The Oral Microbiome, Biofilms, Gingivitis and Periodontitis

Question 1

Explain the symbiosis of man and microbes?

Answer 1

Healthy digestive tract
Resistance to colonisation of pathogens
Regulates CVS
Support host defence
Anti-inflamm properties
Additional metabolic potential
Antioxidant activity

Question 2

Name and explain different types of respiration?

Answer 2

Aerobic: in oxygen
Obligate aerobes: require oxygen
Obligate anaerobes: killed by oxygen
- o2 final electron acceptor 
- fermentation
Facultatice anaerobes: tolerate oxygen and switch to co2
Capnophilic: preferes co2

Question 3

Saliva functions?

Answer 3

ADD

Question 4

Biofilm definition?

Answer 4

Community of microbes characterised by cells that are attached to a surface or to each other and embedded in a matrix of extracellular polymeric substances

Question 5

Process of biofilm formation - bacterial formation and development?

Answer 5

Bacteria approach surface
Contact and attachment
Adherence and change in cell surface
Metabolic activity changes environment
Quorum sensing and development
Mature biofilm can seed new cells into environment

Question 6

Number of bacterial species? Genus examples?

Answer 6

770
Streptococcus
Staphylococcus
Bacillus
Aspergillus

Question 7

Number of fungal species? Genus examples?

Answer 7

9-23
Candida
Saccharomycrs
Aspergillus

Question 8

Viruses? Oral examples?

Answer 8

Herpes 90%

HPV 25%

Question 9

Priming of microbiome may originate in-uterine?

Process of priming?

Answer 9

Loosen of epithelial cells due to preg hormone (bacterial penetration)
Bacteria reach lamina propria and vasc tissue
Transfer bac to placenta via bloodstream
Oral bac trapped in placenta tissue
PACs acquire the allergenic info in placenta
APCs return to feral peripheral lymphoid organ
Fetal T regs recognised maternal microbiome as safe and generated in fetal lymphoid tissue

Question 10

Bacteria in buccal mucosa?

Answer 10

Streptococcus

Question 11

Bacteria in hard palate?

Answer 11

Streptococcus

Question 12

Bacteria in keratinsied gingiva?

Answer 12

Streptococcus

Question 13

Bacteria in saliva?

Answer 13

Streptococcus

Porphyromonas

Question 14

Bacteria in sibgingival plaque?

Answer 14

Strep
Fusobacterium
Prevotella

Question 15

Bacteria in supragingival plaque

Answer 15

Strep
Fuse
Coryne

Question 16

Bacteria in throat?

Answer 16

Strep

Question 17

Bacteria on tongue?

Answer 17

Strep

Question 18

Species of streptococcus?

Answer 18

Mutans: Alpha haemolysis, mutans, sobrinus, cricetus, dental caries
Salivarius: alpha, salivarius, vestibularius, keratibised surfaces and vestibule mucosa
Oralis: alpha, borealis, sanguis, mitis, gordonii and cristacus, early colonisers produces glucans, non-kerat, dental plaque
Anginosus: beta, anginosus, intermedius and constellatus, purulent infections (abscesses)

Question 19

Factors which cause the shift from symbiosis and dysbiosis?

Answer 19

Major ecological pressures
Inflammation
Increased temperature or pH
Diet and reduces pH

Question 20

Carbohydrate sources?

Answer 20

Glucose
Fructose
Sucrose
Lactose
Galactose
Mannose
Celliobiose 
B-glucosides
Trehalose 
Maltose
Raffinose 
Ribulose
Starch

Question 21

Pellicle? Description? Characterisitics?

Answer 21

The layer of material acquired by a cleaned tooth
- mucin, proline rich proteins, statherin and amylase (lysozyme, albumin, Ig, glucans)
Prerequisite for bacterial attachment

Question 22

Structure of pellicle?

Answer 22

90% salivary glycoproteins

- d domain, cys rich, O-glucans (VNTR) and cys rich

Question 23

Proline rich proteins? Characterisitics?

Answer 23

Acidic 16kD: saliva, affin for hydroxyapatite, Ca and PO4 levels and antibacterial activity
Basic 6-9kD: saliva and nasal secretions, complex with tannin
Glycosylated 36kD: newly formed pellicle

Question 24

Alpha amylase?

Answer 24

Alpha 1-4 glycosidic bonds
Digestive function of starch and amylase
Essential component of salivary pellicle
Bacterial receptor
Forms heterotypic mixed micelle like structure

Question 25

Bacterial adhesion?

Answer 25

Pellicle at the enamel allows adhesion to a bacteria, that can form a chain of bacteria

Question 26

Stages of development in plaque biofilm?

Answer 26

``` Start: Clean enamel surface 2s: Pellicle formation 1m: Pioneer bacteria (strep sangius) 2h: icrocolones and extracellular polysaccaride > 2h: biofilm 48h: mature plaque 2-7d: microbial succession and diversification > 7d: climax community ```

Question 27

Dysbiosis? Definition?

Answer 27

A condition in which the normal microbiome pop structure is disturbed often through external burdens such as disease states or medications

Question 28

Holobiont? Defintion?

Answer 28

Host organism and all its symbiotic microbial resident

Question 29

Microbiome? Defintion?

Answer 29

Sum of microbes and their genetic information and the environment in which they interact

Question 30

Symbiosis? Defintion?

Answer 30

Two or more species living closely together in a long term relationship

Question 31

Biofilm related diseases?

Answer 31

Periodontal disease | Dental caries

Question 32

Assessing a person's health?

Answer 32

By frailty

Question 33

What does the oral healthcare team gave to consider?

Answer 33

Weight loss, smoking cessation, exercise and controlling disease and glycaemia

Question 34

Educational programmes? Professional targets?

Answer 34

Mothers to be New mothers Care home workers People whom have dependable people

Question 35

Dental check ups? Key touch points?

Answer 35

2, 5, 12, 26, 40 and 70

Question 36

Toothbrush storage? Location and why?

Answer 36

Separately in bathroom to avoid horizontal transmission

Question 37

Saliva levels? Why?

Answer 37

Oral microbiome

Question 38

Bacteria colonisation? Location?

Answer 38

Teeth, gingival crevice and hard palate

Question 39

Dental biofilm? Defintion?

Answer 39

Masses of microorganisms that bind to and multiply on a solid surface, typically with a fluid bathing thr microbes Free flowing microorganisms are called planktonic cells These communities form microcolonies and interact with each other (quorum sensing)

Question 40

Acquired salivary pellicle? Characterisitics?

Answer 40

``` Thin layer Forms on teeth within seconds Smooth, colourless and translucent Bacteria free Derived from salivary glycoportrind Affinity for hydroxyapatite ```

Question 41

Initial stage of biofilm formation?

Answer 41

Attachment of acquired pellicle, which is a thin coat of salivary glycoprots, to a clean tooth surface Bind to buccal, but list due to desquamantion Non-shedding surfaces permit extensive development (plaque at retention sites) - susceptibility for disease

Question 42

Acquired pellicle formation? Host and bacterial origin?

Answer 42

Host: - glycoprot, phosphoprot, statherin, amylase, protein rich peps, and host defence components Bac: - glucotransferase and glucan

Question 43

Oral habitats? Location and characterisitics?

Answer 43

Buccal mucosa: - sparse, desquamates and masticatory friction Dorsum tongue: - highly, rough papillary surface, refuge, reservoir for -ve, low redux potential (anaerobic) Crevicular epith: - pioneer bacteria for initiation, and development of gingival and periodontal disease Dentures, restorations and orthodontic Tooth surfaces: supra and subgingival (non-shed)

Question 44

Teeth as a habitat? Characteristics?

Answer 44

Only non-shed area of the oral cavity Masses of bacteria constantly accumulate at surface to produce biofilm Biofilm is the initatiting factor in caries and periodontal disease Shoft from symbiotic to dysbiotic

Question 45

Areas of tooth decay?

Answer 45

Smooth surface cavity Pit and fissure cavity Root cavity

Question 46

Factors modulating microbial growth - anatomical characteristics?

Answer 46

Anatomical: - shape and topography of teeth, misalignment, poor restorations, and non keratinised sulcular epith

Question 47

Factors modulating microbial growth? Saliva characterisitics?

Answer 47

Saliva: - mix of inorganic ions Ca, Na, K, bicarbonate, PO4, Cl and proteins/glycoprots - forms salivary pellicle (adhesion site) - food source - aggregation of bac - growth inhib (lysozymes and histatins) - pH maintenance (buffering)

Question 48

Factors modulating microbial growth? Gingival crevicular fluid characterisitics?

Answer 48

Healthy continuous slow flow, and increases with inflammation - similar to serum - flushes bac out of sulcus - source of nutrients - maintain pH - defence (IgG/M/A) - phago

Question 49

Factors modulating microbial growth? Microbial factors characterisitics?

Answer 49

Interaction in promoting and suppressing other bacteria - competition; prevent latecomer attachment - produce toxins; bacteriocins, kill - metabolic end prods; antagonistic agents lower pH/nutrition - coagg with bac - quorum sensing - colonisation resistance; commenasl bac inhibit other bacteria

Question 50

Factors modulating microbial growth?

Answer 50

pH: microbes need neutral pH (6.7), pH can fall and acidophilic will flourish Oxidation: fluctuations favour growth Antimicrobial therapy: remove commensal bac and allow colonisation of fungus Diet: fermentable carbs allow acidogenic bacteria to produce extracellular polysacc allow adherence

Question 51

Progression of the oral biofilm? Characterisitics?

Answer 51

Remnants from the host diet always present (sucrose and starch) Constituents if saliva (glycoprot and mineral) Crevicular exudate (proteins) Low level oxygen Extracellular microbial by products Intaceluular food sources And back to top

Question 52

Pioneer bacteria?

Answer 52

``` Streptococci Staphylcocci Neiserria Lactobacillus Anaerobes: veillonella and fusobac ``` Oral microbiome changes at the eruption of teeth

Question 53

Plaque biofilm? Defintion?

Answer 53

Tenacious microbial community embedded in an inter microbial matrix attached to either soft or hard tissue Dead and living bacteria and their extracellular products together with compounds from the host (salivary derived)

Question 54

Dental plaque? Distribution?

Answer 54

Found on all dental surfaces and applicants (Abscence if hygiene and protected areas) Interproximal.areas (contact between 2 teeth) - occlusal fissures, smooth surfaces buccal and palatal Supra and subgingival: above and below gingival margin

Question 55

Comparison of supra and subgingival plaque?

Answer 55

``` Matrix: 30-50 vs 0 Flora: +ve vs -ve Motile bacteria: few.vs common Respiration: aerobic (unless thick) vs anaerobic Meta: carbs vs prots Species diverse: little vs lots ```

Question 56

Subgingival plaque? Characterisitics?

Answer 56

``` Hardest to investigate As the gingival crevice depends a new environment is created (pocket - BPE) - protected from friction - attachment and adherence less important - different nutrients - low o2 - alkaline pH - different host defence mech ``` ``` Established 4 weeks after gingivitis -ve, cocci and spirochetes Over time plaque more complex and becomes obligate or facultative anaerobes No matrix prod 50% of bac motile ```

Question 57

Composition of matrix?

Answer 57

Organisms embedded in matrix Derived from his factor and biofilm - variety - different/same sites on same/diff teeth

Question 58

Plaque matrix? Characterisitics?

Answer 58

Derived from salivary glycoprots, dead cells and serum prots and polysacc 30-50% of supragingival plaque None found in deep subgingival plaque

Question 59

Plaque matrix? Functions?

Answer 59

Nutrients Chemical scaffold for shape and structural integrity Tolerance for environmental factors Bio active and retains water, nutrients and enzymes Restrict or exclude penetration of other molecules (antimicrobials)

Question 60

Host factors that prevent colonisation?

Answer 60

``` Desquamantion Salivary flow Mastication Immunoglobulins in slaiva Commensal bacteria ```

Question 61

Mechanisms in which bacteria adhere and attach?

Answer 61

Electrostatic Hydrophinuc Receptors Fimbriae

Question 62

Process of biofilm formation?

Answer 62

1. Film formation adsorption of acquired pellicle 2. Transport microbes 3. Reversible phase - long range physio chem forces 4. Irreversible- adhesion receptor 5. Secondary colonisation 6. Biofilm maturation 7. Detachment, colonise other sites

Question 63

Pioneer bacterial species?

Answer 63

``` S. Sanguinis S. Oralis S. Mitis bioval 1 Actinomyces Haemophilus Neiserria ```

Question 64

Plaque biofilm timeline?

Answer 64

2s - acquired pellicle and bacterial adhesion 2 hrs - initial plaque formation (irreversible colonsiation) 6 hrs - supragingival plaque 2 days - plaque mass doubles 5-7 days - plaque mayriatuon by filamentous bacteria 21 days - bacterial rep slows that plaque accumulation becomes relatively stable 12 weeks - well differentiated subgingival plaque formed, -ve

Question 65

How do bacteria cause disease?

Answer 65

Quantity and quality of colonies in sulcus and pockets contribute to disease Local inflammation in gibgival tissue Production of virulence factors such as enzymes and toxins which stimulate an immune response

Question 66

Gingivitis? Characterisitics?

Answer 66

Plaque induced gingivitis is a non specific reversible inflammatory response to an increased accumulation to biofilm around the gingival area due to poor oral hygiene No specific pathogen associated Many possess inflammatory modules Not all gingivitis cases progress to periodontitis

Question 67

Periodontitis? Characterisitics?

Answer 67

Localised or generalised Different stages and grades and associated risk factors Studies show a high diversity of colonies with increased proteolytic and obligate anaerobe bacteria present

Question 68

Role of oral flora in systemic infection?

Answer 68

Evidence linking oral.microbiome to systemic infection CVD: infective endocarditis, CHD, stroke, atherosclerosis and myocardial infection Hospital acquired bacteria pneumonia Diabetes Adverse preg outcomes

Question 69

Oral microbiome's effect on the systemic health?

Answer 69

Metastatic infection: - microbes entry to circulation, placenta barrier Metastatic injury: - exo/endo toxins across CV susten in individual with periodontitis Metastatic inflammation: - locally protected inflammatory products reach and contribute to atherosclerosis or intra uterine inflammation

Question 70

Periodontal diseases? Affect tissues? Most common diseases?

Answer 70

Tissues: - Alveolar bone - Periodontal ligament - Cementum - Gingivae Diseases: - Plaque induced gingivitis - Periodontitis

Question 71

Clinical gingival health? Anatomy and characterisation/

Answer 71

Anatomy: - shallow gingival sulcus (3mm deep) Characterisation: absence - bleeding on probing - erythema and oedema - attachment and bone loss Intact periodontium: - pale pink gingiva - stippled and firm - knife edge dental papillae - low level plaque and calculus - no bleeding - full bone support - JE attached at CEJ

Question 72

Stable reduced periodontium - to ensure stability it must have an absence of?

Answer 72

Absence of: - bleeding - erythema and oedema - symptoms - no increased loss of attachment and bone loss (stop progression of periodontitis) Must remain on maintenance

Question 73

Dental plaque biofilm-induced gingivitis? Definition?

Answer 73

- An inflammatory lesion resulting from interactions between the dental plaque biofilm and the host's immune‐inflammatory response, which remains contained within the gingiva and does not extend to the periodontal attachment (cementum, periodontal ligament and alveolar bone) Such inflammation remains confined to the gingiva and does not extend beyond the mucogingival junction and is reversible by reducing levels of dental plaque at and apical to the gingival margin

Question 74

Further classifications of gingivitis? Types?

Answer 74

- Gingivitis on an intact periodontium - Gingivitis on a reduced periodontium in a non-periodontitis patient (e.g., recession, crown lengthening) - Gingival inflammation on a reduced periodontium in a successfully treated periodontitis patient

Question 75

Gingivitis - clinical signs? visual signs?

Answer 75

Clinical signs: - Erythema - Oedema - Pain - Heat - Loss of function - Halitosis - Accumulation of plaque and calculus - Red and swollen gingiva - increased gingival crevicular flow Visual signs: - swelling (loss of knife-edged papillae) - bleeding on probing (discomfort) - redness

Question 76

Plaque induced gingivitis? Definition?

Answer 76

- Inflammation of the gingival tissues caused by the presence of the oral biofilm (dental plaque) Varies with: Oral Hygiene, Age, Gender, Race, Systemic Factors, Certain Drug Therapies, Local Risk Factors

Question 77

How is inflammation determined clinically? Tests and instruments?

Answer 77

Tests: UNC15 - Plaque index (location and distribution of plaque deposits) - Gingival index (gingival bleeding)

Question 78

Defining the difference between an intact periodontium and a reduced periodontium?

Answer 78

- Attachment loss: No for both - Pocket depths: less than 3mm for both - Bleeding on probing: Health less than 10% and Gingivitis greater than 10%

Question 79

Healthy periodontium? Classifications?

Answer 79

Sulcus: 1-3mm Attachment: No loss PDL: No loss Alveolar bone: No loss

Question 80

Gingivitis? Classifications?

Answer 80

Sulcus: 1-3mm with plaque Attachment: No loss PDL: No loss Alveolar bone: No loss

Question 81

Mild periodontitis? Classifications?

Answer 81

Sulcus: 4-5mm Attachment: 1-2mm loss PDL: loss Alveolar bone: No loss

Question 82

Severe periodontitis - sulcus? attachment? PDL? bone?

Answer 82

Sulcus: >6mm Attachment: 3-4mm loss PDL: loss Alveolar bone: loss

Question 83

Loe et al. 1965? Experimental Gingivitis?

Answer 83

- All patients developed gingivitis - 3 within 10 days - 9 between 15 and 21 days Shift in microbial composition: - pre: +ve cocci and short rods - gingivitis: +ve cocci and short rods fell and remainder -ve cocci and short rods, +ve filments, fusobac, vibrios and spirochaetes Results: - patients return to clinical gingival health - plaque causes gingival inflammation - plaque removal leads to resolution

Question 84

Plaque induced gingivitis? Microflora changes?

Answer 84

Increase in plaque mass (10-20 fold) and a shift from Gram+ve streptococci-dominated plaque seen in health to: - Actinomyces spp - Capnophilic (esp. capnocytophaga spp.) - Obligately anaerobic G-ve bacteria As the lesion progresses and bleeding is seen Bacteroides - Porphyromonas gingivalis Prevotella intermedia together with Spirochaetes increase (believed to be involved with Periodontitis)

Question 85

Local risk factors of gingivitis? Definition? Examples?

Answer 85

Those that encourage plaque accumulation at a specific site by either inhibiting its removal during daily oral hygiene practices, and/or creating a biological niche - Dental plaque biofilm retention factors - Oral dryness

Question 86

Characteristics which -ve impact the immune-inflammatory response - systemic health factors?

Answer 86

Characteristics present in an individual, which negatively influence the immune-inflammatory response to a given dental plaque biofilm burden, resulting in exaggerated or “hyper” inflammation. - Smoking - Metabolic factors – hyperglycemia in people with or without diabetes. - Nutritional factors – Severe Vitamin C deficiency, or scurvy - Pharmacological agents - Elevations in sex steroid hormones – at puberty, during pregnancy, - Haematological conditions associated with signs of excess gingival inflammation in the absence of excessive plaque biofilm accumulation.

Question 87

Bacteria present during periodontitis that cause damage - How?

Answer 87

Porphyromonas, Prevotella, Tannerella - Black pigmented bacteroides species, often isolated from periodontal pockets in large numbers intimately involved with all forms Periodontitis can impair host defences and damage components of the periodontium by production of collagenases, proteases, hyaluronidase and cytotoxins

Question 88

Periodontal health - What is clinical gingival health? Definition?

Answer 88

- Absence of clinically detectable inflammation - Biological level of immune surveillance 'State free from inflammatory periodontal disease that allows an individual to function normally and avoid consequences due to current or past disease'

Question 89

Periodontium pristine health - Definition? Clinical gingival health?

Answer 89

Absence of histological evidence of inflammation and no anatomical change of the periodontal structures Absence of inflammation on an intact or reduced periodontium (<10% BOP)

Question 90

Gingivitis - Clinical signs? Maintenance?

Answer 90

A non-specific inflammatory response to indigenous bacteria Resultant inflammation and periodontal breakdown (shift in microbial composition occurs several pathogens appears leading to a host driven tissue damage) Maintenance: - composition of subgingival plaque needs to be redirected towards one compatible with gingival health

Question 91

Periodontitis - Clinical signs? Management?

Answer 91

Plaque-induced inflammation of periodontal tissues: - loss of CT attachment and alveolar bone Preceded by plaque biofilm induced gingivitis Slow to moderate or rapid rate of progression Life-long disease and requires supportive care No cure

Question 92

Does plaque cause periodontitis - Factors? Interplay?

Answer 92

Complex disease of a multifactorial nature involving interplay between subgingival microbiota, the host immune and inflammatory responses and environmental modifying factors

Question 93

Subgingival biofilm - Definition? Formation? Progression? Combat?

Answer 93

Definition: - The microbial composition is a collection of commensal organisms that coexist in relative harmony Formation: - The bacterial biofilm formation initiates gingival inflammation Progression: - periodontitis initiation and progression depend on dysbiotic ecological changes in the microbiome in response to nutrients from gingival inflammatory and tissue breakdown products that enrich some species Combat: - anti‐bacterial mechanisms that attempt to contain the microbial challenge within the gingival sulcus area once inflammation has initiated

Question 94

Microflora - Definition? Change? Sigmund Socransky's pyramid of bacteria?

Answer 94

Definition: - the composition of bacteria present in the oral cavity that may or may not contribute to disease Change: - progressive change in microflora between health, to gingivitis to periodontitis Pyramid: involvement in the periodontal disease progression, and categories based on their pathogenicity and role in plaque development - Aa; A.actinomycetemcomitans - Green; Capnocytophaga (gingivalis, ochracea, sputigena) - Orange assoc; C. rectus, E. nodatum - Orange; P. intermedia/micra and F. nucleatum - Red; P. gingivalis, T. forsythia/denticola

Question 95

Pyramid of bacteria - Orange assoc? Green?

Answer 95

Adhere to pellicle by fimbriae and so avoid flushing by GCF (early colonisers in the sulcus)

Question 96

Pyramid of bacteria - Orange?

Answer 96

Bridge species, that form a link between colonisers and highly pathogenic bacteria Responsible for attachment loss and increased pocket depth

Question 97

Pyramid of bacteria - Red?

Answer 97

Previous bacteria form ideal living conditions for strictly anaerobic bacteria (red) and allow their colonisation Significantly involved in destruction of the periodontium (destruction of soft tissues and bone) Treponema, Porphyromonas and Tannerella (black-pigmented anaerobes)

Question 98

Periodontitis pathogens - Description? Role? Growth? Secretions?

Answer 98

Description: - non motile, pleomorphic, spindle shaped -ve rod Role: - induce apoptosis, invades epithelial cells and endotoxin (high virulence) Growth: - anaerobically aggressive periodontal pathogens fimbriae mediate adhesion and the capsule defends against phagocytosis Secretions: - collagenase, endotoxin fibrinolysis, phospholipase (destroys Ig)

Question 99

Specific plaque hypothesis?

Answer 99

Only a few species out of the collection comprising the resident oral microflora are involved in the disease process

Question 100

Non-specific plaque hypothesis?

Answer 100

Disease is considered to be the outcome of the overall activity of the total plaque microflora

Question 101

Ecological plaque hypothesis?

Answer 101

Organisms associated with disease may also be present at sound sites, but at levels too low to be clinically relevant. Disease is a result of the shift in the balance of the resident microflora due to the response in a change in local environmental conditions e.g. nutrients available, pH

Question 102

Risk factors for periodontal disease - Description? Factors?

Answer 102

``` Description: - multifactorial influences and on multiple immunoinflammaotry responses that make the dysbiotic microbiome changes Factors: - Smoking - Alcohol - Diabetes ```

Question 103

Periodontitis - Clinical definition? Detection? Clinical features?

Answer 103

``` Definition: - characterised by microbially-associated, host-mediated inflammation that results in loss of periodontal attachment Detection: - circumferential assessment of the erupted dentition with a standardised periodontal probe with reference t the CEJ Clinical features: - gingival swelling - blood on brushing - blood on probing - loss of stippling - loss of knife edge margins - plaque and calculus deposits - subgingival calculus - pocketing (apical migration) - bone loss - mobility - furcation - suppuration ```

Question 104

Periodontitis Stage I - Description? Clinical signs? Susceptibility?

Answer 104

Description: - borderland between gingivitis and periodontitis and represents early stages of attachment loss - periodontitis response to persistence of gingival inflammation Clinical signs: - interproximal bone loss - <2mm attachment loss from CEJ Susceptibility: - show a degree of clinical attachment loss, heightened susceptibility for progression

Question 105

Periodontitis Stage II - Description? Clinical signs? Management?

Answer 105

``` Description: - established periodontitis in which a carefully performed clinical periodontal exam identifies the characteristic damage Clinical signs: - interproximal bone loss - moderate coronal third of tooth Management: - application of standard treatment - professional bacterial removal - monitoring for arrest of disease progression ```

Question 106

Periodontitis Stage III - Description? Clinical signs? Management?

Answer 106

Description: - significant damage to attachment and without advanced treatment, tooth loss may occur Clinical signs: - interproximal bone loss - deep periodontal lesions that extend the middle portion of the root Management: - complicated due to intrabony defects, furcation and history of tooth loss (periodontally)

Question 107

Periodontitis Stage IV - Description? Clinical signs? Management?

Answer 107

Description: - considerable damage to periodontal support and significant tooth loss, translating to loss of masticatory function - without proper control and rehab, the dentition is at risk of being lost Clinical signs: - apical third of root - deep periodontal lesions extending to the apical portion of the root - hypermobility (from biting)

Question 108

Grades of periodontitis - Description? A? B? C?

Answer 108

Progression may differ depending on the rate and may respond differently to treatment Rate of progression: % bone loss/ patients age (using worst bone loss site) A - slow, max % bone loss is < half the age B - medium, all other situations C - rapid, max % bone loss is > patients age

Question 109

Periodontal health- 4 levels - Pristine health? Clinical health? Periodontal stability? Periodontal control?

Answer 109

``` Pristine health: - total absence of inflamm and physiological immune Clinical health: - absence of inflammation - normal support Periodontal stability: - in reduced perio (control of factors) Periodontal remission: - reduce progression ```

Question 110

Gingival health following successful treatment of periodontitis - clinical features? modifying factors?

Answer 110

``` Clinical features: absence - BOP - erythema, oedema, suppuration - adequate OH - manageable pocket <4mm Control modifying factors: - reduce smoking and good diabetic control ```