant be removed by water spray or mouthwash mechanical removal has to take place ,,, and this plaque if it lift for more time it will form dental calculus which is the topic in the next lecture EnshAllah - .

So again we have Materia Alba (soft tissue can be removed by water spray mouthwash and toothbrush less organized ) + time well form dental plaque (more organized cant be removed by water spray mouth wash but we can remove it mechanically by tooth brush ) ++ time well form dental calculus (more organized calcified dental plaque one and cant be remove even by tooth brush ) .

** Dental plaque is a type of biofilm and biofilm is the bacteria when they are attached to the surface basically matrial to cover themselves to change the environment & make it resistant to external forces also become resistant to inter microorganisms so basically this biofilms is able to attach to hard tissue and soft tissue ( gingival tissue ) ; but the mechanism of attachment of bacteria is or facilitate attachment to hard tissue rather than soft tissue. ***free flouting bacteria in the oral cavity dont causing disease , it has to be adhere to surface in order to coz disease ; once they are attached they form a community of the bacteria , the coz of disease not single bacteria the couse is the community , these bacteria which have the ability to attach to a surface are called initial colonizer not all bacteria has the ability to attach to the surface and those colonizer are basically not disease causing bactiria ( not violent ) they secrete extracellular material then secondry colonizers become and attached themselves and these are the bad one (secondary colonizers ) ; they multibly and form anew more complex community and cause disease .. and this is generally how biofilme formed .

Plaque composition :

1- 70% of the plaque is composed of micro-organisms, mainly bacteria .

>500 species

 108 bacteria (in diseased crevice) -bacterial species: mycoplasma, yeasts, protozoa , parasites and viruses . 2- Extracellular matrix 30 % : *epithelial cells. **macrophages . ***Leukocytes . ****embedded in a matrix .

Calcification of dental plaque :

1- supragingival (above the gingival margine )
Coronal related to calculus and caries. Marginal related to gingivitis. The supragingival is the mostly associated to gingivitis(inflammation of the gingival soft tissue ) .

2-subgingival when the plaque when the plaque is accumulate and

extend below gingival margin ; related to preiodontitise (the inflammation of the periodontal complex more sever) .

We can find bactria adher to the soft tissue (gingival ) hard tissue (tooth ) or in between < look at the pic in the next page

unattached 3- tissue attached 1-tooth attached 2Dental plaque and biofilms Biofilms is very important the beginning of infection is start by forming biofilmes . Where can we see biofilms : 1-pt with hemodialysis in the tubes that are used in this process 2-R.T infection . 3- U.T infection . 4-PD. *** Biofilms are: matrix-enclosed bacterial populations adherent to each other and / or to surfaces or interfaces .

**** They are ecological communities that evolved to permit survival of the community as a whole .
*** the most important information is the fluid filled channels in the inner most

layer we have channels they are like tunnels under ground (subways ) , these are very important to the bacteria to receive there nutrients (fluid filled channels ) which supply the bacteria by its nutrient ,, and this well make innermost layer away from the surface this channels is away from the surface and when we use mouthwash it kill the bacteria at the surface but dont reach to the inner most layer & it was found that the bacterial in the biofilms is much more resistance to antimicrobial compared to bacteria on the out surface . Ex ( if u make single bacterial culture in the microbiology lab u need for example [x] of amoxicillin to kill it but if these bacteria are in the biofilms they needs [500x] amoxicillin to be killed )

Fluid filled channels

This pic shows how the biofilms is formed and stast irritating the gingiva .

Intercellular Matrix 20 30 % of the plaque

mass Organic and inorganic material from saliva, GCF and bacterial products .

Organic

Inorganic

-polysaccharide -protiens -glycoprotiens -lipid

Ca , P and traces of Na , K , F Primary source saliva

Note : in the supraginival mineralization the source of minerals is saliva while in the supgigival the source of minerals is the GCF . dental plaque formation
1- Formation of the pellicle . 2- Initial bacterial adhesion and attachment 3- Secondary Colonization 4- Plaque Maturation

1- Formation of the pellical :

The initial phase of plaque formation . All surfaces of the oral cavity are coated with a glycoprotein pellicle . The pellicle comes from saliva, GCF, bacterial, and host tissue cell products & debries . The hydroxyapatite surface: -ve charged phosphate groups Salivary and crevicular fluid macromolecules components : +ve charged . They interact directly or indirectly Mechanisms involved the following forces:

. Dental pellical is important to protect and lubricate tissue BUT Also a substrate to which bacteria can attach and accumulate to form dental plaque ..

Note eno dental pellicle it is not bacterial derivative its only salivary matrial and sub tissue !

___________________________________________________________

2-initial adhesion of bacteria

 Within a few hours, bacteria are found on the dental pellicle (primary colonizers) . Mechanisms not fully understood Suggested stages: of bacteria to the surface Initial (reversible) adhesion Attachment Colonization and plaque formation Initially, Gram positive, e.g. Actinomyces vicosus, Streptococcus sanguis

*** The primary colonizers are 1- aerobics because they have capacity to use oxygen for there living and u know that oxygen is presented in an aerobic environment its simple u ca imagine the superfacial layer that is exposed to the O2 is have to be aerobic but the areas in the tooth are away from O2 so they cant live so that the secondary colonizers become anaerobic they dont need O2 for live and this will make them worse gays 2- G+ bacteria have the ability to use sugar and saliva to get there nutrients again imagine the inner most layer is away from saliva so they have to depend in something else other than sugars and saliva so environment change from G+ to G- change also there nutrient . At the End of this stage (bacterial adhesion ) : Shift will occur from primary aerobic (G+) colonizers to secondary anaerobic (G-) colonizers .

3- secondary colonizers
Primary colonizers cant cause disease by their own they need help from other gays and those what we call secondary colonizers they start modify the environment and they have lived in organized pattern they are co aggregate in protein and bacterial biofilm and this create empty space for other bactria to come and co aggregate . Examples of these secondary colonizers : Prevotella intermedia, Prevotella loescheii, Capnocytophaga spp., Fusobacterium nucleatum and Porphyromonas gingivalis .

4-blaque formation and maturation

A- Co aggregation ; (just understanding )
ex if I belong to Al-shmary family any gay who is related to the Al.shamry area is welcome by me so here in bactira colonize we see : F. nucleatum with S. sangius . P. loescheii with A. viscosus .

Capnocytophaga ochracea with A. viscosus . F. nucleatum with P. gingivalis F. nucleatum with Treponema denticola .

** look here streptococcus actinomyces produce lactate and formate by metabolism lactate is used by veillonella which produce many mineral used by prophyromonas gingivalis and so on .. so this is interactive community of bacteria that make them able to live tolerant (Agonist

interaction see later *)

B- adhesion
Adhesion start by which the bacteria start to attach themselves to other bacteria on the surface and its suggested that this Bactria have adhesive function .

Streptococcus species are the most predominant pellicle colonizers and provide an array of adhesins after attachment .

microbial interreaction

Agonistic Interactions
Cooper ation in the metabol ism of digeste d proteins Providin g favorabl e growth conditio ns

Antagonistic Interactions

Providi ng growth factors

Inhibition of growth:

Competitio n on nutrients

Inhibition of attachme nt

In the pic above you can see 'corncob ' configuration : growth of cocci on the surface of filamentous microorganisms .

here you see test tube brushes are gram negative filamentous bacteria, some of which may be flagellated .

long filaments held together by an amorphous extracellular matrix .

Subgingival plaque
Subgingival ______ away from O2 _____ better environment to danger bacteria _____ provide more than one surface to bactria ( hard & soft tissue and in between ) . Subgingival niches : The tooth (or implant) surface

Subgingival bacteria have the capacity to invade dentinal tubules plaque occurs during pregnancy.

levels

intermedia proportions ensitive indicator of altered systemic hormonal situation than clinical parameters of gingivitis. Non specific plaque hypothesis 1890

Plaque as a whole is the important factor! * non specific means any type of bacteria cause dieses , but it has been found that this is not the case it is seen that:

develope destructive periodontitis . odontitis have affected sites next to unaffected sites . These findings indicate that not all plaque is equally pathogenic .

Spasific plaque hypothsis 1979

. depends on the presence of or increase in specific microorganisms . link with localized aggressive periodontitis .

Ecology plaque hypothesis 1991

Disease can be attributed to changes in the environment which disrupt homeostasis between the plaque microflora and host .

to periodontal disease , we need to have a susceptible host to have a disease . *** how dose plaque grow ?!! In the past, it was thought that plaque grows by apposition of new bacteria at the plaque surface .

division of adherent bacteria .

Clinical aspects of plaque formation

Topography of supragingival plaque then supgingval formation take place .

. ex enamel is more smooth than cementom if there is gingival recession is easier to bacteria to colonize . . . ttability of tooth surface is another factor .

Variation within dentition - more on: . . . .

. not really! & Thats it Done by : zain salameen