Oral physiology Flashcards
Structure of acinus
12+ Acinar cells around a central lumen. Zygomen granules (digestive enzymes) Mucus cells (downstream of acinar cells) Myoepithelial cells to contract and squeeze stuff into the main duct.
Types of ducts (salivary glands)
Intercalated, striated, excretory
The rate of flow vs composition
Increased flow = increased conc of NaCl and HCO3
Movement of substances from blood to the lumen of the acinus
Na+ to the lumen through tight junctions.
Cl- and HCO3- from blood to acinus via co-transporters e.g. transcellular.
Primary saliva is isotonic
Modification of primary secretion
In the duct.
Reabsorption of NaCl
Secretion of K+ and bicarbonate (= high pH).
Ductal cells impermeable to water so final saliva is hypertonic.
What is oral mucosa
The soft tissue of the mouth
What is oral mucosa composed of
Stratified squamous epithelium
What’s the function of oral mucosa
Barrier to bacteria and mechanical irritation and protects against dryness.
The different classifications of oral mucosa
Masticatory mucosa, lining mucosa and specialized mucosa
Lining mucosa properties
Can be stretched, compressed and is moist.
Location of lining mucosa
Buccal surfaces, Ventral surface of tongue, Floor of mouth, Labial Alveolar mucosa, Soft palate.
Histology of lining mucosa
Non-keratinised SSE
Elastic fibres in lamina propria and sub-mucosa = a movable base.
Fordyce spots/granules (misplaces sebaceous glands usually associated w hair follicles)
Masticatory mucosa locations
Attached gingiva, hard palate, dorsal surface of tongue
Transduction mechanism for Umami tastant
G-coupled protein receptor.
T1Rs = T1R2, T1R3
Transduction mechanism for Sweet tastant
G -coupled protein receptor
T1R1, T1R3
Transduction mechanism for Salt tastant
Ion channel = NaCl, KCl (inorganic salts)
Transduction mechanism for Sour tastant
Ion channel = H+
Transduction mechanism for Bitter tastant
G-coupled protein receptor.
TR2’s
Which tastant are we most sensitive to.
Bitter
Sour produces most saliva bc needs to buffer the H+
Mechanism of AP from eating food
- Chewing the food = mechanical and chemical stimulation so saliva released.
- Molecules from broken down food dissolve in saliva and enter taste pore.
- Molecules interact with Ion channels/protein receptors.
- Ca2+ released from stores so increase in conc.
- Increase in [Ca] = exocytosis of transmitters.
6 = AP
Factors affecting taste
Genetics Saliva composition, quantity, etc. Disease Past experience Olfaction Adaption
Structure of acinar/secretory system
~12 acinar cells (serous) around an intercalated duct
Mucous cells further downstream
+Zygome granules
+myoepithelial cells to squeeze saliva downstream
Intercalated then striated then excretory duct.
Movement of substances from blood to the lumen of the acinus
Na+ and water travel straight through.
Na+/K+ enter basolateral membrane, Na+/Cl- exchanged (Cl- in)
HCO3, K+, and Cl- exit to the lumen at luminal membrane.
Movement of substances from the lumen of the duct to blood
Luminal membrane: H+/K+ exchanger (H+ in), H+/Na+ exchanger (H+ out), HCO3/Cl- exchanger (Cl- in).
Basolateral membrane/to blood: K+ moves into the duct, Na+ and Cl- move out.
Impermeable to water.
Stephan’s Curve: Rate of drop of pH due to ?
- Metabolic activity of plaque microbes.
2. Complexity/type of substrate
Stephan’s Curve: pH reached depends on?
- Type of bacteria e.g. acidogenic = lower pH
- The complexity of the carbs
- The rate of diffusion e.g. affected by plaque thickness, clearing rate of saliva, etc.
Stephan’s Curve: Time taken for normal pH to return
- The activity of bacteria inhibited by low pH
- Saliva flow and composition
- Plaque/rate of diffusion.
What is the critical pH
pH where CaPO4 crystals dissolve.
= 1/[Ca] or [PO4]
Benefits of the enamel pellicle
Physical barrier e.g. against abrasion Barrier against bacteria Neutralises bacterial acids Reduces demineralization Inhibits calculus growth
Properties of parasympathetic saliva
A Larger volume as it’s more watery (serous)
Secreted via Ach pathways.
Properties of sympathetic saliva
Smaller volume but rich in mucins so feels thick
Via noradrenaline pathways
Problems caused by xerostomia
Difficulty/pain eating, swallowing, speaking
More gingival infections/tooth decay/poor oral health
Diminished taste
Advantages of the structure of salivary glands
- The epithelium of luminal membrane can be accessed non-invasively
- Well encapsulated = less spread of vectors.
- Non-vital e.g. can be removed.
- Cells are well differentiated and slow dividing = a stable population.
Types of acini
Serous, mucous, mixed
Serous Acini
Dark staining
Nucleus in basal third
Secrete a-amylase and water rich saliva to digest starch.
Small central duct
Mucous acini
Light foamy stained appearance.
Nucleus at base
Large central duct
Secretes mucins (glycoproteins) and water for lubrication
Composition of primary saliva
Isotonic, NaCl rich plasma like fluid
What does whole saliva contain
Acinar secretions/saliva Blood Cell fragments Microorganisms Food remnants Electrolytes Mucins Antibacterials e.g. lysozyme Enzymes
Role/structure of intercalated ducts
Cuboidal cells
Secretory duct e.g. connects acini to the larger striated ducts.
Role/structure of striated ducts
Basal membrane highly folded into microvilli = more surface area for active transport.
NaCl absorbed, HCO3 and K+ secreted.
Impermeable to water so resulting saliva is hypotonic.
Rich in mitochondria due to all the active transport.
Name 5 salivary glands
Parotid Sub-mandibular Sub-lingual Von-Ebner Weber's
Parotid gland secretions
Serous secretions.
Stenson’s duct (crosses masseter and pierces buccinator before entering the oral cavity)
Von-Ebner’s glands
Minor salivary glands Serous secretions (the only minor salivary gland not mucus). Found at the base of tongue, underlying the circumvallate papillae.
Weber’s glands
Mucous secretions
Found in tonsils.
Types of damage to salivary glands
Obstructive, degenerative, infectious, drug side-effects
Types of damage to salivary glands: Obstructive
E.g. calculus stones blocking the ducts
Types of damage to salivary glands: Degenerative
E.g. after radiotherapy or due to Sjogren’s syndrome (affects post-menopausal women and their glands)
Types of damage to salivary glands: inflammatory
Infection, swelling
Types of damage to salivary glands: Drug side-effects
Affect the Ach or noradrenaline pathways
What do acinar cells also secrete
Electrolytes IgA/IgG Mucins Cystatins Histatines Statherins Enzymes e.g a-amylase or lipase Antimicrobial proteins
What are the functions of Statherins, Histatines, and Cystatins in saliva?
All of a mineralization function.
Histatines = buffer
Cystatins = tissue coating
Statherins = Lubrications and vasoelasticity
Sub-mandibular
Unstimulated saliva mostly from here.
Mixed e.g. mucous and serous
Wharton’s duct
Deep and superficial lobes separated by posterior surface of mylohyoid muscle.
Sub-lingual
Mostly mucous
Joins Wharton’s duct and has some small ducts that go directly to the mouth.
What affects saliva composition/amount
Age Time of day Gender Diet Drugs Gland size/type Stimulation type and duration Circadian rhythm (24h cycle) Flow rate
the role of saliva
Lubrication and tissue coating A solvent for taste Digestive Defensive Immunity (antibacterials/antifungal/etc) Buffering Remineralisation Mechanical cleaning Needed to hold dentures in place
How can we determine the composition of saliva
2D/1D electrophoresis
functions of salivary proteins
Taste and digestion
Lubrication - mucins
Immunity/defensive - IgA, IgG, lysozymes
Host protective features during periodontal disease/gingivitis
A complete layer of epithelium = physical barrier
Saliva flow and contains neutrophils/innate immunity
Crevicular fluid increases and contains neutrophils etc = innate immunity.
For periodontitis, phagocytes etc activated (active immunity)
Histological features of Gingivitis
Dilated capillaries = red and bleeding gums
Inflammatory cells
Leaking crevicular fluid (containing neutrophils)
No migration of junctional epithelium
No bone loss
Clinical features of gingivitis
False pocketing
Bleeding
Histological features of periodontal disease
Migration of jucntional epithelium
Bone loss = wobbly teeth or drifitng teeth
True pocketing (7mm)
Ulceration and bleeding gums
Chronic inflammation = plasma cells, lymphocytes
Clinical features of periodontal disease
True pocketing (7mm)
Bone loss - can be checked using a bitewing x-ray
Bleeding
Accumulation of calculus
The appearance of healthy gingiva
Pale pink
Firm and stippled
Knife edge gingival margin
The appearance of gums w periodontal disease
Red, inflamed and bleeding
Lost the stippled appearance
Rolled gingival margins
Types of gingival disease
Hereditary or acquired. Plaque-induced or not. Infective e.g. herpes. Affected by systemic illnesses etc e.g. pregnancy or diabetes. Inflammatory or not hyper or hypoplastic. Allergic Traumatic
Chronic periodontitis features
Localised or generalized (>30%)
Bad bacteria > good bacteria
Affected by systemic factors e.g. smoking, stress, plaque levels, diabetes.
Progressive bone/attachment loss consistent w local factors
Acute periodontitis
Aggressive and rapid bone/attachment loss, not consistent w local factors.
The patient appears to be healthy.
Localised or generalized.
Macrophage/neutrophil abnormalities.
Steps needed in a treatment plan
- Care of the pain
- Prevention (finding and stopping the cause)
- Stabilisation
- Rehabilitation
- Maintenance.
Why do systemic illnesses affect oral health
Affect the saliva.
Affect host responses e.g. inflammatory response, antibodies/neutrophils etc.
Affects strength of the tissues e.g. how easily they get infected etc.
Changes in epithelium
Atrophy Hyperplasia Hyperkeratinised Ulcers/loss of epithelium When epithelium separates from underlying CT
Atrophy of oral epithelium
Red fragile epithelium
When rate of loss of cells > rate of new cell production
Reasons = immune mediated, vitamin B12 deficiency, age.
Oral epithelium hyperplasia
Appearance = normal, maybe whiter (hyperkeratinised)
When rate of new cell production > rate of loss of cells.
Reasons = trauma, infection/fungal e.g. candidia
Oral epithelium hyperkaratinised
White appearance
Reasons = immune-mediated, trauma, infection/virus, unknown, etc.
Loss of epithelium/ Ulcers
Covered in fibrin and neutrophils instead so has a white appearance surrounded by red inflamed surrounding tissues.
Reasons = immune-mediated, infection/virus e.g. herpes, trauma.
Separation of epithelium from underlying tissues
Blister - can burst to form an ulcer.
Reasons = immune-mediated, virus/infection.
Changes to oral connective tissues
Inflamed
Hyperplasia
Inflamed oral connective tissues
Red appearance - increased blood flow
Swollen and firm - due to oedema and increased pressure
Yellow due to the pus
Causes = Trauma, ulcers or gingival/periodontal disease
Hyperplastic oral connective tissue
Swelling, nodule or lump, normal color or red
Due to trauma e.g. rubbing dentures or hormones.
What does red oral mucosa indicate
Atrophic epithelium, hyperplastic or imflamed connective tissue.
What does a white patch intraorally indicate
Hyperkeratosis due to immune-mediated, fungal infection e.g. candida, trauma.
Neoplasia definition
Unregulated proliferation/replication of cells due to genetic changes
Benign neoplasia
Cells in a capsule so don’t grow into neighboring cells or metastasize.
Cells resemble the original tissue type - well differentiated
Overlying mucosa looks normal
It compresses surrounding structures.
Malignant neoplasia
Cells metastasize e.g. not localized and grow, invade and infiltrate into neighboring cells.
Cells don’t resemble original cells.
Cancer in glandular tissue
Adenoma - spreads via lymph nodes
Cancer in connective tissue
lipoma, schwannoma - invades the bloodstream and spreads from there.
Cancer in epithelium
Carcinoma - infiltrates lymph nodes and vessels and spreads
Aetiology of neoplasia
Multifactorial: Age Nutrition/diet Alcohol Smoking Sunlight/UV (lip) Genetics Viruses (HPV)
Histology of neoplasia
Thicker epithelium bc uncontrolled cell growth
Ragged epithelium/CT edge bc epithelium cells grow into CT
Islands of epithelium break off and lodge in CT e.g. in bone or muscle and stop them working.
What occurs during dysbiosis of an early lesion in the mouth.
A quiescent site/early lesion in mouth turns into active caries.
Due to a change in the host (e.g. starts smoking, pregnancy) or due to a change in the microbes (e.g. increased plaque levels)
Periapical disease definition/summary
Infection in pulp (via caries in the enamel/dentine). Causes necrosis of pulp and travels out the apices and infects surrounding tissues.
Types of pre-cavitation enamel caries
Smooth surface caries
Fissure caries
Features of pre-cavitation enamel caries
Conical shape
Most spreading at the ADJ
Surface is zone is reistant to demineralisation (until dentine is involved)
Body of lesion = 4-20% demineralised. Demineralisation in the prism cores = enhanced striae of retzius and cross-striations.
Dark zone surrounded by transluscent zone at base of lesion.
Pre-cavitation smooth surface caries vs fissure caries
Both have a conical shape but smooth surface caries’ apex is towards ADJ and fissure caries’ base is towards ADJ.
Fissure caries starts in the walls of the fissure (not the base).
How do caries spread into the dentine
Most spread along the ADJ = secondary enamel caries starting from the ADJ.
Acid diffuses through the porous enamel.
Dentine/pulp’s reaction to caries
Tertiary reactionary dentine forms as the odontoblast cells get reacted and retreat as they detect the stimulus (makes pulp shrink)
Sclerotic dentine = inter and peritubular dentine forms and mineralization of odontoblast processes/calcification of tubules.
Dead tracts = dead odontoblasts and empty tubules.
Features of cavitation of a carious lesion
More demineralisation (1st wave) and proteolytic enzymes degrade collagen matrix (2nd wave). Bacteria invade and grow in tubules and widen them until they collapse = liquefaction foci. Tubules grow and join = transverse/dentine clefts.
Types of arrested caries
Type 1 = dentine caries self cleanses
Type 2 = enamel caries/white spot lesion remineralises
The 3 zones of the body of the cavitation
Demineralisation = sterile e.g. no bacteria (furthers from the enamel/ center of the body)
Bacterial penetration = bacteria invade and grow in tubules.
Destruction = liquefaction foci, transverse clefts, discolouration.
Cementum/dentine caries
Starts at the amelocemental junction.
The direction of tubules is towards apex and pulp so difficult to see and treat.
PDL means infection can go straight to cementum/dentine.
The colonisation of bacteria onto teeth
Host-bacteria adhesion: irreversible if just chemical/physical interactions e.g. not specific protein-protein. Bacteria adhere to acquired pellicle via IMF, protein-carb interactions, etc.
Bacterial-bacterial adhesions - co-aggregations.
Growth and multiplication.
Source of nutrients for the bacteria in plaque
The waste of other bacteria
By-products of the breakdown of stuff e.g. salivary glycoproteins.
Urea/ammonia
Dietary constituents - diff bacteria work together to break up food quicker.
Progression of plaque formation
- decrease in host response
- primary adherance
- metabolism = a change in environment
- bacterial succession
- climax community
Progression of caries through the tooth
- White spot lesion - reversible using fluoride and better oral health.
- Early coronal lesion collapses the enamel surface.
- Caries progresses into dentine and then pulp.
Caries management
- Assessment e.g. plaque score (disclosing tablet), diet diary, x-rays to identify the causes and how to stop them - preventative.
- Diagnose and come up with a specific treatment plan for that patient.
- Inform the patient and of their options etc.
- Restoration/treat the symptoms.
- Future prevention e.g. oral hygiene instructions, topical fluoride application.
- Review and assess at each visit and recall time specific to each patient.
Types of caries risk factors
Primary = stuff that affects the biofilm directly e.g. saliva, oral-health, bacteria. Modifying = indirectly affect the biofilm e.g. SES, job, background, etc.
Pulp pathology types
Inflammatory = pulpitis Degenerative = fibrosis, calcification, internal resorption.
Pulp pathology causes
Infectious = via caries or fracture
Trauma = a blow, cold/hot
Chemical = fillings
Mechanical
Pulpitis
Chronic = usually due to infection. Open or closed. Acute = usually due to trauma. Open or closed e.g. if due to a fracture or a blow.
Periapical pathology types
Inflammatory = periapical periodontitis Reactive = Hypercementosis
Periapical pathology causes/ aetiology
Infectious = Periodontitis or via root canal e.g. pulp necrosis.
Trauma, chemical or mechanical
Periapical pathology on a non vital tooth w periapical periodontitis
Chronic periapical granulation = Periapical cyst = Chronic abscess.
Acute periapical abscess = Acute alveolar abscess = Chronic abscess or Cellulitis (face infection).
Chronic periapical granulation can lead to acute periapical abscess and vice versa.
Non-invasive diagnosisi of caries techniques
Radiographs
Caries detection dye that stains demineralizing areas
Laser fluorescence or transillumination
Interproximal impression.
Periodontal tissue injuries
Avulsion = tooth falls out Intrusion/extrusion = tooth pushed in or out Concussion = inflammation of PDL only Luxation = tooth displaced e.g. lateral or buccal Subluxation = tooth not displaced but is mobile.
Soft tissue injuries
Abrasion
Laceration
Contusion
Types of tooth fractures
Uncomplicated # = just in enamel/ a bit chipped off Complicated # = enamel-dentine Root # = just through root Enamel infraction = crack in the enamel Crown-root #
Trauma to primary teeth and effects on primary teeth
U1’s most common site, infarcation, due to accidents.
Effects on primary teeth = discolouration, early/delayed exfoliation.
Trauma to primary teeth’s effect on secondary teeth.
Discoloration or enamel opacity Hypoplasia/incomplete enamel development Early/delayed eruption and diff order. Abnormal root morphology/dilaceration. Benign tumors.
Trauma to secondary teeth and effects
U1’s most common, due to RTA, assault or sports injury
Effect on tooth = pulp death, discoloration, fracture, inflammation, hypersensitivity
Effect on patient = image, time, money, pain
Epidemiology
Study of distribution, risk factors and outcomes of a disease on a population (i.e. not individuals)
How to decide if an oral health condition is of public health importance
Frequency, severity, and distribution. Study epidemiology, prevalence (people w it/people at risk) and incidence (new cases/people at risk). Use an index to measure the disease. Impact on individuals and society. Prevention and treatment options etc.
What index is used to measure caries
DMFT/DMFS = permanent (teeth/surfaces) dmft = decidiuous teeth
Pros of DMFT
DMFS > DMFT bc bigger range and more specific
Used for a long time so accepted and a lot of data to compare to.
Easy to use and view data etc.
Disadvantages of DMFT
Age-specific so hard to compare across populations e.g. w/ aging populations or not.
Irreversible and cumulative
Doesn’t take into account:
- The severity of disease e.g. a small filling or a crown.
- How the tooth was lost e.g. trauma or decay
- The dentist’s treatment style
- Improvements in oral health
- Further treatments
- Treated or untreated decay
Index for measuring gingivitis
Plaque and bleeding score.
Plaque is more unreliable bc patient can brush teeth before coming to the dentist.
Index for measuring periodontitis
Loss of attachments e.g. recession or probing depths.
Non-carious tooth loss types and risk factors
Attrition, erosion, abrasion
Risk factors = anything that affects pH or saliva e.g. diet and medication. Teeth-brushing habits, acid reflux, teeth strength, etc.
Measuring non-carious tooth loss
O’Sullivan index
- A-F sites in the mouth (buccal, lingual, occlusal, buccal+occlusal, lingual+occlusal, multi).
- 0-5, 9 severity (9=crown/can’t tell).
- +/- = amount of mouth affected.
Oral cancer risk factors and effects on people/society
Risk factors = smoking, alcohol, sun, diet
Effects on individuals =
- death
- Time off work etc
- Surgery = physical and functional changes
- Radiotherapy = diminished tase, saliva and worse oral health.
Effects on society =
- NHS
- People not working/dead.
Centric Relation
The most anterior-superior position of the condyle in the glenoid fossa. Movement here is rotation around the horizontal axis.
RCP
Retruded contact position
Occlusion when TMJ is in centric relation.
ICP
Max cuspal contact.
Posterior teeth in contact, anterior teeth in light contact (posteriors have more molars and are sturdier so can withstand forces of mastication whereas anterior’s can’t)
Why is ICP important to maintain
Stops teeth drifting or over-erupting because there’s cuspal contact.
Protrusion of mandible
Condyle moves forward.
Incisor guidance - the palatal surface of upper incisors guides the mandible.
Anterior teeth in contact but not posteriors.
Sideways movement of the mandible
Canine guidance (only canines on the working side are in contact).
Canines > posteriors:
- Have a better morphology so less likely to fracture/recession/bone resorption when a sideways force applied (than posteriors).
- Longer larger root so can withstand force
- Further from the muscles and TMJ/hinge so less force applied to them than posteriors.
- More innervated. Masseter only works when posteriors are in contact, to protect anterior teeth.
Class I jaw
“Normal”
Molars = mesiobuccal cusp of U6 sits in buccal groove of L6.
Incisors = Lowers occlude at or below the upper cingulum
Class II jaw
Small mandible, large maxilla.
Molars = mesiobuccal cusp of U6 occludes in front of L6 buccal groove.
Incisors Division 1 = Uppers are at a normal inclination or proclined, so overjet increased.
Incisors Division 2 = uppers are retroclined so deep overbite.
Class III jaw
Molars = mesiobuccal cusp of U6 sits behind the buccal groove of L6. Incisors = lowers occlude in front of uppers.
Anterior guidance/protrusion with a Class II jaw
Division 1 = Mandible needs to protrude more so more occlusal contact between incisors so careful when doing incisal edge restorations.
Division 2 = Mandible needs to open more before protruding so more contact between lowers and posterior surface of uppers so careful when doing restorations here.
Anterior guidance/protrusion with a Class III jaw
Contact between all the teeth = bad.
Mandible movements dictated by
The position of the condyle in the fossa
Condylar guidance (from fossa to eminence)
Teeth guidance
How can fluoride act on teeth in general
Topically = directly affects the enamel on the tooth Systemically = incorporated into the enamel structure when the tooth was developing.
Effects of fluoride on teeth
- Replaces the OH- in calcium hydroxyapatite to make calcium fluoroapatite which is less soluble in acids.
- In bacteria, it affects some reactions e.g. glycolysis (less glycolysis = less acid)
- Catalyst for remineralization
- When demineralization happening, HA is lost so F binds to the Ca and PO4 lost and redelivers them to the tooth.
Sources of fluoride
Natural e.g. food and drinks
Added to stuff e.g. toothpaste, water, salt, milk
Supplements
Dental treatments
Water fluoridation pros
Breaks SES barriers e.g everyone can have it.
Proven to reduce caries (by 15%)
Easy to give to a large population and cheap
Safe
Water fluoridation cons
Associated with some health problems e.g. fluorosis
Mass medication means people don’t have a say
Not the same as naturally fluoridated water
Only benefits children because their teeth are still developing.
Problems caused by excess fluoride
While developing = fluorosis. More porous, weaker enamel that appears chalky white w striations and brown in severe cases.
A high F dose is toxic e.g. can cause respiratory problems. > 1 mg/kg is can cause nausea and vomiting.
Fluoride in dentistry
toothpaste - high F toothpaste can be prescribed to high risk patients (2800 ppm if >10yrs, 5000ppm if >16yrs).
Normal toothpaste = 1000ppm for <3yrs, 1350-1500ppm for 3-6yrs.
fluoride varnish - given to children and high risk patients/on high risk sites or white spot lesions. V V V high [F]
supplements - need to be prescribed. Not for < 6 months. Only effective until 6 years/while teeth are developing.
mouthwash - alternate time to brushing. 0.05% daily, 0.2% weekly.
What are white spot lesions and why do they appear white
Signs of demineralisation but not necessarily caries. White because the enamel becomes more porous as it loses minerals e.g. PO4 and Ca.
Are caries an infectious disease
No, because you need more than just the right bacteria to cause caries.
What are the requirements for caries to occur
Change in host response/susceptible tooth
Bacteria
Sugar
Historical theories of cariogenesis
- Acidogenic - the acid produced from fermentation of sugars causes caries
- Proteolytic - enzymes break down the matrix.
Dental plaque benefits and how it can cause caries.
Stops other bacteria colonising the tooth surface
If exposed to lots of acid frequently, the good acid sensitive bacteria get inhibited and the aciduricity and gram-negative anaerobic bacteria get selected for
= bad bacteria > good.
How to prevent the process of plaque becoming cariogenic
Prevent the low pH environment e.g. use fluoride and no snacking/sweeteners etc.
Stop the bacteria colonizing using antibacterials.
Cariogenic properties of mutan strep
Sugar transport systems are v efficient.
Aciduricity
Acidogenic
Make EPS and IPS.
What is dental plaque
Matrix of polymers with bacteria embedded into it.
What is the enamel pellicle
Selectively absorbed salivary proteins.
Plaque matrix’s role in making EPS
Produces enzymes glucosyl and fructosyl transferase that breaks down sucrose into fructose and glucose.
The glucose then joins w other glucose molecules to make a chain w side chain etc.
More side chains = more rigid = more insoluble.
These chains = EPS
EPS functions
- Sticky so harder to physically remove plaque from tooth.
- Sticks the microcolonies together.
- Diffusion barrier keeps low pH trapped near tooth.
- Makes it harder for immune cells and antibiotics to get in.
- Store of energy - glucan chains can be broken down if needed (via glucanase)
- Creates spaces b/w the bacteria so more sugars can diffuse in.
- Reduces surface area of bacteria so less Ca can stick to them so less Ca released when low pH = less buffering.
IPS roles
When there’s lot of sugar availible, bacteria cells lay down IPS in their cells which can be broken downa nd used as an energy source during times of low sugar availibiltiy.
What carciogenic properties of bacteria are most useful/needed
Aciduricity and acidogenicy.
How does sugar get fermented when there’s little glucose availibility
Permease used to allow glucose to enter cell (ATP dependent)
Pyruvate to Acid pathway uses a diff pathway that makes a diff acid (acetate, via PFL instead of LDH)
How does sugar get fermented when there’s a lot of glucose availability
PEP.PTS pathway used to get glucose into the cell.
LDH used to make lactate from pyruvate.
How do artificial sugars work and give an example of one?
Xylitol.
Compete/use up the PEP.PTS when they’re taken into the cell but don’t undergo phosphorylation so not ATP or acid made but the PEP.PTS is still used up.
How does aciduritity work?
The bacteria cells still work best intracellularly at a normal pH.
- Active pump system removes lactic acid and works best at low pH.
- Protein pump and glucose permease work best at low pH.
- Bacteria makes alkalis to neutralize the acid/increase pH e.g. breaks down arginine into ammonia.
- Pumps out acids actively and passively (gradient)
What in the saliva neutralizes the acid
HCO3, K+
How is dental tartar formed
Saliva pools and the ions can ppt out into the teeth but if ou aren’t brushing your teeth, it will solidify.
Problems with restorative materials
Water damages them:
- Poor surface retention e.g don’t stick well so gaps can form between it and the cavity walls and bacteria can live in these spaces.
- Water disrupts the setting process (polymerisation)
- Water absorbed into the material causes it to swell, weaken and crack.
How can you diagnose a salivary stone/sialolith e.g. investigations to do
Sialography, radiography ultrasound to see any soft tissue swellings Intra/extraoral examinations Take a history Measure flow rate
What is a mucocele
Damage to the salivary duct so when it tries to secrete saliva, it bursts
What is it called when there is damage to a salivary duct that causes it to burst if it tries to secrete saliva
mucocele
What is a swollen parotid gland called
Suppurative parotitis
Pediatric dentist’s patients
Specialist medical condition
- at higher risk of complications
Specialist dental condition
- abnormal facial bone growth e.g. cleft palate
- abnormal teeth e.g. morphology, position, number
- severe trauma
- excessive dental or periodontal health
- oral pathology e.g. infections, abscess, etc.
Behavioral or learning disability
- In pediatric clinics, the dentist is more trained and has more time.
Special cases e.g. safe-guarding, language communication barrier.
Preventative dentistry in paeds
Can be done on an individual or large population (water fluoridation).
Healthcare is important - educate, advice, preventative treatments.
Must be the first thing considered when treating a patient, and must be specialized for that patient esp w high-risk cases.
Should be evidence-based.
Benefits of preventative dentistry
Improves patient’s quality of life.
Better outcomes for the dentist
Cheaper for NHS etc.
Methods of prevention of oral conditions
Fissure sealants Smoking cessation Mouthguards Dietary advice Mechanical/chemical removal of plaque or calculus Regular screening (for cancer) Early intervention Fluoride
What sugars are most/least cariogenic
Sucrose (fructose and glucose) is most cariogenic.
Added sugars or non-milk extrinsic sugars are bad
Lactose and intrinsic sugars e.g. in fruits aren’t a threat.
How can sugar be eliminated from the mouth
Chewing
Saliva rinsing
Using foods/elements e.g. cheese, fluoride, phosphates, xylitol (in chewing gum)
What does clearance time depend on
Time of day Age The stickiness of the food Conc. of the sugar Saliva flow rate
