Oral Disease Flashcards
What is the basic structure of a tooth?
Mineralised ‘Hard’ Tissue which contains;
-Enamel
-Dentine
-Cementum
-Alveolar Bone
Non-mineralised ‘Soft’ Tissue
-Gingivae (gums)
-Periodontal ligament*
-Pulp
-Oral mucosae
What are the 3 main parts of a tooth:
Crown
Root
Pulp Chamber
What are The 4 TOOTH-specific tissues:
Enamel
Dentine
Cementum
Dental Pulp
Enamel 1
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
Enamel 2
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
Dentine 1
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)
Dentine 2
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.
Cementum 1
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.
Cementum 2
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
Dental Pulp
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)
Gingivae
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.
Periodontal Ligament
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
Alveolar Bone
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)
Etiology and Pathogenesis of Caries
The three general disease categories of focus in dentistry are currently:
Tooth decay
Periodontal disease
Oral cancer
Why should you brush your teeth at night
you don’t produce saliva when you sleep so the salivary gland shut down
Dental Caries
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
What are the stages of decay?
decay in enamel
advanced decay
decay in dentin
decay in pulp
Plaque
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.
What are the stages of Plaque formation
Pellicle formation
initial adhesion
maturation
dispersion
What is a good defence for biofilm
saliva
Production of lactic acid
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
Hydroxyapatite resistance to acid dissolution
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.
How does Fl- protect the tooth?
Inhibition of bacterial metabolism
Inhibition of demineralization of enamel
Promoting remineralization of the enamel surface
Demineralisation vs. Remineralisation
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
Promoting remineralisation
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.
gingivitis and periodontitis
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.
What causes Periodontitis?
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
What pathogens can you get in your mouth
Fungi
Candida
Viruses
Herpes
HIV
Hepatitis
Protozoa
The oral cavity: structures and host defence
-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
Formation of dental plaque
-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
The initial lesion
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
The early lesion
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
The established lesion
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
The advanced lesion
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
The ‘Balance’ between Health and Disease
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
Model of pathogenesis of periodontitis
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.
Describe the Inflammatory Reaction
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
Describe Initial cellular activity
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.
Pathogenesis (& severity) of microbial disease is dependent on
Host factors – including genetic factors and host physiology
The virulence of the micro-organism
The ecological plaque hypothesis: periodontal disease
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.
Periodontitis & Systemic Disease
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
Role of cytokines in pathogenesis
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.
What are the potential mechanisms linking oral disease to non-oral disease
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)
Periodontitis & systemic disease susceptibility
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
Examples of Periodontitis & Systemic Disease
(N.B. correlation NOT causation)
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
Summary
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
Conclusions
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
