oral and dental disease for medical students
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Oral and Dental Disease
Victor Lopes PhD FRCS FDSRCS
Clinical Director, Head & Neck.
TOOTH CHARTING
Each arch is divided in half at the midline,forming FOUR QUADRANTS
maxillary right
maxillary left
mandibular right
mandibular left
PERMANENT DENTITIONFour quadrants and withineach quadrant there is
8 teeth
1= Central Incisor
2= Lateral Incisor
3= Canine
4= First Premolar
5= Second Premolar
6= First Molar
7= Second Molar
8= Third Molar / Wisdom
Tooth
PRIMARY DENTITIONOnly 5 teeth per quadrant
a / 1 = Central Incisior
b / 2 = Lateral Incisor
c / 3 = Canine
d / 4 = First Primary Molar
e / 5 = Second Primary Molar
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Examples of complete tooth names are:
- mandibular left permanent first molar
- maxillary right primary canine
Because their names are cumbersome,teeth are frequently referred to by number
The tooth numbering systems primarilyused today are the:
- Palmar Notation
- Fdration Dentaire Internationale (FDI)
PALMAR NOTATIONPermanent Teeth
R L
PALMAR NOTATIONPrimary Teeth
R L
e d c b a a b c d e
e d c b a a b c d e
FDI SYSTEMR L
RADIOGRAHICINTERPRETATION
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OPG OPGamalgam restoration
unerupted canine
composite restoration
3. THE APICAL TISSUES
a) integrity of lamina dura
b) radiolucencies assoc. with theapices
4. THE PERIODONTAL TISSUES
a) width of the periodontal ligamentb) level and quality of crestal bone
c) vertical and horizontal bone loss
d) furcation involvement
MIXED DENTITION DENTAL CARIES
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BASIC DENTAL ANATOMY
ENAMEL: hardest and most impermeable ofthe tissues
DENTINE: tubular structure, highly permeable
PULP: connective tissue within a pulp cavitysurrounded by dentine, communicateswith periradicular tissue through apicaland lateral canals
SUGAR
AETIOLOGY OF DENTAL CARIES
TOOTH
BACTERIA
TIME
CARIES
Dental caries is a sugar-dependantinfectous disease
Acid is produced as a by-product ofcarbohydrate metabolism by plaquebacteria
Results in a drop in pH at the tooth surface
In response, Ca and P ions diffuse out ofthe enamel => DEMINERALIZATION
Process is reversed when the pH rises
again
Caries is a dynamic process with episodicdemineralization and remineralization
If demineralization predominates
Disintegration of the mineral component
Cavitation
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TOOTHACHE
Pain may be arising from a variety ofdifferent structures:
- Pulpal pain
- Periapical / periradicular pain
- Non-dental pain
CLASSIFIACTION OF DENTAL PAIN
The sensory response of teeth iscontrolled by myelinated (A) nerve fibresand unmyelinated (C) fibres
Differences between the two fibres assistin the classification of dental pain
Disturbances in the pulp dentine complexinitially have their effects on the lowthreshold A fibres, which produce
- quick pain
- sharp pain
Inflammatory tissue damage in the pulpinvolves the high threshold C fibres, which
produce- spontaneous pain
- lingering pain
NORMAL PULP
Never spontaneously symptomatic
Reacts to thermal and electrical testing
Percussion does not cause pain
Radiographic picture is normal
REVERSIBLE PULPITIS Suggests the presence of mild inflammation
Thermal / electrical stimuli produce short,sharp pain for the period of stimulation
(This is a typical A nerve response)
Radiographically no evidence of pathology
Removal of the cause of inflammation (egdental caries) leads to resolution of thecondition
Rx OF REVERSIBLE PULPITIS
Remove any caries present and restorewith a suitable lining
Vitrabond (RMGI)
GI
ZnO
Ca(OH)
Then place permanent restoration Amalgam
Composite Resin
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IRREVERSIBLE PULPITIS
Inflammation that results in the dull throbbingpain of toothache
Spontaneous pain
May last several hours, often worse at nightand may keep the patient awake
Difficult to localize source of pain
Pain is elicited by hot and cold at first, butin later stages heat is more significant andcold may actually ease the symptoms
A characteristic feature is that the painremains after the removal of the stimulus
Radiographic changes may be evident ifthe inflammation extends to theperiodontal ligament e.g. widening of thelamina dura
Rx OF IRREVERSIBLE PULPITIS
Extirpation of the pulp and RCT
OR
Extraction
PULP NECROSIS
Progression of irreversible pulpitisultimately leads to death of the pulp
At this stage pt may experience RELIEFfrom pain and thus may not seek attention,HOWEVER INFECTION STILL REMAINS
If neglected, the bacterial and pulpalbreakdown products leave the root canalsystem via the apical foramen or lateralcanals and lead to inflammatory changesand possibly pain.
PULPAL NECROSIS WITH
PERIAPICAL PERIODONTITIS Dull ache, exacerbated by biting on the tooth
No response to hot / cold
Tender to percussion
Radiographically apical PDL may be widenedor may be a periapical radiolucency (granulomaor cyst)
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Rx OF PULPAL NECROSIS WITHPERIAPICAL PERIODONTITIS
Extirpation of the pulp and RCT
OR
Extraction
ACUTE PERIAPICAL ABSCESS
Severe pain
Will disturb sleep
Extremely tender to touch
ACUTE PERIAPICAL ABSCESS
May be associated localised / diffuseswelling
Radiographically varies from widening ofPDL / Lamina Dura to an obvious
radiolucency
Rx OF ACUTE PERIAPICALABSCESS
Drain pus
a) Enter pulp chamber with high speeddiamond bur. After drainage, prepare thecanal and place temporary dressing
NOTE:
Open Drainage should be avoided ifpossible, but if absolutely necessary for
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RECURRENT ORAL ULCERATIONS
MINOR APHTHAEMAJOR APHTHAE
HERPETIFORMBEHCETS SYNDROME
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FACTORS ASSOCIATED WITH APHTHAE
Hereditary Hypersensitivity
Psychological Chemicals in foodSocio-economic Trauma
Endocrine Strep. SanguisAIDS
BEHCETS SYNDROMECLINICAL FEATURES AND POSSIBLE
COMPLICATIONS
1. ORALAphthous Stomatitis
2. OCULARUveitis
Retinal VasculitisOptic atrophyBlindness
3. GENITALUlcers
BEHCETS SYNDROMECLINICAL FEATURES AND POSSIBLE
COMPLICATIONS (cont.)
4. NEUROLOGICALSyndromes resembling multiple sclerosisSyndromes resembling psudobulbar palsy
Benign intracranial hypertensionBrain-stem lesions
5. CUTANEOUSPustulesErythema nodosum
6. PSYCHIATRICDepression
BEHCETS SYNDROMECLINICAL FEATURES AND POSSIBLE
COMPLICATIONS (cont.)
7. JOINTSArthralgia (large joints)
8. VASCULAR
AneurysmsThromboses of vena cavae
9. RENALProteinuriaHaematuria
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APHTHAE WITH GI DISORDERS
COELIAC DISEASECROHNS DISEASE
ULCERATIVE COLITISMALABSORPTION SYNDROME
NUTRITIONAL DEFICIENCIESASSOCIATED WITH APHTHAE
IRONB12
FOLATEB1 B2 B6
LOCAL THERAPY: chlorhexidine mw &orabase, NOT BONJELA
SYSTEMIC THERAPY FOR APHTAE
COLCHICINELEVAMISOLETHALIDOMIDE
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LICHEN PLANUS
LICHENOID REACTIONLICHENOID DYSPLASIA
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DRUGS CAUSING LICHENOID REACTIONS
Allopurinol Gold Practolol
Amiphenazole Hydroxychloroquine PropanololAtorvastatin (Lipitor) Ketoconazole PyrimethamineCaptopril Labetanol QuinidineCarbamazetine Mercury QuinacrineChloroquine Methyldopa SpironolactoneChlorpropamide Metopromazine Streptomycin
Cyanamide NSAID TetracyclineDapsone Oxyprenolol ThiazidesEnalapril Palladium TolbutamideErythromycin Para-amino salicylic acid TriprolidineFenclofenac Penicillamine ZoloftFurosemide Phenothiazines
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PEMPHIGUSVULGARISVEGETANS
FOLIACEOUSERYTHEMATOSUSPARANEOPLASTIC
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PEMPHIGOID
MUCOUS MEMBRANE OR CICATRICIALBULLOUS
LINEAR IgA DISEASE
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ERYTHEMA MULTIFORME
STEVENS JOHNSON SYNDROME
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LUPUS ERYTHEMATOSUS
DISCOIDSUBACUTE CUTANEOUS
SYSTEMIC
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SCLERODERMA
CIRCUMSCRIBED (MORPHEA)SYSTEMIC SCLEROSIS
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BENIGN MIGRATORY GLOSSITIS
(ERYTHEMA MIGRANS, GEOGRAPHIC TONGUE)STOMATITIS AREATA MIGRANS
PSORIASIS
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GEOGRAPHIC TONGUEERYTHEMA MIGRANS
BENIGN MIGRATORY GLOSSITIS
STOMATITIS AREATA MIGRANSPSORIASIS
Morris, LF, et al. Oral Lesions in patients with psoriasis: acontrolled study. Cutis 49:339-44, 1992
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SUMMARY OF FINDINGS
- GT was 4 times more frequent in psoriatics.- Male psoriatics had 2.5 times the incidence of
GT than female psoriatics.- Males with GT had 10 times the incidence of
psoriasis than females with GT.- Ectopic lesion were 5 times more frequent in
psoriatics.
- Incidence of FT was the same in both groups.- Incidence of FT increased with age in both
groups.