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DISEASES OF PERIODONTIUMPrepared by:Dr Sundeep s Bhagwath : 

DISEASES OF PERIODONTIUMPrepared by:Dr Sundeep s Bhagwath


OVERVIEW INTRODUCTION ETIOLOGY CLASSIFICATION GINGIVITIS – Various types, their etiology, clinical, radiological and histological features. PERIODONTITIS - Various types, their etiology, clinical, radiological and histological features. JUVENILE PERIODONTITIS PAPILLON – LEFEVERE SYNDROME

What is periodontium? : 

What is periodontium? Defined as a group of such tissues that support and surround the teeth. Comprised of 4 connective tissues, out of which 2 are mineralized (Cementum & Alveolar bone) and 2 are soft tissues (PDL and Lamina propria of gingiva)


AETIOLOGY Pulpitis (infection spreading from pulp) Trauma Endodontic treatment. Drug induced


CLASSIFICATION 1. GINGIVITIS: - - Plaque related - Acute necrotizing ulcerative gingivitis (ANUG) - Drug related - Specific infection related - Dermatosis related

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2. PERIODONTITIS: - - Chronic (Localized & Generalized) - Aggressive (Localized & Generalized) - Periodontitis as manifestation of systemic diseases (hematologic, genetic etc) - Necrotizing ulcerative periodontitis - Abscesses of periodontium (Gingival, Periodontal, pericoronal) - Periodontitis associated with endodontic lesions.


GINGIVITIS Refers to inflammation of soft tissues surrounding the teeth. Does not include inflammation of alveolar ridges, PDL or cementum. Various types of gingivitis have already been listed.

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FACTORS RELATED TO GINGIVITIS: - Hormonal (progesterone) Smoking Stress Poor nutrition Medication Diabetes mellitus Tooth malpositioning Masticatory injury Mouth breathing

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CLINICAL FEATURES: - Age incidence: increases with age, but puberty related gingivitis occurs between 9 – 14 years. Sex incidence: occurs less in females. This may be due to better oral hygiene than physiologic difference. Female susceptibility increases with increased levels of progesterone associated with pregnancy or oral contraceptives.

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Signs & symptoms: Inflammation of gingiva can be localized (marginal or papillary gingivitis) or diffuse. Earliest signs are – loss of stippling and bleeding on minimal probing. In early inflammation, gingiva is light red and as inflammation progresses, it becomes darker red and edematous.

Gingivitis can take various forms : 

Gingivitis can take various forms Mouth breathing related Puberty associated Chronic hyperplastic gingivitis Hyperplastic gingivitis with Pyogenic granuloma

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HISTOLOGICAL FEATURES: - Early gingivitis shows presence of PMNL’s in the connective tissue adjacent to sulcular epithelium. With progression of inflammation, infiltrate becomes mixed, composed of lymphocytes, plasma cells and PMNL’s. Fibrosis, edema and hemorrhage may also be seen.

Gingivitis progressing to periodontitis : 

Gingivitis progressing to periodontitis Epithelial attachment on CEJ and inflammatory cells in gingiva. Epithelial attachment extends to cementum & inflammation spreads deeper.

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TREATMENT & PROGNOSIS: - Elimination of causes. Improvement of oral hygiene by self administered plaque control programs as well as professional aid (scaling & polishing). Mouthwashes containing chemicals like chlorhexidine, triclosan etc can be used to aid mechanical plaque removal. Surgery may be required if gingiva becomes hyperplastic and fibrotic.


ACUTE NECROTIZING ULCERATIVE GINGIVITIS Also called “Vincent’s infection” & “Trench Mouth”. Infection caused by bacteria like – Borrelia vincentii, Fusobacterium nucleatum, Prevotella intermedia and species of Treponema and Selenomona.

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CAUSATIVE FACTORS: - Psychological stress Immunosupression Smoking Local trauma Poor nutritional status Poor oral hygiene Inadequate sleep Recent illness

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CLINICAL FEATURES: - Age incidence: Young & middle aged Sex predilection: no predilection Site of occurrence: Typically involves the interdental papillae.

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Signs & symptoms: Typically, interdental papillae are inflamed, edematous & hemorrhagic. Involved papillae show punched out, crater like necrotic areas covered by grayish pseudomembrane.

There is a fetid odor, extreme pain and spontaneous hemorrhage. Associated features like lymphadenopathy, fever and malaise may also be present. Involvement of PDL leads to necrotizing ulcerative periodontitis. If infection spreads through mucosa to skin of face, then the infection is called “Cancrum oris” or Noma.

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HISTOLOGICAL FEATURES: - Non specific features. Interdental papillae show surface ulceration covered by a fibrinopurulent membrane. Underlying connective tissue shows acute or mixed inflammatory infiltrate along with extensive hyperemia.

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TREATMENT & PROGNOSIS: - Compared to other PDL diseases, ANUG resolves quickly after removal of bacterial infection. Tissue debridement is done by scaling or curettage. Chlorhexidine, warm saline or diluted H2O2 rinses are beneficial in enhancing therapeutic response. Antibiotics may be given in cases of fever or lymphadenopathy. Patient education, motivation and removal or causative factors are also done.


DESQUAMATIVE GINGIVITIS This term used to describe gingival epithelium that spontaneously sloughs off or can be removed after minimal manipulation. Most probably represents one of the several vesiculobullous lesions. Histological and immunological examinations often reveal features of either lichen planus or pemphigoid and sometimes of SLE, pemphigus vulgaris, epidermolysis bullosa.

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CLINICAL FEATURES: - Age incidence: Older than 40 years Sex incidence: Female predilection Site of occurrence: Mostly affects facial surface of gingiva. May be multifocal or generalized.

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Signs & symptoms: Affected areas show smooth erythema with loss of stippling. With progression, there is blister formation, spontaneous desquamation or zones of erosion. Blisters are filled either with clear fluid or blood.

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Manipulation of affected gingiva with cotton swab or compressed air can cause desquamation. Areas of erosion are often covered with a yellowish fibrinopurulent membrane. Significant pain is present.

To : 

To HISTOLOGICAL FEATURES: - Histological and immunological features of desquamative gingivitis are quite variable. Most patients report features of lichen planus or pemphigoid.

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TREATMENT & PROGNOSIS: - Incisive biopsy specimen should be submitted for histological examination, followed by immunological studies. Thorough evaluation of dermatologic and mucosal surfaces should be carried out to check other sites of involvement. Many patients respond well to topical corticosteroids.


GINGIVAL HYPERPLASIA(DRUG INDUCED) Refers to abnormal growth of gingival tissues related to use of systemic medications. Misleading term since, neither the epithelium nor the CT is hyperplastic. Increased gingival size is due to overproduction of extracellular matrix, mainly collagen. The severity of hyperplasia is linked to patient’s susceptibility and level of oral hygiene.


CAUSATIVE DRUGS 1. Anticonvilsants - Phenytoin - Carbamazepine - Ethosuximide - Sodium valporate 2. Cyclosporine 3. Erythromycin 4. Oral contraceptives 5. Calcium channel blockers - Nifedipine - Verapamil - Amlodipine

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CLINICAL FEATURES: - Age incidence: Depends on the drug used. Therefore, phenytoin induced hyperplasia occurs in younger patients, while nifedipine induced hyperplasia occurs in middle and older aged persons. Cyclosporine has a variable age predilection. Sex & race predilection: Nil

Enlargement begins 1-3 months after drug usage. Originates initially in interdental papilla and then spreads across tooth surface. In severe cases, hyperplasia can cover almost entire tooth surface.

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When inflammation is absent, hyperplastic gingiva appears normal in color and consistency. In presence of inflammation, enlarged gingiva appears dark red, edematous and bleeds readily.

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HISTOLOGICAL FEATURES: - Histological examination of hyperplastic tissue shows excessive tissue of normal composition. Overlying epithelium shows elongation of rete ridges.

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In secondary inflammation, there is increased vascularity and infiltration with lymphocytes and plasma cells.

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TREATMENT & PROGNOSIS: - Causative drug must be discontinued, which often results in cessation of hyperplasia and occasionally some regression. If drug use is mandatory then professional cleaning and home plaque control is essential. Surgical removal of hyperplastic tissue may be done in cases where regression does not occur.


GINGIVAL FIBROMATOSIS Also called “Elephantiasis gingivae” and “Fibromatosis gingivae”. Slowly progressing gingival enlargement caused by overproduction of collagen.

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CLINICAL FEATURES: - Age incidence: Before 20 years of age. Sex incidence: Nil Signs & symptoms: May occur alone or with other syndromes like Zimmermann-Laband, Murray-Puretic-Drescher, Rutherford, Multpile hamartoma and Cross syndromes.

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Other findings include hypertrichosis, epilepsy, mental retardation, sensorineural deafness, hypothyroidism, growth hormone deficiency etc.

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Gingival changes may be local or generalized. Either of the jaws can be affected, but maxilla is affected more, especially the palatal aspects. The affected gingiva is firm, normal in color and covered by a either a smooth or a stippled surface.

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HISTOLOGICAL FEATURES: - Enlarged tissue consists of hypocellular, hypovascular collagenous tissue with long, interlacing collagen bundles. Surface epithelium shows elongated rete ridges, extending deeply into the underlying CT. Inflammation is usually absent or mild.


PERIODONTITIS Refers to inflammation of gingival tissues in association with some loss of attachment of PDL and alveolar bone. Due to progressive loss of attachment, destruction of PDL and adjacent alveolar bone occurs. The sulcular epithelium shifts apically along the root surface, resulting in formation of periodontal pockets.

CAUSATIVE FACTORS: - Dental Plaque / calculus Advancing age Smoking Diabetes mellitus Lower socioeconomic status Poor oral hygiene Other systemic diseases like bleeding disorders, sarcoidosis, Hypophosphatasia etc. AIDS

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PATHOGENESIS: - For more than a century, periodontitis has been associated with dental plaque. But periodontitis has been shown to be absent in patients with extensive plaque also. Recent evidence indicates periodontitis results not from mere presence of plaque but from changes in proportions of bacterial species in plaque. Chronic periodontitis is associated with Actinobacillus actinomycetecomitans, Bacteroides forsythus and Prevotella intermedia.

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The pathogenic bacteria exist inside the plaque where they are protected from host defenses. Here they also show increased resistance to local / systemic antibiotics. These bacteria then release lipopolysaccharides which bring about the release of catabolic inflammatory mediators as host response.

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However, only presence of pathogenic bacteria is not sufficient to cause periodontitis. Other host factors like smoking, diabetes and heredity predilection are also significant in leading to periodontitis.


CLASSIFICATION 1. CHRONIC PERIODONTITIS - Localized - Generalized 2. AGGRESSIVE PERIODONTITIS - Localized - Generalized 3. PERIODONTITIS WITH SYSTEMIC DISEASES - Associated with hematologic disorders - Associated with genetic diseases - Diabetes mellitus

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4. NECROTIZING PERIODONTAL DISEASES - Necrotizing ulcerative gingivitis - Necrotizing ulcerative periodontitis 5. ABSCESSES OF PERIODONTIUM - Gingival abscess - Periodontal abscess - Pericoronal abscess 6. PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS

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CLINICAL FEATURES: - I. CHRONIC PERIODONTITIS: Age incidence – Adults, especially after 35 years Sex incidence – Slight male predilection

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Signs & symptoms – Generalized gingivitis present. Typically, gingival margins are blunted along with gingival recession.

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PDL disease is said to be present when loss of PDL attachment can be demonstrated by perio probe in the absence of significant gingival hyperplasia. Pocket depth > 3-4 mm indicates PDL destruction and resorption of alveolar bone.

High quality dental x rays reveal bone loss of the alveolar bone surrounding the affected teeth. With advanced bone loss, tooth mobility is present

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Normal alveolar bone Alveolar bone after periodontitis

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II. NECROTIZING ULCERATIVE PERIODONTITIS: - Similar features as ANUG, but also shows loss of PDL attachment and alveolar bone loss. Can arise within pre existing periodontitis or as a sequela of ANUG. Affects younger persons, especially those with immunosupression or malnutrition.

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III. PERIODONTAL ABSCESS: - Usually arises in preexisting PDL lesion. Occurs probably due to change in sub gingival micro flora, host resistance or both.

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CAUSATIVE FACTORS: Closure of entrance to periodontal pocket Furcation involvement Diabetes mellitus Superinfection by opportunistic organisms due to use of systemic antibiotics. Trauma Developmental anomalies of teeth like enamel pearl, dens invaginatus etc

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CLINICAL FEATURES: Mostly occurs in adults. Involved gingiva appears erythematous and edematous with a red surface or it may be hemorrhagic. Probing on gentle pressure results in expression of pus from the sulcus.

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Other symptoms include - Throbbing pain - Extreme sensitivity to palpation - Sensitivity, mobility of adjacent tooth (due to bone loss) - Foul taste - Lymphadenopathy - Fever & leukocytosis

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III. PERICORONITIS: Infection similar to periodontal abscess can occur around impacted or partially erupted teeth when food debris and bacteria collect between gingiva and tooth. Most commonly seen on third molars. Pain, foul taste and inability to close the mouth are common symptoms.

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HISTOLOGICAL FEATURES: - Gingivitis is seen and the sulcular epithelium is hyperplastic. Underlying connective tissue is hyperemic and shows an inflammatory infiltrate consisting of lymphocytes and plasma cells.

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TREATMENT & PROGNOSIS: - I. PERIODONTITIS: First, risk factors like smoking, diabetes etc must be eliminated. Next, loss of attachment of PDL should be stopped by scaling, root planing and curettage. In deep periodontal pockets, surgical flap may have to be raised to access the root surfaces.

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II. NECROTIZING ULCERATIVE PERIODONTITIS: Elimination of causative factors like immunosupression, malnutrition etc must be eliminated. Patients usually respond well to oral antibiotics like metronidazole.

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III. PERIODONTAL ABSCESS: Cardinal principles of incision and drainage are followed. Analgesics and antibiotics are prescribed to reduce the pain and fever, if present. Treatment for underlying periodontitis is undertaken after the abscess is treated satisfactorily.

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IV. PERICORONITIS: Acute pericoronitis is treated with antiseptic lavage under under the gingival flap to remove food debris and bacteria. Once the acute phase passes, either the impacted tooth is extracted or the gingival flap is surgically removed.


JUVENILE PERIODONTITIS Also called as “Early onset periodontitis” or “Aggressive periodontitis”. By definition it occurs in younger persons with no association with any systemic disease.

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Diagnosis is by exclusion and all systemic diseases known to cause premature loss of PDL attachment must be ruled out first. This disease is associated more with deficiency of immune response rather than plaque / calculus. Suspected pathogens are – Actinobacillus actinomycetecomitans, Prevotella intermedia, Porhyromanas gingivalis etc.

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CLINICAL FEATURES: - I. LOCALIZED AGGRESSIVE PERIODONTITIS Age incidence: Begins around 11 - 13 years. Sex predilection: Nil

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Signs & symptoms: This type of disease is localized around the incisors and first molars Typically the oral hygiene is good and there may be mild or no gingival inflammation. The rate of bone loss is 5-10 times more than chronic periodontitis.

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RADIOGRAPHIC FEATURES: - Radiographs usually reveal bilaterally symmetrical vertical bone loss. Similar involvement is seen around anterior teeth also. Tooth mobility and migration is common. In 1/3rd of cases, disease progresses to a more generalized pattern.

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II. GENERALIZED AGGRESSIVE PERIODONTITIS: Age incidence: Occurs before 30 years Sex predilection: Nil Signs & symptoms: Compared to localized variant, more teeth are involved. Bone loss is not limited to specific areas of jaws.

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HISTOLOGICAL FEATURES: - Histological features of tissue removed from sites of aggressive periodontitis is similar to that of chronic periodontitis. In spite of this, histological examination of material from affected is essential to rule out other systemic diseases.

ose : 

ose TREATMENT & RROGNOSIS: - Unlike chronic periodontitis, scaling and root planing alone do not stop the disease. Combination of antibiotics along with mechanical removal of subgingival plaque and inflamed periodontal tissues is needed to counteract the effects of leukocyte defect and pathogenicity of involved organisms. Generally, patients with localized disease show stable course, while those with generalized disease continue to lose PDL attachment and teeth.


PAPILLON-LEFEVRE SYNDROME Autosomal recessive disorder. Shows oral and dermatological manifestations. Similar dermatological findings are also seen in absence of oral findings – Meleda’s disease.


PATHOGENESIS Oral manifestation are due to accelerated periodontitis that appears to be due to - Impaired T and B lymphocyte reactivity - Chemotactic defect - Reduced intracellular killing of bacterial and fungal organisms

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CLINICAL FEATURES: - Age incidence: Dermatological manifestations develops by 3 years of age, while oral findings begin to appear soon tooth eruption. Prevalence: 1-4 per million people

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Skin manifestations appear as diffuse palmar-plantar keratosis. Oral findings consist of rapidly advancing periodontitis , seen in both deciduous and permanent dentitions.

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Widespread hyperplastic and hemorrhagic gingivitis is seen

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Radiologically, teeth appear to “float” in soft tissue, due to loss of PDL attachment and bone support. Tooth mobility, migration and eventual loss of teeth occurs without therapy.

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HISTOLOGICAL FEATURES: Features resemble those of adult periodontitis. Tissue shows hyperplastic sulcular epithelium and infiltration with WBC’s. Underlying CT shows hyperemia and a mixed inflammatory infiltrate composed of PMNL’s, lymphocytes, plasma cells and histiocytes.

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TREATMENT & PROGNOSIS: - In spite of aggressive therapy, in many patients, the disease progresses until all the teeth are lost. Two treatment approaches have been used until now. 1. Removal of all periodontally involved teeth and administration of tetracycline to remove the causative organisms.

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2. Directly attack the pathogenic organism especially, A.actinomycetecomitans. Culture sensitivity testing has shown the combination of amoxicillin-clavulanic acid to be most effective against this organism. By use of mechanical plaque control and specific antibiotic, course of disease MAY be altered.


BIBLIOGRAPHY Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 6th ed. W.B. Saunders Company. Phil, London, Toronto, 2005. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd ed. WB Saunders Company. Phil, London, Toronto, 2007. Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology: Clinical Pathologic Correlations. 4th ed. Saunders Company, 2003. ACKNOWLEDGEMENT: All pictures in this presentation are courtesy of above mentioned authors.

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