Oral Disease

Dental caries (tooth decay)

- bacterial disease of the mineralised tissues of the tooth -> where strong crystal structure found in both enamel
& dentine is demineralised (dissolved) by the action of acids.
Acids (waste product produced by oral bacteria) are relatively weak, but organic ones : lactic acid / citric acid
are strong enough to attack enamel & dentine.
Bacteria production of these acids :
 Streptococcus mutans (initial stages of cavity formation)
 Streptococcus sanguis
 Some lactobacilli (later stages of cavity formation).

Factors in the development of dental caries :
 the presence of certain types of bacteria
 carbohydrate foods
 the production of weak organic acids by these bacteria
 adequate time or frequency for the acids to attack the tooth.

Bacterial plaque
Combination of bacteria (colonies) & food debris on a tooth surface forms a thin, transparent, protein-containing,
soft & sticky film - plaque.
Areas (where it cannot be easily dislodged): at the gingival margins (gingivitis & periodontal disease), in the
fissures & around the edges of dental restorations---stagnation areas (O fissures & the spaces between the M & D
surfaces of adjoining teeth (the interproximal areas, or contact points)).

Sugars

 Protein – meats, fish & various dairy products & pulses (beans, peas, lentils).
 Fat –animal fats & vegetable oils.
 Carbohydrate (cariogenic - capable of causing caries) – natural sugars from fruit & vegetables, & artificial
sugars from processed foods.
+++ acid- producing carbohydrates -> artificially added during food preparation - based on non-milk extrinsic
sugars (NMEs) .The most damaging : the refined sugars sucrose (proceed->beet, cane) & glucose (dextrose).
Naturally occurring sugars (produce so little organic acid) - considered harmless to teeth:
 Intrinsic sugars – found naturally in foods - fructose in fruits.
 Milk extrinsic sugars – especially lactose.
Any food containing added sugar can cause caries & some obvious ones are: cake, biscuits, jam & sweets,
breakfast cereals, pastry, desserts, syrups & ice cream, soft drinks, hot beverages sweetened with sugar.
Hidden sugar : soup, sauces, breakfast cereals; medicines.
Naturally sugar : milk, fruit & vegetable (potatos, carrots, peas, beans).

Acid formation
Carbohydrate source is eaten - the oral bacteria take the sugar component into the plaque structure and begin to digest it.
In 1-2 min it is turned into acid by the plaque bacteria & then attacks the enamel surface beneath the plaque.
Enough acid is produced in 20 min & in this initial acid attack-a microscopic layer of enamel is dissolved
away----- demineralisation (destruction). The end of meal – acid is persist from 20 min to 2h.

Saliva maintain the mouth at a neutral level - pH 7.The measure of acidity/alkalinity of a solution - pH level.
When the weak organic acids are produced by the oral bacteria - the pH level starts to fall & once it passes the
critical pH 5.5, the environment is acidic enough to attack the enamel & dentine of teeth, and produce cavities.
Once neutralisation has occurred, no further demineralisation can take place, some natural healing takes place;
mineral constituents naturally present in saliva enter demineralised enamel & restore the part lost by the initial
acid attack. This healing phase - remineralisation.
 Caries and cavity formation

Process of cavity formation:

 Acid attacks -> ‘white spot lesions’ ( enamel surface).-> enamel prism ; exposed cementum
 Demineralisation -> of remineralisation (brown lesions on the teeth- contact point)
 Enamel destroyed & caries enters the tooth -> extends deep ->> amelodentinal junction (ADJ)
(no pain) -> enters dentine (spread rapid) =fracture off pieces of the tooth surface, leaving a hole
in the tooth structure - cavity
 Odontoblast cells at the ADJ react to the bacterial attack by laying down secondary dentine
(protect the underlying pulp tissue) (feel sensitivity to temperature changes and to sweet foods)
 The pulp tissue will become irritated & inflamed – pulpitis.
 Caries can be removed by the dentist & the cavity restored with a filling, the inflamed pulp will
settle & the tooth will be restored to its normal function – the inflammation -reversible pulpitis.
 -> pulp chamber (severe pain of longer duration, unable to bite with the affected tooth -
irreversible pulpitis (removing the caries)
 The pain - constant & throbbing in nature, disturbing the patient’s sleep.
 Once the pulp chamber itself is breached by the caries, a carious exposure of the contents
occurs & the pulp will eventually die.->RCT / extraction

Irreversible pulpitis
Pulpitis occurs when caries extends through the dentine to reach the pulp. The pulp is cariously exposed.
 There is an increased blood flow through the apical foramen into the pulp.
 Swelling cannot occur.
 Pressure therefore builds up instead-> causes intense pain.
 Compression of blood vessels passing through the tiny apical foramen – this cuts off the blood
supply & causes death of the pulp (severe toothache stops abruptly). -> The dead pulp
decomposes & infected material (pus) passes out of the tooth through the apical foramen & into the
alveolar bone at the apex of the tooth – alveolar abscess:
- painful condition
- tooth become loose
- surrounding gum - red & swollen
- raised temp + side of face-infl swelling
-
Pulpitis acute / chronic; always ends in pulp death.
- If acute abscess not treated -> chronic abscess by the drainage of pus through a sinus

(small hole in the gum) ‘‘ gum boil ’’

Diagnosis of caries
Methods detect smaller carious lesions:

 Close visible inspection under magnification (white matt appearance)

  Various blunt dental probes

 Transillumination - anterior teeth ( curing light to shine through their contact points)

 Caries dyes wiped into prepared cavities to stain any residual bacteria & allow their removal.
 Periodical horizontal bite-wing radiographs - detect interproximal caries in posterior teeth;
(detect recurrent caries beneath existing restorations ; caries beneath occlusal fissures)
Prevention of caries
 Modification of the diet – (cariogenic foods & drinks containing sugars – reduce)
 Control of bacterial plaque – (good oral hygiene techniques)
 Increase the tooth resistance to acid attack – (incorporating fluoride into its crystal structure)

Non-carious tooth surface loss

Erosion

- action of extrinsic acid (food / drinks) on the enamel : bacteria

 Carbonated fizzy drink
 Acid fruits (lemon, orange, lime, grapefruit)
 Pure fruit juise
 Wines
 Vinegar excessive consumption.

Condition & disorders : (gastric juices of stomach =pH2) - (Intrinsic)

 Obesity & eating/drinking too much
 Bulimia (vomiting) & Anorexia
 Reflux oesophagitis
 Hiatus hernia
 Stomach ulcers
 Pregnancy / Hormones
 Rumination (anxiety) & Regurgitation

- The tooth surface - pitted & worn but shiny & clean, with no plaque present.
- Affects the labial / palatal surfaces - U incisors ; O surfaces - L M
- The tooth – hypersesnsitive to hot, cold &swwet.

Treatment :
 Dietary and/or medical advice.
 Desensitisation of the dentine.
 Use of high-concentration fluoride toothpastes & mouthwashes to help restore the pH balance of o cav.
 Abrasion

- scrub their teeth using excessive side-to-side sawing forces bacteria

* smokers -> brush with a sawing action / use abrasive smokers’ toothpastes to remove the stains.

- Affects the cervical necks of the teeth ( deep ridge on the B & L surfaces) O surfaces - L M
- The tooth – hypersesnsitivity with temp changes
- Restore : GIC / composite
Attrition

- loss of enamel from the biting surfaces

Cause:
 Normal ‘‘wear & tear’’ of chewing, especially (old –patient)
 Occlusion of natural teeth onto ceramic restorations ( crowns & bridges)
 Bruxing – the abnormal & subconscious action of clenching & grinding the teeth (stress).

Abfraction
- loss of tooth in the cervical (neck) region, due to the shearing forces - overloading single standing teeth.

- can affect B, L, P -> occur suddenly

The teeth affected are usually single standing premolars-> molars have been lost in the same jaw.
Treatment : restoration of the affected tooth ;replacement of any missing teeth to reduce the occlusal loading of
the affected tooth and prevent a recurrence of the tooth loss.

Periodontal disease
- bacterial infection of supporting structures of the teeth caused by an initial accumulation of bacterial plaque

(tenacious transparent film of saliva + micro-organisms + oral debris )

at the gingival margin of the tooth - the gingivae, the perio ligam & the alv bone, anat cementum too.
Caries - major cause of tooth loss in children & young adults ; periodontal disease - major cause in older people.
Juvenile periodontitis – begins in childhood.
The earliest stage of periodontal disease - chronic gingivitis (chronic inflammation involving the gingivae alone)
Localise – affect a few teeth Generally – affect the majority of the dentition

chronic periodontitis - chronic inflammation spreads then deep into the underlying cementum & periodontal
ligament, and eventually to the alveolar bone.
These structures are gradually destroyed and the teeth become very loose - supporting tissues are lost.

Causes of periodontal disease

Plaque + Saliva =>Calculus(tartar) - (hard rock-like deposit commonly seen on the lingual surface of L incisors).
Supragingival plaque & calculus - bad oral hygiene – above the gum margin
Subgingival calculus --------------------------------------- - beneath the gum margin

Role : passive -> calculus ; active -> plaque micro-organisms

Iatrogenic factors : additional reasons for plaque form - not the patient’s fault caused by imperfect dentistry:
- fillings / crowns -> have an overhanging edge at their cervical margin,
- fillings / crowns with loose contact points,
- ill-fitting / poorly designed partial dentures.
Periodontal tissues in health

Gingivitis - first stage of periodontal disease (inflamed gingiva).->no pockets

Diagnosis of periodontal disease - is based on the medical history, appearance and recession of the gums,
depth of gingival pockets, amount of bone loss, tooth mobility and the distribution of plaque.
Periodontal pockets

Disclosed agents on teeth

Periodontal charting
The mouth is divided into quarters (quadrants) for tooth charting, sixths (sextants) U & L:
 molar sextant (876)
 premolar and canine (543)
 incisor (21).

Basic periodontal examination (BPE) coding system:

Code 0 – healthy gingival tissues with no bleeding on probing.
Code 1 – pocket no more than 3.5 mm, bleeding on probing, no calculus. >3,5
Code 2 – pocket no more than 3.5 mm but plaque retention factor detected. >3,5
Code 3 – pocket present up to 5.5 mm deep. >5,5
Code 4 – pocket present deeper than 5.5 mm. <5,5
Code * – gingival recession / furcation involvement.

Tooth mobility:
 Grade I – side-to-side tooth movement less than 2 mm. <-> >2
 Grade II – side-to-side tooth movement more than 2 mm. <-> <2
 Grade III – vertical movement present.
Non-surgical treatment of periodontal disease
- Accessible plaque - removed by tooth brushing & interdental cleaning.
- Subgingival plaque & calculus - during scaling.
- Application of antimicrobial drugs directly into the gingival crevice & pockets => Periochip, Dentomycin gel &
Gengigel applications.
Supragingival plaque control
At home = twice-daily tooth brushing - keep plaque under control + dental floss(between teeth – keep contact
area clean), wood sticks (large space) , interspace & interdental brush(TePe) .
Supragingival calculus & any overhanging cervical margins of restorations - removed in the surgery
->Scaling hand instruments ->: sickle , cushing’s push, jaquette.(SCALER)+ultrasonic -> polished with
prophylactic polishing paste (abrasive & removes any residual surface stains) + a rubber cup / bristle brush in

the slow handpiece

Subgingival plaque control
Instruments:

- gracey curette 1 cutting surface ->scraped away root cementum

- other subgingival curettes
- periodontal hoe
- ultrasonic scaler (vibration -> help loosen the plaque + water -> flash away).
 Other periodontal conditions
Subacute pericoronitis - infection of the gingival flap(operculum) that lies over a partially erupted tooth

->trismus (unable to fully open mouth)

Treatment (depending on the severity of the infection):
 Irrigation of any food debris from under the operculum - chlorhexidine-based disinfectant (Peroxyl).
 Oral hygiene instruction for the area = hot salt water / disinfectant / oxygen-releasing mouthwashes
 Anti – inflammatory analgesics (ibuprofen)
 Antibiotics if the patient has a raised temp (metronidazole ).
 Operculectomy
 Alternatively, the extraction of the opposing tooth to break the cycle of trauma and inflammation.

Acute herpetic gingivitis

– “Cold Sore”– Herpes Simplex (labialis) Virus – painful ulcers infectious

ANUG acute ulcerative gingivitis (AUG) or Vincent’s disease.

- pain & halitosis.

- gingiva a bright red + covering layer of yellow/grey sloughing membrane where the gum margin has been
destroyed by bacterial action.
- Bacillus fusiformis & Treponema vincenti.

Treatment :
 Antibiotic specific for anaerobic bacteria ( metronidazole).
 If pregnant - no mitranidazol( penicillin substituted).
 Long-term disinfectant chlorhexidine mouthwash & adequate brushing technique.

Acute lateral periodontal abscess

- complication of chronic periodontitis in which pus formation in a deep pocket is unable to drain
through the gingival crevice.
The pus accumulates instead at the base of the pocket to form an abscess.
- on a vital tooth at the side of the root (the lateral region of the root).

Treatment:
 Drainage of the pus present,
 Subgingival scaling of the affected tooth
 Local administration of antibiotic into the pocket itself ( metronidazole),
 Oral hygiene instruction,
 if all else fails => extraction of the affected tooth.
 Operculectomy
surgical removal of the gingival flap (operculum) overlying a partially erupted tooth (LM3)
+ electrosurgical cautery unit

Alveolectomy and alveoplasty

- remove pieces of the alveolar ridge / smooth & alter its shape

teeth extracted -> the edges of the sockets can remain - sharp spicules of bone ( radiograph ) which

make the wearing of dentures impossible without discomfort.

A mucoperiosteal flap must be raised to gain access to the ridge & bone rongeurs /
surgical burs are used to remove all the bony projections.
Gingivectomy and gingivoplasty
- periodontal surgery techniques -> adjust the shape of the gingivae & aid oral hygiene measures, so
that more effective plaque removal is possible.
- removal of a strip of gingival margin level with the the point of the epithelial attachment

Excessive overgrowth of gum (gingival hyperplasia) caused by drugs :

phenytoin (for epilepsy), nifedipine (for hypertension) & ciclosporin (following organ transplant).

/scalpel / laser - excess of gum remove ->

area covered –ZOE periodontal-pack 1week (Coe – Pak) (promote healing)
Gingivoplasty – surgical recontouring of the gingival.