Gingivitis & Periodontitis

💡Gingivitis vs periodontitis

Exam pearl: Bleeding on probing does not, by itself, establish periodontitis. Assess attachment levels and radiographic bone loss.

💡Color changes in gingivitis

The appearance of inflamed gingiva depends on vascular changes, tissue edema, chronicity and fibrosis.

Remember the color sequence: Normal coral pink → acute bright red → chronic bluish-red.

Fibrotic tissue may appear relatively pale even when inflammation persists.

💡EXOGENOUS PIGMENTATION OF GINGIVA

Exogenous pigmentation occurs when substances from outside the body accumulate in gingival or oral tissues. This differs from endogenous pigmentation, which results from internal pigments such as melanin, hemosiderin or bilirubin.

💡PATHOGENESIS OF PERIODONTAL DISEASE

💡Stages of periodontal inflammation

💡Cells involved in periodontal disease

💡Mechanism of alveolar bone loss

The central pathway is the RANK–RANKL–OPG system.

1. Bacterial biofilm stimulates host inflammatory responses.
2. Inflammatory mediators, including IL-1β and TNF-α, promote tissue destruction.
3. RANKL binds RANK on osteoclast precursors.
4. Osteoclast differentiation and activation increase.
5. Alveolar bone is resorbed.

OPG (osteoprotegerin) acts as a decoy receptor that binds RANKL and limits osteoclast activation.

MCQ tip: Osteoclasts resorb alveolar bone; RANKL promotes their activation, whereas OPG inhibits it.

💡ACUTE NECROTIZING ULCERATIVE GINGIVITIS (ANUG)

💡Definition and etiology

ANUG is an acute, painful, necrotizing gingival infection historically called Vincent infection or trench mouth.

It is associated with a fusospirochetal microbial community, particularly:

• Fusobacterium nucleatum
• Treponema species, including organisms historically called Borrelia vincentii

Prevotella intermedia may also be involved.

Predisposing factors

• Psychological stress.
• Smoking.
• Poor oral hygiene.
• Malnutrition.
• Sleep deprivation.
• Immunosuppression, including HIV infection.

Clinical features

Classic diagnostic combination

Pain + bleeding + punched-out papillae + halitosis strongly suggests ANUG.

Histological zones of ANUG

The describes four zones, from the surface toward deeper tissues.

Treatment of ANUG

• Gentle professional debridement, initially as tolerated.
• Oral hygiene instruction.
• Antiseptic rinses such as chlorhexidine when appropriate.
• Metronidazole may be indicated when systemic antimicrobial treatment is clinically warranted.
• Address smoking, nutrition, stress and other predisposing factors.
• Assess for systemic illness or immunosuppression when indicated.

Complications

Untreated necrotizing gingival disease can extend into the periodontium as necrotizing ulcerative periodontitis (NUP). In severely malnourished or immunocompromised patients, advanced necrosis may progress to noma.

FCPS tip: In a young patient with ANUG, consider whether HIV testing or other evaluation for immunosuppression is indicated; ANUG alone does not establish HIV infection.

💡DRUG-INDUCED GINGIVAL OVERGROWTH

💡Drugs

Certain medications promote excessive gingival enlargement, particularly in the presence of plaque-induced inflammation.

Clinical features

• Enlarged gingival margins and interdental papillae.
• Often more prominent in the anterior gingiva.
• Plaque-induced inflammation can increase the severity.
• Fibrotic enlargement may persist even after inflammation is reduced.

Management

1. Improve plaque control and perform professional cleaning.
2. Review the medication with the prescribing clinician; consider an appropriate alternative if medically feasible.
3. Reassess gingival enlargement after inflammation control and any medically supervised medication change.
4. Gingivectomy or another periodontal surgical procedure may be considered if enlargement persists and interferes with function, hygiene or appearance.

FCPS mnemonic: P-C-N = Phenytoin, Cyclosporine, Nifedipine.

Exam pearl: Plaque is an important cofactor. Do not advise a patient to stop an anticonvulsant, immunosuppressant or antihypertensive independently.

💡COLOR CHANGES IN PERIODONTITIS

Clinical appearance

Periodontal inflammation can change the appearance of the gingiva and periodontal pocket.

Remember: Gingival color alone cannot determine whether attachment loss is present. Periodontal probing and appropriate radiographs are needed to assess periodontitis.

💡PERIODONTITIS: 2017 CLASSIFICATION

Staging: severity and complexity

The 2017 classification replaced the older categories of chronic and aggressive periodontitis with a unified periodontitis diagnosis classified by stage and grade.

Staging reflects the severity of attachment/bone loss and treatment complexity.

Tooth-loss and furcation criteria as additional stage indicators. Stage assignment should use the complete classification criteria rather than CAL alone.

Grading: rate of progression

Grade estimates the risk and rate of progression, including evidence of progression over time and the relationship between bone loss and age.

The following approximate bone-loss progression figures:

Clinical grading should follow the formal classification criteria and available longitudinal or radiographic evidence.

Grade modifiers

• Smoking: more than 10 cigarettes per day supports Grade C.
• Diabetes: HbA1c above 7% supports Grade C in the classification framework.

FCPS tip: Stage = severity and complexity; grade = progression rate and risk.

💡AGGRESSIVE PERIODONTITIS

The older classification divided aggressive periodontitis into localized and generalized forms. Although the 2017 classification no longer treats aggressive periodontitis as a separate diagnostic category, the terminology remains relevant to some examination questions.

💡Localized aggressive periodontitis (LAP)

Classic pattern

• Usually begins around puberty or during adolescence.
• Classically affects first permanent molars and incisors.
• Interproximal attachment loss is concentrated around these teeth.
• The amount of plaque may be relatively small compared with the extent of destruction.
• A strong host immune response against Aggregatibacter actinomycetemcomitans (Aa).

Key organism: Aggregatibacter actinomycetemcomitans

• Gram-negative, facultative anaerobic, capnophilic coccobacillus.
• Produces leukotoxin, which damages neutrophils and monocytes.
• May produce collagen-degrading and bone-resorption-associated factors.
• Host neutrophil/monocyte dysfunction can contribute to severe disease.

FCPS tip: Adolescent + first molars and incisors + rapid bone loss disproportionate to plaque = classic localized aggressive periodontitis.

💡Generalized aggressive periodontitis (GAP)

Clinical pattern

• Usually affects individuals younger than 30 years in the classic description.
• Attachment loss affects at least three permanent teeth other than first molars and incisors.
• Destruction may occur in episodes, with periods of relative quiescence.
• Plaque levels may vary.
• A. actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia.

Systemic associations to remember

Consideration of systemic conditions associated with early-onset aggressive periodontal destruction, including:

• Papillon–Lefèvre syndrome.
• Hypophosphatasia.
• Cyclic neutropenia.
• Leukocyte/neutrophil disorders, including relevant immune deficiencies.

💡PERIODONTAL PATHOGENS

💡High-yield organisms

💡Microbial complexes

Socransky's complexes classify subgingival bacteria according to their association with periodontal health and disease.

Key relationships

• Red complex: Porphyromonas gingivalis + Tannerella forsythia + Treponema denticola.
• Orange complex: Includes Fusobacterium nucleatum and Prevotella intermedia.
• Orange-complex organisms can help establish conditions that favor red-complex colonization.
• F. nucleatum is a bridge organism because it interacts with both early and late plaque colonizers.

FCPS tip: Memorize the three red-complex organisms together; this is a classic microbiology MCQ.

💡Pregnancy gingivitis

Pregnancy can exacerbate plaque-induced gingival inflammation because increased estrogen and progesterone modify the host response and gingival vascularity.

Key organism

Prevotella intermedia is the classic organism associated with pregnancy gingivitis.

Mechanism

• Increased estrogen and progesterone.
• Greater gingival vascular permeability and altered inflammatory response.
• P. intermedia can use steroid hormones as growth factors.
• Existing plaque produces an exaggerated gingival inflammatory response.

Clinical features

• Red, swollen gingiva.
• Increased bleeding.
• Exaggerated response to plaque without necessarily having a greater plaque burden.
• Pregnancy-associated pyogenic granuloma (pregnancy epulis) may develop, often on the gingiva.

Exam pearl: Pregnancy gingivitis is primarily an exaggerated response to plaque under hormonal influence; it is not simply an infection caused by pregnancy alone.

💡MASTER COMPARISON TABLES

💡Gingivitis vs periodontitis vs ANUG