Periodontal disease

Periodontology

Study of healthy and diseased periodontium

Periodontium

Group of tissues that support the teeth (gingivae, periodontal ligament, cementum, alveolar bone)

Periodontal disease

An inflammatory disease of periodontium

Periodontal disease and caries are

The most common disease of man

Periodontal disease is the major cause of

Tooth loss in older people

Plaque

A tenacious film of micro organisms, saliva and oral debris

Stagnation areas

Areas where plaque cannot easily be dislodged- pits and fissures, gingival margins, fixed appliances, overhangs

Chronic

Long duration- chronic gingivitis and periodontitis

Acute

Quick onset- NUG, perio abscess, pericornonitis

Factors that may lower a patients resistance to periodontal disease

Pregnancy (hormone imbalance), diabetes, HIV/ aids, leukaemia, vitamin deficiencies, drugs (anti depressants), smoking, age, stress

Healthy gingivae

Pink, stippled, pointed papillae, firm, no bleeding on probing or brushing

Periodontal disease only occurs in

The presence of plaque

Plaque is made of

70% micro organisms, 30% inter bacterial substances (proteins, carbohydrates cells, enzymes, toxins and acids)

Plaque is housed in

Stagnation areas

Plaque initial film only visible with

Disclosing agents- if left becomes thicker

Sucrose has marked effect on

Plaque formation

Factors lowering resistance to plaque

Diabetes, smoking, pregnancy, drug induced, blood disorder

Progression of plaque- pellicle

Thin organic salivary layer forms within minutes of brushing, no micro organisms, stains slightly with disclosing agents

Progression of plaque- 3-8 hours

Bacteria attaches to the pellicle, bacteria is non pathogenic/ gram positive

Progression of plaque- 24 hours

A clinical detectable layer of plaque now formed. At end of 24 hours, flora becomes increasingly complex- introduction of gram negative/ pathogens can be detected

Progression of plaque- 3 days

Number of organisms present continue to increase. Presence of pathogens/gram negative greater. At this stage pathogens can release toxins that irritate soft tissues

Progression of plaque- 7 days

Final phase of plaque maturation before calculus formation occurs. Further decrease in percentage of gram positive cocci/ rods present

Gingivitis may be considered to be

First stage of chronic periodontal disease

Gingivitis characterised by

Inflammation of gingival tissues

Gingivitis restricted to

Gingivae only and doesn't affect other supporting structures

Bacteria in mature plaque produces

Substances (toxins) which irritate the gingivae and produce an inflammatory response

Gingivitis is reversible by

Carrying out effective oral hygiene

Gingivitis clinical signs

Bleeding, halitosis, redness, spongey&glossy gingivae, swelling, false pocketing

False pocketing

An enlarged gingival crevice due to inflammation. It provides a bigger stagnation area for plaque and debris to collect

Gingivitis treatment

Scale & polish, plaque control via OHI, correction of tooth relationships, correction of appliance

Periodontitis

Periodontal disease is an inflammatory disease of supporting structures of the teeth

If chronic gingivitis is not treated

Microbes will affect the deeper tissues

Periodontitis clinical signs are same as gingivitis as well as

Gingival recession, tooth mobility, bone loss, true periodontal pocketing, drifting, lateral periodontal abscess, furcasion lesion

Furcation lesion

Exposed bifurcation/ trifurcation area that can be accessed by a periodontal probe. Cannot necessarily be seen

Bacteria associated with periodontal disease

Porphyromonas gingivalis, actinomyces, treponema denticola, prevotella intermedia

Cause of periodontitis

Poor oral hygiene, calculus, caries, malalignment, high fraternal insertion, lip apart posture, gingival recession

Calculus

Hard mineralised dental plaque

Calculus can adhere to

Teeth, restorations and appliances

Calculus made up of

70% inorganic salts and 30% microorganisms and organic material

Calculus main minerals

Calcium and phosphorus

Calculus covered by

A film of plaque, also occupy its porous structure

Presence of calculus makes

Effective oral hygiene impossible

Calculus removal to prevent or assist in the

Control of inflammatory periodontal disease is of great importance

Calculus is usually classified according to

It's relationship to the gingival margin

Supra gingival

Calculus above gingival margin on clinical crowns of teeth

Supra gingival colour

White or pale yellow, unless stained by tobacco tar or food pigments

Supra gingival calculus is

Relatively soft and can be removed easily with a scaler

Supragingival calculus occurs most commonly on

Buccal aspect of upper molars and lingual aspect of lower anteriors

Reason for why supragingival calculus occurs most commonly where it does is due to

The fact that the ducts of the major salivary glands open into the mouth in these areas

Sub gingival calculus

Much darker, harder and more difficult to remove than supra

Sub gingival calculus colour

Black to brown and more evenly distributed throughout mouth

Sub gingival calculus forms

Below gingival margin in periodontal pockets and may be present as small discreet deposits or form a band running round the tooth

Sub gingival calculus dark colour is caused by

The breakdown products of blood lost from the ulcerated pocket epithelium

False pocket

Enlarged gingival crevice- only affects gingivae. If plaque not removed and gingivitis not halted- free gingivae will become swollen to produce illusion of a pocket. Allows food debris to accumulate

True pocket

Microbes from plaque penetrate deeper tissues detaching the gingivae from the tooth and causing destruction of the periodontal ligament and alveolar bone

Gingival recession

Gingivae becomes detached from tooth and starts to move away from the source of irritant. Will expose root, visible clinically

Bone resorption

Irritation of supporting tissues by microbes in plaque will destroy bone. Visible root surface and root Furcation. Loss of supporting structures will increase mobility

0

No pockets exceeding 3mm, no bleeding, no plaque or calc- no treatment required

1

No pockets exceeding 3mm, no calculus, bleeding on probing- oral hygiene instructions required

2

No pockets exceeding 3mm, bleeding and calculus and plaque present- 1 visit scaling required

3

Pockets exceed 3mm, bleeding, calculus and plaque present- 2 visit scaling, root planning and pocket chart required

4

Pockets exceed 6mm, bleeding calculus and plaque present- 3+ scaling, rootplanning, 6 point pocket chart and radiographs required

X

No teeth/ only 1 in sextant

Full periodontal charting

Readings taken at 6 points on each tooth, measured using Williams probe or cpc12 probe. Recorded above and below tooth on chart.

Scalers

Jacquette, push scaler, sickle scaler, curettes, periodontal hoes, chisels, implant scalers and ultrasonic scaling tip

Jacquette and push scaler

Removes supra gingival calculus and used in a pulling action

Sickle scaler

Removes supra gingival calculus and is excellent interdentally

Curettes

Main function for sub gingival scaling also suits supra, good for root planning

Periodontal hoes

Push/pull action, TC tipped, different angled tips, good for root planning

Chisels

Heavy deposits of supra gingival calculus

Implant scalers

Doesn't scratch or damage implants, plastic or gold tipped

Ultra sonic scaling tip

Removes stains and calculus using ultra sonic waves, washes away blood, debris and dead tissue, cooled with water

Prevention of periodontitis

Toothbrushing, interdental aids, disclosing agents, chlorhexidine (mouthwash and gel)

Chlorhexidine

Inhibits growth of plaque and slows down the progress of the disease. Can cause staining

Acute periodontal conditions

Acute pericoronitis, acute herpatic gingivitis, NUG, acute lateral periodontal abscess, pregnancy gingivitis, epulis

Acute pericoronitis

Infection of gingival flap of tissue lies over partially erupted tooth called operculum (particularly wisdom teeth) difficult to clean and allows plaque to stagnate

Acute pericoronitis treatment

Irrigation, talbots iodine, OHI, antibiotics, extraction, operculectomy

Acute herpatic gingivitis

Caused by herpes simplex virus, most commonly affects infants. Signs- acute inflammation & tiny blisters that leave painful ulcers. Symptoms- pain, unwell, unable to eat solids, resolves without treatment

Necrotising ulcerative gingivitis

Occurs mainly in young adults(18-30) factors are poor OH, smoking, stress, immune suppression

NUG signs and symptoms

Neurotic ulcers affecting interdental papillae, painful ulcers may be covered in grey slough, gingival bleeding, halitosis, lymph node involvement

NUG treatment

Ultrasonic scaling, root planning, metronidazole

Acute lateral periodontal abscess

Localised infection within tissues adjacent to periodontal pocket. May lead to further destruction of periodontal ligament and alveolar bone

Acute lateral periodontal abscess cause

Imp action of food debris, foreign body (fish bone), incomplete removal of calculus, bacterial invasion of tissues, systemic factors

Acute lateral periodontal abscess treatment

Drainage, antibiotics or metronidazole, subgingival scaling, OHI

Pregnancy gingivitis

Gingivitis or inflammation of gingivae, hormonal changes that occur lead to increased blood flow to gingival tissue and increased inflammation in response to reserve of plaque.

Epulis

Localised hyperplasia (overgrown gingivae) quite often occurs with pregnant women. (Second or third trimester) often bleed easily and very red/inflamed- not painful. Usually disappears after childbirth.

Surgical treatment

Open flap curettage, gingivectomy

Open flap curettage

Gingival flap is raised to expose bone, root surface, subgingival calc. Curettage or ultrasonic scale of calc, plaque and granulation tissue. Perio chip may be placed, flap is sutured back, review in a week

Gingivectomy

Surgical removal of gingival tissue. Pre op scale, excess gingivae removed with knife/scalpel, area covered with a gingivectomy pack (Coe pack), review in a week