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Chronic periodontitis is the most common form, usually occurring in people over the age of 35

Pain is NOT a symptom of chronic periodontitis, hence why patients don’t seek treatment early on or don’t follow through with treatment after diagnosis.

Clinical appearance is not a reliable indicator for presence or severity of chronic periodontitis

May exhibit pronounce changes in appearance.

May exhibit minimal changes in appearance.

CLINICAL APPEARANCE IS NOT A RELIABLE INDICATOR OF DISEASE.

Pus represents dead WBCs and occur in any infection, including PD.

Exudate AKA suppuration is the accumulation of pus.

The seriousness of chronic periodontitis is determined by:

Rate of disease progression over time.

The response of tissues to treatment.

Treatment goals for chronic periodontitis:

Control bacterial plaque to a level compatible with periodontal health.

Alter or eliminate contributing risk factors.

Arrest disease progression (stop attachment loss from worsening).

Prevent recurrence of disease.

Reduction in probing depth.

Long-term outcome of periodontal therapy depends on:

Patient compliance with self-care.

Periodontal maintenance – recall appointments at appropriate intervals.

Not all disease sites respond equally to therapy. Signs that disease site is not responding successful to therapy include:

Inflammation

Increasing attachment loss

High plaque levels

Recurrent chronic periodontitis involves new signs of destructive periodontitis that reappear after therapy because:

Disease was not adequately treated and or patient did not practice adequate self-care.

Refractory periodontitis was a disease classification category that was eventually removed in 1999.

Referred to all types of periodontal disease that do not respond to treatment.

Refractory chronic periodontitis involves cases of chronic periodontitis that do not respond to periodontal therapy.

This means, there was continued attachment loss at one or more sites even with appropriate and adequate therapy, self-care, and full completion of periodic maintenance visits.

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3 basic states of periodontium:

1. Periodontium in health:

Clinical picture of health: pink, firm, no bleeding.

Histological picture of health - healthy sulcus: JE coronal to CEJ, supragingival fibers intact, alveolar bone intact, and PDL intact.

2. Gingivitis: a type of PD characterized by changes in colour, contour, and consistency of gingival tissues.

Observed clinically from 4 to 14 days after biofilm builds up in the gingival sulcus.

Bacterial infection confined to the gingiva.

Reversible damage.

Clinical picture of gingivitis: red, swollen, bleeding likely

Histological picture of gingivitis – gingival pocket: JE at CEJ, supragingival fiber destruction, alveolar bone intact, PDL intact

Acute gingivitis: lasts for short period of time, characterized by fluid in gingival connective tissues, and tissue appears swollen.

Chronic gingivitis lasts for months or years, new collagen fibers are formed resulting in more fibrotic tissue.

Gingivitis may persist for years without progressing to periodontitis.

3. Periodontitis: a type of PD characterized by apical migration of JE, loss of connective tissue attachment, and loss of alveolar bone.

Tissue damage is permanent.

Bacterial infection of all parts of the periodontium.

Clinical picture of periodontitis: pink or purplish, swollen or fibrotic, and bleeding.

Histological picture of periodontitis – periodontal pocket: JE on cementum, supragingival fiber destruction, alveolar bone destruction, and PDL destruction.

2 types of periodontal pockets:

1. Suprabony: occurs when there is horizontal bone loss.

JE located coronal to crest of alveolar bone (above crest of bone).

2. Infrabony: occurs when there is vertical bone loss.

JE located apical to the crest of alveolar bone (below the crest of bone).

Base of pocket located within cratered-out area of bone alongside root surface.

Current view/theory of disease progression is known as Intermittent Theory of Disease Progression, and states that:

PD is characterized by periods of disease activity and inactivity.

Tissue destruction can be sporadic/random, progressing at different rates throughout the mouth.

Most cases of untreated gingivitis DO NOT progress to periodontitis.

Susceptibility to periodontitis varies greatly between individuals.

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Gingival diseases are the most common and mildest form of PD.

Plaque-induced gingival diseases: PD involving inflammation to gingiva in response to dental plaque.

Plaque-induced gingivitis:

On a periodontium with no attachment loss:

Most common form

Plaque at GM

Red, tenderness

Swollen margins

BOP

Damage reversible with good homecare

On a reduced but stable periodontium:

Occurs in patients who have been successfully treated for periodontitis, but then at a later time, develop gingivitis (but NO periodontitis is present at the same time).

All other signs of plaque-induced gingivitis, and the attachment loss from history of periodontitis.

Gingival disease modified by systemic factors:

Less common type.

Plaque initiates the disease and then specific systemic factors in the host modify the disease process (usually exaggerating it).

i.e. puberty-induced gingivitis, pregnancy-induced gingivitis, pregnancy-associated pyogenic granuloma AKA “pregnancy tumor”, diabetes-associated gingivitis, and leukemia-associated gingivitis.

Gingival diseases modified by medications:

Drug-influenced gingivitis: exaggerated inflammatory response to dental plaque and a systemic medication.

Drug influenced gingival enlargement: an increase in size of gingiva resulting from systemic medications. This could even occur without plaque accumulation – meticulous plaque control can reduce but will NOT eliminate gingival overgrowth. Examples of medications that cause this are:

Anticonvulsants, i.e. phenytoin

Calcium channel blockers, i.e. nifedipine

Immunosuppressants, i.e. cyclosporine

Gingival disease modified by malnutrition:

Those at risk for vitamin deficiencies, i.e. infants, institutionalized elderly, alcoholics.

Example: ascorbic acid-deficient (chronically low vitamin C levels) gingivitis.

Non-plaque-induced gingival lesions:

Gingival disease of a specific bacterial origin:

Characterized by a bacterial infection of gingiva by specific bacterium that is not common component of bacteria plaque biofilm, AKA not a periodontal pathogen.

Gingival diseases of viral origin:

Primary herpetic gingivostomatitis: the initial oral infection with the herpes simplex type-1 virus (HSV-1).

This infection is contagious during the vesicular stage.

Linear gingival erythema (LGE): gingival manifestation of immunosuppression, that is characterized by inflammation that is exaggerated for the amount of plaque present.

Does NOT respond well to better homecare or professional therapy.

Usually associated with HIV infection.

Lichen planus: a disease of the skin and mucous membranes without an exact cause that is characterized by an itchy, swollen rash on skin or in mouth.

May be an allergic or immune reaction.

Erythema Multiforme: a disease of the skin and mucous membranes caused by an allergic reaction or infection.

Characterized by large, symmetrical red blotches, (target-like), that appear all over the sin in circular pattern.

Other non-plaque induced lesions include:

Gingival diseases of fungal origin

Gingival diseases of genetic origin

Gingival manifestations of systemic conditions

Traumatic lesions

Foreign body reactions

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Aggressive periodontitis is a bacterial infection characterized by the rapid destruction of PDL and supporting alveolar bone.

High risk for tooth loss with this form of periodontitis.

Less common than chronic periodontitis.

Poor response to periodontal treatment.

Previously known as early onset periodontitis (EAP).

Thought to occur only in individuals under the age of 30 years.

Renamed because it can really occur at any age.

Primary features of aggressive periodontitis:

Rapid destruction of attachment.

No obvious signs/symptoms of systemic disease.

Other family members with aggressive periodontitis, i.e. parents, siblings.

Secondary features of aggressive periodontitis:

Relatively small amounts of plaque but disease severity is exaggerated.

Elevated proportion of Aggregatibacter actinomycetemcomitans (Aa).

Phagocyte abnormalities.

Lack of clinical signs of disease – tissue appears healthy, but probing shows deep PPDs.

Key difference between chronic and aggressive:

CHRONIC: a very slowly progressing disease.

AGGRESSIVE: attachment loss is episodic, occurring in a succession of acute destructive phases with intermittent inactive phases.

Localized aggressive periodontitis (LAP):

Onset of disease around puberty.

Localized, rapid tissue destruction around permanent first molars and/or incisors.

Involving NO more than 2 teeth other than first molars and incisors.

Lack of tissue inflammation and minimal amounts of plaque that seem inconsistent with around of periodontal destruction.

Usually associated with Aa.

Vertical bone loss around first molars and incisors – beginning around puberty.

Previously called localized juvenile periodontitis.

Generalized aggressive periodontitis (GAP):

Onset usually occurs in people under the age of 30 years.

Generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors.

Episodic disease progression.

Minimal amounts of plaque that seem inconsistent with amount of periodontal destruction.

Bone loss around most teeth.

2 types of appearances:

Type 1: gingival tissues may appear acutely, inflamed, ulcerated, and fiery red.

Believed to occur in destructive phase of disease progression.

Type 2: Gingival tissues appear pink, deep pockets are detected with probe. This appearance occurs during periods of disease inactivity.

Previously called generalized juvenile periodontitis or early-onset periodontitis.

GENERALIZED AGGRESSIVE PERIO= GENERALIZED JUVENILE PERIO = EARLY-ONSET PERIO.