UOL PRD Flashcards
Dental Plaque
A soft layer composed mainly of bacteria which forms on the hard structures of the mouth and is present in all mouths
Dental Biolfilm
A complex association of many different bacteria in a single environment
Features of Biolfim
Bacteria more resistant to environmental changes
Reduced susceptibility to antimicrobial agents
Lower nutritional requirements
Materia Alba
Soft accumulation of bacteria, dead cells and food debris that is loosely adhered to teeth
Pellicle
A thin layer of salivary proteins
Calculus
A hard deposit of mi realised plaque which is invariable covered with a layer of soft plaque
Composition of dental plaque
Bacteria
Inorganic
Organic
Organic components of plaque
Polysaccharides
Glycoproteins
Lipids
Inorganic components of plaque
Calcium Phosphate Sodium Potassium Fluoride
Plaque formation
Pellicle
initial colonisation by pioneer bacteria
Secondary colonisation
Maturation of plaque
How does the dental pellicle adhere to teeth
Electrostatic affinity
Initial pioneer bacteria
Gram positive facultative bacteria
Streptococcus sanguis
Actinomycetes viscosus
Streptococcus Oralia
Secondary colonisation bacteria
Fusobacterium nucleatum Porphyromonas gingivalis Prevotella intermedia Prevotella losechii Capnocytophagya
Tooth associated bacteria
Streptococcus sanguis
Streptococcus mitus
Actinomycetes viscosus
Actinomycetes naeslundi
Tissue associated bacteria
Gram negative rods, cocci, filaments, flagellated rods, spirochetes
Prevotella intermedia
Porphryomonas ginigvalis
Bacteriodes Forsythus
Aggregebacter actinomycetesmcomitans
Cariogenic bacteria
Streptococcus mutans
Actinomycetes sp
Lactobacillus acidophilus
Which study is the evidence of bacteria role in caries
1950s Orland and Keyes Germ Free Rats
High risk of caries
2-10% proportion of s.mutans in plaque
Low caries risk
0.1% s.mutans In plaque
Predominant bacteria in enamel pits and fissures
Streptococcus mutans
Predominant bacteria on approximately smooth surfaces
Actinomycetes
Predominant bacteria on exposed root surfaces
Streptococcus mutans
Actinomycetes
Lactobacillus sp
Local risk factors
Influence which sites develop disease
Systemic risk factors
Influence which individuals develop disease
Modifies the host response to plaque
Periodontal pathogens
Porphyromonas gingivalis
Prevotella intermedia
Aggregebacter Actinomycetemcomitans
3 plaque hypothesis
Specific
Non-specific
Ecological
Non Specific plaque hypotheses
The quantity of plaque matters - gingivitis
Specific plaque hypothesis
The quality of plaque matters - aggressive periodontitis
Ecological plaque hypothesis
Small number of interacting species may cause destruction (unified theory) - chronic periodontitis
Medications that cause DIGO
Calcium channel blockers
Phenytoin
Cyclosporine
Systemic diseases that effect the host response
Diabetes Infections Osteoporosis CV disease Haematological diseases
Inherited syndromes effecting the immune response
Leukocyte adhesion deficiencies Checliak - Higashi syndrome Ehlers-Danlos syndrome Hyphophosphatasia Down’s syndrome Papillon-lefevre syndrome
What % of damage is caused by host response
80%
What % of damage is caused by bacteria
20%
Nutritional deficiency in periodontal disease
Lack of Vit C / scurvy
Pro-inflammatory foods
Saturated fats
Refined carbohydrates
Anti inflammatory foods
Fruit and veg
Adipose tissues store what
Cytokines
Cytokines and adoteases are anti inflammatory or pro inflammatory
Pro inflammatory
Increased prevalence in periodontal disease in what race
Chinese
Asians
Afro-Caribbean’s
Systemic risk factors (11)
Smoking Diabetes Medications Systemic diseases Nutrition Obesity Race Gender Genetics Stress Hormonal changes
second biggest risk factor after smoking
Diabetes
What % of people have diabetes
5%
What is the relationship between perio and diabetes
Bi-directional
Test for diabetes
HBA1C
AGES stands for
Advanced glycated end products
Severity of gingivitis correlates with which hormone
Progesterone
Junctional epithelium
Highly specialised Non-keratinised Fast turnover 20-30 cells thick Attached via hemidesmasomes
Compact bone
Oral and buccal cortical plates
Thin compact layer lining the socket
Cancellous bone
In between contact layers
Gingival fibres (4)
Transeptal fibres
Circular fibres
Dentogingival fibres
Alveolar crest fibres
Lamina Dura
A radiographic term denoting the thin plate of compact bone that lies adjacent to the PDL and lines the socket
PDL features
0.1-0.3mm wide Constantly breaks down and renewed Cells - fibroblasts, cementoblasts, osteoblasts, osteoclasts Blood vessels Nerves Lymphocytes
Principal Periodontal Fibres (5)
Dento-alveolar crest Horizontal Oblique Apical Interradicular
Composition of calculus
80% inorganic
20% organic
Inorganic calculus salts
Calcium phosphate
Calcium carbonate
Magnesium phosphate
Fluoride
Principal crystalline forms (4)
Calcium hydroxyapatite
Magnesium whitlockite
Octocalcium phosphate
Calcium brush it every
Organic portion of calculus
Proteins Carbohydrates Non-vital organisms Dead epithelial cells Leukocytes
When does precipitation of calculus begin
1-14 days after plaque growth
May be as early as 4-8 hrs
Theories of calculus formation
Nucleation theory - most likely theory (seeding)
Precipitation theory - precipitation of mineral ions from saliva
Attachment of calculus to tooth
Acquired pellicle
to irregularities in tooth surface
Holes in roots where sharpeys fibres were inserted
Direct contact - calcium deposit interlocked with crystals of tooth
Stain
Discolouration spot or mark caused by contact with foreign matter
Not easily removed
Extrinsic
Originating from without
Mineralised and can be removed by scaling or polishing
Intrinsic stain
Integral part of tooth structure cannot be removed by scaling
Examples of extrinsic stain
Metallic
Tobacco
Food and drink
Examples of intrinsic stain
Non vital tooth
Tetracycline
Fluorosis
1989 classifications of periodontitis
Adult Early onset Systemic disease ANUG Refractory
1999 classification of periodontitis
Chronic Aggressive NUG/NUP Systemic Periodontal abscess Perio endo legions
Severity of disease
Mild 1-2mm CAL
Moderation 3-4mm CAL
Severe >5mm CAL
Localised %
<30%
Generalised %
> 30%
Aetiology of periapical abscesses
Insult to tooth Acute pulpitis Pulpal necrosis Acute periapical periodontitis Acute periapical abscess Acute chronic
Aetiology of periodontal abscess
Pre-existing periodontal pocket
Foreign body impact ion
Compromised immune system
Response to incomplete treatment
Symptoms of pulpal \ periapical abscess
Non-vital Swelling over apex Sinus over apex TTP+++ Bone loss at apex