Oral Disease

Question 1

What is the basic structure of a tooth?

Answer 1

Mineralised ‘Hard’ Tissue​ which contains;
-Enamel ​
-Dentine​
-Cementum
-Alveolar Bone

Non-mineralised ‘Soft’ Tissue​
-Gingivae (gums)
-Periodontal ligament*​
-Pulp​
-Oral mucosae​

Question 2

What are the 3 main parts of a tooth:​

Answer 2

Crown​
Root​
Pulp Chamber​

Question 3

What are The 4 TOOTH-specific tissues:​

Answer 3

Enamel​
Dentine​
Cementum​
Dental Pulp​

Question 4

Enamel 1​

Answer 4

Structure​
-Highly calcified and hardest tissue in the body​
-Crystalline in nature​
-Enamel rods​

Not innervated​ (no nerves)
-Acid-soluble - demineralizes at pH5.5 and lower ​
-Cannot be renewed​
-‘Darkens’ with age ​
-Fluoride and saliva can help with remineralization​

Question 5

Enamel 2​

Answer 5

Enamel can be lost by:​
Physical mechanisms​
Abrasion (mechanical wear)​
Attrition (tooth-to-tooth contact)​
Abfraction (lesions)​
- Chemical dissolution ​
Erosion by extrinsic acids from diet​
Erosion by intrinsic acids from the oral cavity/digestive tract​

Multifactorial etiology​
- Combination of physical and chemical factors​

Question 6

Dentine 1​

Answer 6

Softer than enamel​
Susceptible to tooth wear (physical or chemical)​
Does not have a nerve supply but can be sensitive​
Is produced throughout life​

Three classifications ​
Primary​
Secondary​
Tertiary​
Will demineralize at a pH of 6.5 and lower​ (tries to protect the pulp of the tooth)

Question 7

Dentine 2​

Answer 7

Dentinal tubules connect the dentin and the pulp (innermost part of the tooth, circumscribed by the dentine and lined with a layer of odontoblast cells)​

The tubules run parallel to each other in an S-shape course​

Tubules contain fluid and nerve fibres​

External stimuli cause hydrodynamic movement of the dentinal fluid, which can result in short, sharp pain episodes.​

Question 8

Cementum 1​

Answer 8

The calcified, avascular mesenchymal tissue that forms the outer layer covering the root.​

2 Types:​
1) Acellular cementum​
2) Cellular cementum​

Composition :​
50-55 % organic composed of proteins;​
45-50% inorganic composed of HAp crystals.​
The collagenous composition of the organic portion is type I (90%) & type III (5%) collagen.​

At cervical margin the thickness of cementum is 50um & at apical margin the thickness progresses to 200um.​

Question 9

Cementum 2​

Answer 9

Acellular Cementum: ​

It is the first cementum that forms; covers one third of the cervical root; more calcified than cellular version.​

Cellular Cementum: ​
It forms after the tooth reaches the occlusal plain. ​
It is more irregular and contains cementocytes in lacunae; can adapt and repair; confined to premolar and premolar teeth​

Question 10

Dental Pulp​

Answer 10

Innermost part of the tooth​
A soft tissue rich with blood vessels and nerves​
Responsible for nourishing the tooth​
The pulp in the crown of the tooth = the coronal pulp​
Pulp canals traverse along the root(s) = radicular pulp​
Typically sensitive to extreme thermal stimulation (hot or cold)​

Question 11

Gingivae​

Answer 11

Gingivae: The part of the oral mucosa overlying the crowns of unerupted teeth and encircling the necks of erupted teeth, serving as support structure for sub-adjacent tissues. ​

Question 12

Periodontal Ligament​

Answer 12

Consists of numerous cells; fibroblasts, epithelial, undifferentiated mesenchymal cells, bone and cementocytes. ​

ECM consists of various groups of collagen fibre bundles embedded in ground substance. ​

The PDL has significant effect on the tooth’s ability to withstand stress loads. ​

The PDL helps provide for the attachment of the teeth to the surrounding alveolar bone via the cementum.​

PDL Functions: Supportive –Formative – Resorptive – Nutritive - Sensory​

​PDL helps teeth move if there isn’t this there is a risk of fracture as there wouldn’t be any give

Question 13

Alveolar Bone​

Answer 13

Bone lining the tooth socket is the “alveolar process”; remainder provides support (alveolar bone)​

i.e. the thickened ridge of bone containing the tooth sockets in both the mandible and maxilla​

Known as Lamina Dura in radiographs (see below)​

Question 14

Etiology and Pathogenesis of Caries​

Answer 14

The three general disease categories of focus in dentistry are currently: ​

Tooth decay ​
Periodontal disease​
Oral cancer​

Question 15

Why should you brush your teeth at night

Answer 15

you don’t produce saliva when you sleep so the salivary gland shut down

Question 16

Dental Caries​

Answer 16

A progressive dissolution of the inorganic component of dental hard tissues mediated by bacteria present in the dental plaque​

Main microbes involved = Streptococcus mutans, Lactobacillus spp.​

Estimated global prevalence of untreated dental caries ~ 40%​

about 700 species of microbes present in the mouth

Question 17

What are the stages of decay?

Answer 17

decay in enamel
advanced decay
decay in dentin
decay in pulp

Question 18

Plaque​

Answer 18

Dental plaque is a biofilm or mass of bacteria that grows on surfaces within the mouth. It is a sticky colourless deposit at first, but when it forms tartar (calculus) , it is often brown or pale yellow. ​

​It is commonly found between the teeth, on the front of teeth, behind teeth, on chewing surfaces, along the gingivae, or below the cervical margins.​

Bacterial plaque is one of the major causes for dental decay and gum disease.​

Question 19

What are the stages of Plaque formation​

Answer 19

Pellicle formation
initial adhesion
maturation
dispersion

Question 20

What is a good defence for biofilm

Answer 20

saliva

Question 21

Production of lactic acid

Answer 21

acid that produces H+ that

you lose minerals when having sweets

Stephan’s curve where there is a critical PH where if you go below you will get demineralization

Question 22

Hydroxyapatite resistance to acid dissolution ​

Answer 22

Hydroxyapatite (HA) is found in nature as a ‘geological’ HA composed of calcium,​

phosphate and hydroxyl groups Ca10(PO4)6(OH)2​

• In human tissues, apatite is similar BUT Crystals are smaller, less well packed and some of the hydroxyl or phosphate ions are replaced with carbonate i.e. ‘carbonated’ hydroxyapatite or ‘carbonatoapatite’.​

However, because the crystals are small, their SA/Vol ratio is greater meaning that more parts of their structure will lie on the crystal surface.​

• It is easier for acid to pass between crystals and come into contact with crystals deeper within the structure.​
• Collectively this means that carbonated HA (in teeth) is more vulnerable to acid attack than the Native form.​

Question 23

How does Fl- protect the tooth?​

Answer 23

Inhibition of bacterial metabolism​
Inhibition of demineralization of enamel​
Promoting remineralization of the enamel surface​

Question 24

Demineralisation vs. Remineralisation​

Answer 24

Demineralisation
mineral salts dissolve into the surrounding salivary fluid ​
enamel at approximate pH of 5.5 or less​
dentine at approximate pH of 6.5 or less ​
erosion or caries can occur ​

Remineralisation
pH recovers to pH7​
saliva-rich calcium and phosphates​
minerals penetrate the damaged enamel surface and ‘repair’ it​
enamel pH < 5.5​
dentine pH < 6.5​

Question 25

Promoting remineralisation

Answer 25

Saliva is supersaturated with calcium and phosphate​

Fl- in the oral environment will be adsorbed onto the surface of the affected enamel​

This will serve to attract Ca2+ to the enamel surface, PO4 2- will follow​

The exposed surfaces of demineralized enamel will act as foci of nucleation for the deposition of calcium and phosphate leading to apatite crystal growth.​

New mineral will be laid down, which will be a ‘fluorapatite’ rather than ‘carbonatoapatite’ to give a demineralized surface layer rich in fluorapatite from which carbonate has been excluded . ​

This will lead to much greater resistance to acid dissolution.​

Question 26

gingivitis and periodontitis

Answer 26

Gingivitis is a chronic inflammatory condition affecting the periodontal tissues. It is reversible however periodontitis is not ​as it involves deeper tissues with loss of bone.

Question 27

What causes Periodontitis?​

Answer 27

Dental Infections - caused by various odontopathogens​

Formation of dental plaque creates environment for pathogens that produce acids and other virulence factors​

Correlation between plaque and gingivitis ​
Antibody response to microbes​
Pathogenic potential of plaque bacteria ​
Experimental animal models ​

Question 28

What pathogens can you get in your mouth

Answer 28

Fungi​
Candida​

Viruses​
Herpes​
HIV​
Hepatitis​

Protozoa​

Question 29

The oral cavity: structures and host defence​

Answer 29

-hard and soft tissues​
-soft tissues: low bacterial load (high cell turnover)​
-hard tissues: stable substrate for colonisation​
-continual flow of saliva: warm & moist but also contains lysozyme, lactoferrin, antimicrobial peptides, IgA​
-shear forces of mastication etc.​
-adherence in dental plaque​​

Question 30

Formation of dental plaque​

Answer 30

-clean tooth surface coated with “salivary pellicle”​
-ordered pattern of colonisation (microbial succession) ​
-pioneer species attach to pellicle eg., Streptococcus oralis, S. gordonii (cell to surface attachment)​
-increasing proportions of Actinomyces, Veillonella sp. (cell to cell interactions)​
-formation of mature community with high levels of Gram negative anaerobes (Porphyromonas, Prevotella) and Fusobacteria​

Microbial composition of plaque from diseased surfaces differs from that found in health​

​

Question 31

The initial lesion​

Answer 31

Within 24 h of plaque accumulation on the gingival third of the tooth surface​

Capillary dilation and increased blood flow (sub clinical gingivitis)​

Margination , emigration and diapedesis​ of neutrophils​

The flow of GCF increases​

Lymphocytes are retained in the connective ​tissues on contact with antigens, cytokines​ or adhesion molecules and are therefore ​not so readily lost through the junctional epithelium and into the oral cavity, as are​ neutrophils​​

Question 32

The early lesion​

Answer 32

Occurs over several days of plaque accumulation ​

Increased redness of the marginal gingiva due to increase in size and number of the blood vessels ​

Bleeding on probing​

Lymphocytes and neutrophils are the predominant leucocytes in the infiltrate at this stage​

Breakdown of collagen fibres occurs in the infiltrated area (this will provide space for the infiltrating cells)​

This stage may persist for long periods and the variability in time required to produce an established lesion may reflect variance in susceptibility between subjects​

Question 33

The established lesion​

Answer 33

Further enhancement of the inflammatory response of the gingival tissue​

Dominated by lymphocytes/plasma cells​

Collagen loss continues as the inflammatory cell infiltrate expands​

Junctional epithelium migrates apically and a ‘pocket’ epithelium forms - not attached to the tooth surface (this allows for a further apical migration of the biofilm)​

Two types of established lesion appear to exist:​

one remains stable and does not progress for months or years ​

the second becomes more active and converts more rapidly to a progressive and destructive advanced lesion​

​

Question 34

The advanced lesion​

Answer 34

The advanced lesion has many​ of the characteristics of the ​established lesion but differs ​importantly in that loss of ​
connective tissue attachment ​and alveolar bone occurs​

​

Question 35

The ‘Balance’ between Health and Disease​

Answer 35

disease=Risk factors (e.g., genetics smoking, diabetes), Overproduction of proinflammatory or destructive mediators and enzymes (e.g IL-1, IL-6, PGE2, TNF-a, MMPs), Underactivity or overactivity of aspects of host response, Poor compliance, Poor plaque control and Subgingivalbioburden

Health=Reduction of risk factors, Expression of host-derived anti-inflammatory or protective mediators
(e.g., IL-4, IL-10, IL- 1ra, TIMPs), Host modulatory therapy, Resolution of Inflammation and OHI, SR, surgery, antiseptics, antibiotics to reduce bacterialchallenge

Question 36

Model of pathogenesis of periodontitis ​

Answer 36

Gingivitis: This is the earliest stage of gum disease, and it involves inflammation of the gums without loss of bone or tissue attachment.

Mild Periodontitis (formerly known as Early Periodontitis): This stage involves slight bone loss and the formation of pockets (spaces between the teeth and gums) of 4mm or less.

Moderate Periodontitis: In this stage, there is more noticeable bone loss, and pocket depths may range from 5mm to 6mm.

Severe Periodontitis: This is the advanced stage of periodontitis, characterized by significant bone loss and pocket depths exceeding 6mm.

Question 37

Describe the Inflammatory Reaction​

Answer 37

Initial tissue reaction to bacteria is a “non-specific reaction” called “inflammation” which is defined as a localized, protective response of the body to injury & infection.​

The main reaction responses seen during inflammatory reactions are:​
* Vascular response​
* Cellular response​
* Immunologic response​

Question 38

Describe Initial cellular activity​

Answer 38

Polymorphonuclear leukocytes​ (granulocytes)​

Neutrophils​
The directed movement of leucocytes from blood​ vessels is a key process of inflammation. ​

Leucocytes push their way between the endothelial cells to exit the blood & enter tissues.​

Chemokines and chemokine receptors in oral tissues: potential involvement in the induction and maintenance of inflammatory reactions.​

Question 39

Pathogenesis (& severity) of microbial disease is dependent on

Answer 39

Host factors – including genetic factors and host physiology​
The virulence of the micro-organism​

Question 40

The ecological plaque hypothesis: periodontal disease​

Answer 40

Periodontal disease: growth of bacteria in the subgingival niche Induces inflammatory response GCF selection of A. actinomycetemcomitans, P. gingivalis, F. nucleatum, B. forsythus, - the “periodontopathic microbota”​

​no single species responsible but disease requires an integrated and orchestrated interaction of this peridontopathic microbiota​

ie. Multifactorial complex disease involving multiple bacterial species and host cell interactions, the combined effect of which is the destruction of soft tissue and bone.​

​

Question 41

Periodontitis & Systemic Disease​

Answer 41

Association between oral disease and systemic disease recognised since 600BC​

Role of microorganisms first realised - 17th Century​
Oral cavity as a source of infection – 20th Century​
Focal infection Theory – 20th Century ​

All have led to a separate branch of Periodontal Medicine which traverses both dentistry and medicine (Offenbacher 1996); a bi-directional relationship in which periodontitis may influence the individual’s systemic health and systemic disease may influence periodontal health​

oral disease can actually link to heart diseases and others
rheumatoid arthritis can also be linked, it shows lots of similarity with periodontitis

Question 42

Role of cytokines in pathogenesis​

Answer 42

Anti-inflammatory cytokines eg., IL-4: ? induced early in infection to promote growth in subgingival niche​

Pro-inflammatory cytokines eg., IL-1, TNF-a: ? function late in infection to promote disease ​

Periodontal disease is a multifactorial complex disease involving multiple bacterial species and host cell interactions, the combined effect of which is the destruction of soft tissue and bone.​

Question 43

What are the potential mechanisms linking oral disease to non-oral disease​

Answer 43

Metastatic Infection (TRANSIENT BACTERIA)​
Oral bacteria enter the periodontal tissues eliciting a transient bacteraemia​
Inflammation/Inflammatory Injury (INNATE immunity)​

Cellular release of cytokines which may impact systemic inflammation​

Adaptive Immunity​
Persistent inflammation leads to processing of bacterial antigens by the ​adaptive immune system (T-cell [cytokines] and B-cell [antibody] activation)​

Question 44

Periodontitis & systemic disease susceptibility​

Answer 44

Shared risk factors e.g. smoking, stress, ageing, ethnicity​
Subgingival biofilm, acts as a reservoir for bacterial toxins​
Chronic inflammation of periodontium, acts as a reservoir for ​inflammatory mediators​

Question 45

Examples of Periodontitis & Systemic Disease ​
(N.B. correlation NOT causation)​

Answer 45

Diabetes Mellitus​
Cardiovascular disease​
Adverse Pregnancy Outcomes e.g. pre-term birth​
Respiratory disease​
Rheumatoid arthritis​
Osteoporosis​
Alzheimer’s disease​
Head/Neck cancer​

Correlations not causations​

Question 46

Summary​

Answer 46

Pathogenesis of microbial disease: pathological changes associated with infectious disease​

Pathogenesis due to:​
the properties of the micro-organism and​
the response of the host​

Pathogenesis of oral infectious diseases: role of host genetic factors, host physiology, bacterial virulence, host immune response​

Question 47

Conclusions ​

Answer 47

Periodontal diseases are complex bacteria-induced infections characterized by an inflammatory host response to plaque bacteria and their by-products​

Genetics and environmental influences play a role in the inflammatory response to the infection​

Initial host responses to bacterial infections include activation and recruitment of neutrophils, leucocytes and macrophages​

Biofilm by-products stimulate host cells to produce proinflammatory cytokines including IL-1β and TNF-α, which can induce connective tissue and alveolar bone destruction​