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118 Cards in this Set
- Front
- Back
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Gram Positive bacteria |
Retain purple colour when stained Have a single, thick cell membrane Are usually associated with periodontal health |
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Gram-negative bacteria |
Red stain Have double cell membranes Associated with periodontitis |
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Percentage of attached vs. free floating bacteria |
More than 99% of all bacteria on earth live as attached bacteria
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What do biofilms consist of
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Many species of bacteria
Other organisms Debris |
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What are the three life cycles of a biofilm?
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1) Bacteria attach to a surface 2) Bacteria growth 3) Detachment |
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What is the film that the attached bacteria secrete? (step 2)
What is its function? |
The extracellular slime layer
- acts as a protective shield - helps anchor bacteria to the tooth |
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What are the 5 phases of plaque biofilm development? |
1) Film coating
2) Binding of single organisms 3) Multiplication (Coaggregation) 4) Continued growth 5) Mature biofilm |
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How long after a cleaning does a film form over the tooth surface?
What is the name of the film? |
Forms within minutes Acquired pellicle |
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What is the main purpose of the acquired pellicle? |
To protect the enamel from acids
Disadvantages: - acts a double-sided adhesive tape - provides a sticky side that aids bacteria in sticking to the tooth surface - alters the charge and energy of the tooth surface |
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How long after pellicle formation do bacteria begin to attach to the surface?
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Within a few hours
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Fimbriae |
Hair-like attachment structures that enable bacteria to attach rapidly upon contact |
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Bacterial Blooms |
Periods when specific series or groups of species grow at rapidly accelerated rates
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Structural elements of mature biofilm
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- Bacterial microcolonies
- Extracellular slime layer - Fluid forces of the surrounding saliva - Fluid channels - Cell-to-cell communication system - Bacterial signaling |
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Differences in microcolony environments
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Oxygen concentration, pH, temperature
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Why is bacterial diversity important?
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Ensures the survival of the plaque biofilm - makes it less likely that a toxic agent or condition could destroy the biofilm
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Benefits of fluid forces (for the bacteria)
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- Influence the shape of the biofilm
- Result in the development of extensions from the main body - Result in cell to cell collisions; which lead to a rapid spread of genes among bacteria |
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Disadvantage of fluid forces (for the bacteria)
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Extensions can break free and be swallowed or expactorated |
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Fluid channels
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-Penetrate the slime layer
- Bring nutrients and oxygen to the bacteria - Carry bacterial waste products away *Included in the fluid is everything from saliva to beverages consumed |
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Cell to Cell communication system
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Direct cell-to-cell interaction occurs among the bacteria within the biofilm
Bacteria use chemical signals to communicate with each other - this communication also results in the transfer of genes among bacteria |
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Bacterial signalling
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Bacteria within a biofilm produce 100s of proteins that free-floating bacteria do not
Function to trigger the adhesion of additional bacteria and form the ECSL Early colonizers send signals to pathogens when conditions are favourable to join |
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Sequence of bacterial colonization |
Early colonizers - adhere to the pellicle coating
Intermediate colonizers - coaggregate with the early colonizers Late colonizers - coaggregate with the late colonizers *Periodontal pathogens cannot colonize the biofilm until the non-pathogenic early colonizers attach to the tooth |
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Which species are early colonizers? |
Streptococcal species have the ability to attach to the tooth pellicle and to each other (a feature other early colonizers dont have) Early gram positive A. viscous, S. sanguis |
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Timeline of attachment |
Within hours - pellicle forms over the crown of the tooth. Early colonizers attach supragingivally. 6 hours- surface of the tooth becomes covered Day 7 - Mature supragingival biofilm occurs 3-12 weeks - subgingival biofilm begins to form |
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Subgingival attachment zones |
- Root surface - Epithelial lining of the periodontal pocket |
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Tooth-Associated plaque biofilms |
•Bacteria attach to the tooth surface extending from the gingival margin to the junctional epithelium at base of pocket •Subgingival bacteria have ability to invade dentinal tubules •Cocci and rod microorganisms dominate tooth-associated biofilms |
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Tissue-Associated plaque biofilms |
•Bacteriaadhere to the epithelium •Adhereloosely to epithelium of pocket wall•Distinctlydifferent microorganisms from tooth-associated biofilms •Bacteriacan invade gingival connective tissues, periodontal connective tissues, andsurface of alveolar bone |
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Where else may bacteria be found? |
Theperiodontal pocket may also have free-floating, unattached bacteriathat is not part of the biofilm. |
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Nonspecific plaque hypothesis |
"Accumulationof plaque biofilm adjacent to gingival margin led to inflammation and thenperiodontal destruction". - Fails to explain why most cases of gingivitis do not progress to periodontitis |
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Specific Plaque Hypothesis |
"Specific pathogenic bacteria present in subgingival biofilms with their toxic products result in periodontal tissue destruction. The shift occurs with bacteria in the biofilm to be predominantly gram-negative anaerobes, from being gram-positive" - Includes Socranksy's microbial complexes - New research shows pathogens can be present in the absence of disease - bacteria more heretogenous and diverse than previously thought |
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Microbial homeostasis-host response hypothesis |
Plaque biofilm is necessary but not sufficient for periodontal destruction. Despitethe presence of plaque biofilm, bacteria do not appear to be the majordetermining factor in the progression of gingivitis to periodontitis. Established gingivitis would not change to periodontitis unless some other unknown factor tipped the delicate biofilm-host balance toward further destruction |
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Periodontal pathogen |
Amicroorganism that causes or can cause disease, or cause damage in a host |
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Commensal organisms |
•Onespecies obtains benefits from the other species without either harming orhelping the host species. •Theorganism may obtain nutrients, shelter, or locomotion from the host species. •Plaquebiofilm is an association of commensal organisms, sometimes transformed intobeing pathogenic. |
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Dental plaque |
Dense, nonmineralized mass of bacterial colonies in a gel-like intermicrobial, enclosed matrix that is attached to a moist environmental surface AKA - microbial plaque, dental plaque biofilm, oral biofilm, bacterial plaque bioflim |
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Soft deposits |
Oral biofilm Materia Alba Food debris |
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Hard deposits |
Calculus - sub and supragingival |
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How is calculus related to periodontal disease? |
Is a local contributing risk factor because it is covered in plaque biofilm *DOES NOT CAUSE PERIODONTAL DISEASE - acts a spot to grow bacteria |
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Local contributing factors |
DO NOT initiate PD - they contribute to the process already inititated by the bacterial plaque |
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How does calculus affect the gingiva? |
Will distend the tissues Often a dark edge may be seen just beneath the tissues Cannot be removed with brushing and flossing |
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Visual examination of calculus |
Can be stained or unstained
Use compressed air to view - small amounts can look invisible in saliva Looks white and chalky |
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Progression of periodontal disease - seven stages
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1) Pellicle formation 2) Bacterial biofilm formation –Mineralization of biofilm leads to calculus formation (supragingival and subgingival) –Bacterial biofilm overlays calculus 3) Inflammation…. Leading to pocket formation 4) Activation of the inflammatory response 5) Ulcerated sulcular epithelium with an increase in crevicular fluids, along with continued inflammation 6) The disease may progress to periodontitis if the JE migrates away from the CEJ and bone destruction occurs 7) The presence of tooth mobility and tooth loss can occur with further destruction |
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Dental plaque induced gingivitis
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Dental plaque leads to inflammation of the gingiva
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Non-plaque induced gingival diseases |
–A small percentage of gingival disease isnot caused directly by biofilm, although the presence of biofilm could increasethe severity of inflammation. - Viral and fungal infections, skindiseases, allergic reactions, mechanical trauma (including vigoroustoothbrushing methods), habits, occlusal forces, inadequate attached gingiva, frenalpull, etc.) |
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Acquired Pellicle and exogenous dental cuticle |
*Acellular Nonmineralized Unstructured, homogenous film adhering to tooth surfaces, firm surfaces in the oral cavity and old calculus May be stained by tar products or tannin |
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Dental plaque biofilm |
Cellular Nonmineralized Dense, transparent,highly organized mass of bacterial colonies in a gel-like intermicrobial, enclosed matrix Host-associated biofilm |
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Materia alba |
Cellular Nonmineralized Loose deposit of microorganisms, desquamated epithelial cells, and broken down food debris White to yellow-ish white in colour Has cottage cheese like appearance Can be displaced with rinsing and water irrigation |
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Food debris |
Cellular Nonmineralized Unstructured particles that remain in the mouth after eating and are removed with irrigation unless impacted between the teeth |
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Extrinsic stain |
Cellular May be mineralized or non-mineralized Discolourations that accumulate on the external surface of the tooth via. pellicle, plaque biofilm, or calculus Can be removed by power toothbrushing, scaling, and/or polishing |
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Supragingival calculus |
Cellular Mineralized layer Mineralized bacterial plaque permeated with moderately hard calcium phosphate crystals Superficially covered with bacterial plaque biofilm, usually white or yellowish-white in colour but may be stained darker *Source of minerals is slaiva |
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Subgingival calculus |
Cellular Mineralized layer Mineralized bacterial plaque, adheres to tooth structure in the gingival sulcus Organic matrix of bacteria permeated with hard calcium phosphate crystals May be stained green to greenish black Superficially covered with bacterial plaque biofilm *Source of minerals is GCF |
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Primary herpetic gingivostomatitis |
•Contagious infection
•Infection can be spread to eyes bytouching mouth and then eyes •Infection can be spread to others bykissing |
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Seven major categories of Periodontitis |
1.Chronic periodontitis – most common form of periodontitis (HPDP1)
2. Aggressive Periodontitis … highly destructive form 3. Periodontitis manifested by systemic disease •Hematological disorders …. ie Leukemia •Genetic disorders … ie. Downs syndrome, Leukocyte adhesion deficiency syndrome 4. Necrotizing Periodontal Disease - involves tissue necrosis 5. Abscess of Periodontium 6. Periodontitis associated with endo (root canal therapy) 7. Acquired deformities and conditions .. ie anatomic features, root abnormalities, restorations, mucogingival deformities, occlusal trauma |
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Chronic periodontitis |
–Previously called ‘Adult Periodontitis’
–May occur in primary or permanent dentition –Progresses at a slow to moderate rate –May be short periods of rapid disease progression –Classified by extent and severity –Smoking can predispose |
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Stable periodontitis (not worsening) |
–Occurrs in patients who have been successfully treated for periodontitis.
–At a later date, after successful treatment of the periodontitis, the patient may develop gingivitis –Pre-existing bone loss from previous history of periodontitis –May be plaque at gingival margin, however the CAL is stable |
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Oral hygiene assessment is the process of determining in the client:
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–Review of client’s medical and dentalhistory related to oral hygiene status
–Identification of local and systemiccontributing factors –Amount of hard and soft tooth deposits –Oral hygiene status& indices –Oral self-care effectiveness –Assessing for non-plaqueinduced problems relatedto oral hygiene –Motivation related to oral self-care |
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How are soft and hard deposits assessed? |
•Location *referencedto the gingival margin (Supragingival/ Subgingival) •Amount •Extentand distribution (Generalized/ Localized) |
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Halitosis |
Most common cause is bacteria present in the mouth, sinuses and throat
- this bacteria feeds on the protein in saliva and tissues - producing sulfur products (VSC) Other possible sources inc. medical and dental conditions, certain drugs, xerostomia, certain foods |
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How is halitosis measured?
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Halimeters Oral Chroma (GC) Organoleptic |
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How is halitosis treated? |
Improved oral hygiene Tongue cleaning Improved diet Antimicrobial rinses Medications Referrals |
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Oral hygiene assessment tools |
•Light •Compressedair •Mouthmirror •Periodontalexplorer *most common method assess biofilm •Gauze •Disclosingsolution |
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Purpose of disclosing agent |
•Biofilm is most commonly assessed by passing a dentalexplorer over the tooth surface•Disclosing agents make oral biofilmclinically visible •Available in liquid or tablet form and containingredients that temporarily stainplaque biofilm so that it can be observed and measured (using an index) •Twotone disclosing agents stain thicker (older) plaque blue and thinner (newerplaque) red |
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How is biofilm assessed? |
By its locations and extent (generalized, localized) |
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What is more important - quality of biofilm or quantity? |
Quality of biofilm is more important than quantity - for example, a client with severe gingivitis and small quantity of plaque will require a different approach to care |
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What are some contributing factors that influence the growth, retention, and removal of oral biofilm? |
malocclusion, mouthbreathing, faulty restorations, systemic factors,calculus (attracts biofilm) |
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How is biofilm changed to calculus? How long does it take? |
Oralbiofilm is mineralized by calcium and phosphate salts from salivaand the oral environment 10-20 days |
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What is the purpose for measuring oral hygiene indices? (index = singular) |
–Establish a baseline for an individual –Survey the oral hygiene status within a population –Establish a baseline for a target population –Evaluate an intervention, drug, or device *Oral hygiene status should be assessed at each visit in order to set goals with the client |
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Categories of indices |
•Screeningfor periodontal health ie:(PSR); •DentalBiofilm ie:PHP, PCR •Biofilm-Debris-Calculus; •GingivalBleeding; •Gingival/Periodontal; •Caries |
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General categories of indices |
Simple - the presence/absense of a condition Cumulative - past and present |
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Difference between PCR and PHP |
PCR - Plaque Control Record Indicates the percentage of tooth surfaces with biofilm -uses the whole mouth PHP - Patient Hygiene Performance - uses 6 teeth |
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Plaque Control Record |
By recording the presence of biofilm on individual tooth surface, it allows the client to visualize biofilm and learn from the OHI All teeth are inculded 4 surf. - facial, lingual, mesial, distal |
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How Plaque Control Record is performed |
*Before beginning - identify the teeth that are present. Draw a box around the missing teeth on the diagram. 1) Apply disclosing solution 2) Examine each tooth surface for plaque at the gingival margin 3) Record by colouring in the appropriate spaces on the diagram 4) Total the number of teeth and x by 4 (F,L,M,D). *available surfaces 5) Count the number of surfaces with plaque 6) Divide surfaces with plaque by the available surfaces to determine an overall percentage * 10% or less considered a good goal |
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Disadvantage of Plaque Control Record |
Time consuming Doesnt look at amount or quality - just location |
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Patient Hygiene performance |
5 surfaces on 6 teeth - Fac. of max 1st molars, R Fac. central incisor, Li of mand 1st molars, L Li central incisor Out of 30 possible, take the number of surface with plaque and divide it by 6 |
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Stains by origin - exogenous and endogenous |
Exogenous - orginiating from outside the tooth Endogenous - originating from within the tooth |
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Stains by location - extrinsic or intrinsic |
Extrinsic - occur on the external surface of the tooth Intrinsic - occur within the tooth substance and cannot be removed by scaling or polishing |
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Endogenous stains |
•ALWAYS INTRINSIC Originate within the tooth from developmental and systemic (ie. diseases or drugs) disturbances while the teeth are forming/developing •Usually discolorations of the dentin reflected through the enamel •Example: tetracycline staining/fluorosis |
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Exogenous stains |
•Develop or originate from sources OUTSIDE the tooth (environmental agents) ie. tobacco •May be extrinsic and stay on the outside of the tooth OR •Can become intrinsic over time and become incorporated within the tooth structure |
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Because more than one type of stain may occur, and there may be more than one etiologic factor - what must be examined? |
•Medical dental hx –Developmental complications, medications, use of tobacco, fluoride history •Food diary: –Contributing factors (soy sauce, tumeric/paprika, red wine, coffee) • Oral Hygiene Habits: – oral hygiene and cleanliness is significant |
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Which staining can be removed? |
•Extrinsic stains are those stains that are on the exterior of the tooth and can be removed. The source of the stain is external (exogenous) and the stain may be removed. Usually can be scaled. –staining from food, drink, tobacco, topical (applied on the teeth) fluoride stain (SnF2) •Intrinsic stains cannot be removed because the stain is incorporated into the structure of the tooth. Stains from …. –endogenous sources; –stains from dental amalgam that has become incorporated into the tooth structure; –extrinsic stains that have become embedded in the tooth … such as tobacco stain, green stain, |
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Significance of stain |
Stains are considered non-disease causing They are primarily a cosmetic concern, unless thickness increases could cause plaque retention |
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Green stain |
Caused by: Chromogenic bacteria and fungi from poor oral hygiene * Penicilium and aspergilus species Most often seen in children with enamel irregularities •Found in the presence of materia alba •May become embedded in enamel (intrinsic, exogenous) •Enamel is often demineralized •DO NOT SCALE AREA! •Daily fluoride regime used to treat |
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3 general forms of green stain |
1) Smallcurved line following the contour of gingival crest 2)Irregular,may cover facial surface 3) Streaked,following grooves and lines in enamel |
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Black stain |
Caused by - iron in saliva - iron containing oral solutions - actinomyces species - Industrial exposure to iron, manganese, and silver |
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Black line stain |
•Very tenacious / retentive •Forms along gingival third, along gingival margin •Composed of micororganisms embedded in intermicrobial matrix (Gram positive rods primarily) •Does not cause oral disease! |
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Orange stain |
Caused by: Chromogenic bacteria from poor oral hygiene |
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Brown stain |
Tobacco stain caused by: Tars from smoking, chewing, and dipping spit tobacco Food stain caused by: Food and beverage pigment and tannins |
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Topical medication |
Caused by: - Stannous fluoride - Chlorohexidine - Cetylpyridinium chloride mouth rinses |
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Yellow stain |
•Dull,yellowish discolouration ofdental biofilm•Commonin all ages, poor oral hygiene •Etiology:food pigments |
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Blue-green stain |
Mercury and lead dust |
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Red-black stain |
Caused by: Chewing betel nut, betel leaf, and lime (pan) Found in Western pacific and South Asian cultures |
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Intrinsic - dental fluorisis |
Appearance - white spotted to brown pitted enamel Cause: excessive fluoride ingestion prenatally (during enamel development) |
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Intrinsic - Hypocalcification |
Appearance - white spots on enamel Cause: high fever in utero |
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Intrisic - Demineralization |
Appearance - white or brown spots on enamel Cause: acid erosion of enamel caused by plaque |
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Intrinsic - Tetracycline |
Appearance: grayish brown discolouration Cause: ingestion of tetracycline in utero |
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Intrinsic - Enamel hypoplasia |
Enameldefect from a disturbance of the ameloblastsduring matrix formation – “incomplete” enamel formation leading to pitted,rough surfaces - can be generalized by systemic sources or localized by traumaor infections that affect uneruptedteeth. |
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Systemic contributing factors |
–effectsof smoking, diabetes, hormone alteration, psychosocial stress, geneticinfluence, systemic medications…. |
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Local contributing factors |
–dental calculus,, developmental defects, dental caries, habits, trauma from occlusion, toothbrush abrasion, and faulty dental fillings/restorations … which are called….(iatrogenic causes) –Oral conditions that increase an individual’s susceptibility to periodontal infection in specific sites |
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When does periodontal disease occur? |
Periodontaldisease results when the balance is changed betweenpathogenic bacteria and the host’sinflammatory and immune responses.Thebalance can also be affected by localand/or systemic risk factors. * Ifan individual’s immune system can effectively deal with a mouthful ofperiodontal pathogens, no destructive periodontal disease will occur. |
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What can cause the balance to swing towards disease? |
–Systemicillness –Medications –Smoking –Poordiet –Stress |
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How can local contributing factors be overcome? |
• Itis possible to eliminate local contributing factors to restore balance.
–Faultyrestoration • Itis possible to compensate for local factors that cannot be eliminated. –Goodhome care around crowded teeth |
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How can systemic risk factors be overcome?
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Patientscan work to eliminate systemic risk factors to restore balance.
–Controldiabetes –Quitsmoking *Ifsystemic risk factors cannot be eliminated, tip the balance toward health by increasing home care and professional care. |
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Risk Factors
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Are attributes or exposures thatsignificantly increase the risk for onset or progression of a specific disease
Influence one’s susceptibility todisease •Identifyrisk factors to determine which patients are more likely to prevent or controltheir dental disease. •Classifypatients into high-risk and low-risk groups. |
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Modifiable (Mutable) risk factors
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•smoking,specific bacterial pathogens, poor oral hygiene, bleeding gums, medications,& most local contributing factors
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Non-modifiable (non-mutable) risk factors
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• age, gender, genetic make-up, history of periodontitis (bone loss in the gums)
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How do local contributing factors contribute to periodontal disease? |
Local contributing factors DO NOT INITIATE periodontal disease.
They contribute to the process already initiated by the bacterial biofilm. They may increase the risk of developing disease. They may increase the risk of developing more severe disease. |
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Three Ways Local ContributingFactors Increase the Risk of Disease
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1) Increasebiofilm retention (rough edge on a restoration)
2) Increasebiofilm pathogenicity (biofilm-covered calculus deposit) 3) Causedirect damage to the periodontium(heavy chewing forces on a tooth) |
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How does calculus contribute to periodontal disease?
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The surface of the calculus deposit is irregular. Rough nature of the calculus tends to harbor bacteria.
The surface of the calculus deposit is always covered with disease-causing bacteria. As calculus builds up, it becomes irregular, forming ledges on the teeth. Plaque control becomes difficult. Plaque retention on irregular calculus increases risk for disease. Controlling disease in the presence of biofilm and calculus is difficult. |
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Three Modes of CalculusAttachment to the Tooth Surface
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1) Attachment to the pellicle
2) Attachment to the tooth irregularities 3) Attachment by direct contact to the tooth |
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Calculus attachment to pellicle
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•Pellicle—athin, bacteria-free membrane thatforms on surface of the tooth during late stages of eruption
•Mostcommon means of attachment to enamel surfaces •Calculusdeposits attached by pellicle are removedeasily because attachment is on surfaceof the pellicle, not locked to the tooth |
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Calculus attachment to irregularities in the tooth surface
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•Calculus deposits in cracks in the tooth surface, tiny openings from PDL detachment, or grooves in the cementum from over-instrumentation •Deposit removal is difficult because deposits lie sheltered in tooth defects |
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Calculus attachment to the tooth surface |
•Thematrix of calculus deposit may interlock with inorganic crystals of the tooth. •Depositsare firmly interlocked in the tooth and aredifficult to remove. |
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Heavy calculus vs. light calculus |
•Heavy calculus formers have a higher salivary concentrations of calcium and phosphate than light formers •Light calculus forms can have higher levels of pyrophosphate, a known inhibiter of calcification… also used in anticalculus toothpastes |
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What is calculus composed of? |
Inorganic components make up about 70% to 90% of the calculus, primarily calcium phosphate, but also contains calcium carbonate and magnesium phosphate, etc.. Organic components make up about 10-30% of the calculus and include non-vital microorganisms, desquamated epithelial cells, leukocytes, salivary mucins, fatty acids, carbohydrates, amino acids… etc… |
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What effect does age have on calculus? |
Crystals in calculus will have different proportions of calcium and phosphate in combination with other ions depending on age: Brushite – newly formed calculus Octocalcium phosphate – a bit more mature but less than 6 months Hydroxyapatite – more than 6 months |
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Supragingival calculus |
Is calculus located ‘coronal’ to the gingival margin Can occur at all ages, however incidence increases with age Often appears whitish or creamy or can be stained Mineral source is primarily from saliva Can occur with or without subgingival calculus Frequently found near salivary duct, although can occur on any tooth surface Shape is often irregular |
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Subgingival calculus |
•Is calculus located ‘apical’ to the gingival margin •Can appear a dark colour if stained by blood pigments •Can be called submarginal or serumal calculus •Can occur with or without associated supragingival calculus •Incidence increases with age •Mineral source is primarily from the gingival sulcus fluid (crevicular fluid) and inflammatory exudate. •Shape can be flattened •Often more difficult to remove |
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Palatogingival groove |
A developmental groove on thepalatal surface of a tooth Developmentalgrooves and root concavities lead to difficulty in patient self-care in thesite. (Naturallyoccurring root concavities harbor bacteria, increasing incidence of disease.) |
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Causesof Direct Damage to the Periodontium |
Food impaction Patient habits (incorrect self care, tongue thrusting) Faulty restorations (exclude biologic width) Inappropriate crown placement Improperly contoured restorations Faulty removable prosthesis (can impinge on gingival tissue and favour biofilm accumulation) Occlusal forces |
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Other contributing factors |
Limitation of normal activity(reduces effectiveness of self-cleansing mechanisms) Saliva Dietary and eating habits Oral Self Care Systemic Contributing Factors Tongue – tieShort upper lip Mouth breathing (often irritationshows up in the maxillary facial areas) Impaired muscular coordination Cognitive or physical disabilities |
