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