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Define periodontitis.

Periodontitis is a chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilms and characterized by the progressive destruction of the tooth- supporting apparatus.

What are the three factors that characterize periodontitis?

The loss of periodontal-tissue support, manifested through clinical attachment loss (CAL) and radiographically assessed alveolar bone loss, the presence of periodontal pocketing, and gingival bleeding.

Which of the following is NOT a sign or symptom of periodontitis?

  • Dry mouth (correct)
  • Bad breath
  • Pink-tinged toothbrush after brushing
  • Spitting out blood when brushing or flossing your teeth
  • Gums that bleed easily
  • Pus between your teeth and gums
  • Gums that feel tender when touched
  • Swollen or puffy gums
  • Bright red, dusky red, or purplish gums

    • What was the classification to define periodontitis for the longest period?

    <p>The American Academy of Periodontology (AAP) 1999 classification</p> Signup and view all the answers

    Which periodontitis classifications are categorized by both localization and generalization?

    <p>Chronic Periodontitis</p> Signup and view all the answers

    The AAP 1999 classification includes periodontitis as a manifestation of systemic diseases, which is divided into three categories: associated with hematological disorders, associated with genetic disorders, and not otherwise specified.

    <p>True</p> Signup and view all the answers

    Describe chronic periodontitis.

    <p>Chronic periodontitis is defined as &quot;an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.&quot;</p> Signup and view all the answers

    How is chronic periodontitis diagnosed radiographically?

    <p>Chronic periodontitis is diagnosed radiographically by localized or generalized loss of alveolar supporting bone, horizontal or vertical.</p> Signup and view all the answers

    What is the difference between localized and generalized periodontitis?

    <p>Localized periodontitis affects less than 30% of the sites, demonstrating attachment loss and bone loss. Generalized periodontitis affects less than 30% or more of the sites, demonstrating attachment loss and bone loss.</p> Signup and view all the answers

    Which of the following is NOT a clinical feature of periodontitis?

    <p>Dental abscess</p> Signup and view all the answers

    Reversible tooth mobility is caused by the spread of inflammation, while irreversible tooth mobility is due to loss of attachment and bone.

    <p>True</p> Signup and view all the answers

    What is meant by bacterial invasion in periodontitis?

    <p>Bacterial invasion refers to the penetration of bacteria into the apical and lateral aspects of the pocket wall. These gram-negative bacteria can include filaments, rods, and coccoids.</p> Signup and view all the answers

    What is the primary mechanism of collagen destruction in periodontitis?

    <p>Collagen fibers are destroyed by collagenases and enzymes secreted by the host cells.</p> Signup and view all the answers

    Phagocytosis of collagen by fibroblasts is a contributing factor in the destruction of periodontal tissues.

    <p>True</p> Signup and view all the answers

    The loss of collagen triggers a cascade of events that leads to the deepening of the periodontal pocket. This includes proliferation of apical cells of junctional epithelium along the root surface, detachment of the coronal portion of the junctional epithelium from the root, and ultimately, a deeper pocket.

    <p>True</p> Signup and view all the answers

    What is the histological appearance of the pocket epithelium in periodontitis?

    <p>Thin and ulcerated</p> Signup and view all the answers

    What is the cause of the bluish-red color of the gingival wall in periodontitis?

    <p>Circulatory stagnation</p> Signup and view all the answers

    What is the primary reason behind bleeding on gentle probing in periodontitis?

    <p>All of the above</p> Signup and view all the answers

    What is the underlying reason for pain when exploring the inner aspect of the wall in periodontitis?

    <p>The pain is caused by ulceration of the inner aspect of the wall.</p> Signup and view all the answers

    What is the direct reason for the presence of pus on digital pressure in periodontitis?

    <p>The presence of pus is due to suppuration and inflammation within the periodontal pocket.</p> Signup and view all the answers

    How is the presence of periodontal pockets diagnosed?

    <p>Only by probing the gingival margin</p> Signup and view all the answers

    Radiographic examination is not a reliable way to determine the presence or depth of periodontal pockets.

    <p>True</p> Signup and view all the answers

    What is the term used to describe the rapid destruction of periodontal tissues and the reason for it?

    <p>The rapid destruction of periodontal tissues is termed &quot;advanced destruction&quot; and is likely caused by the patient's poor antibody response to the pathogens present.</p> Signup and view all the answers

    What is the key differentiating factor for localized aggressive periodontitis?

    <p>A striking lack of clinical inflammation despite the presence of deep periodontal pockets and advanced bone loss.</p> Signup and view all the answers

    Explain the significance of the "arc-shaped loss of alveolar bone" in localized aggressive periodontitis.

    <p>This distinctive pattern of bone loss, extending from the distal surface of the second premolar to the mesial surface of the second molar, is a common radiographic finding in localized aggressive periodontitis.</p> Signup and view all the answers

    The rate of bone loss in localized aggressive periodontitis is significantly faster than in chronic periodontitis.

    <p>True</p> Signup and view all the answers

    What is a common clinical feature observed in localized aggressive periodontitis?

    <p>All of the above</p> Signup and view all the answers

    What is a common radiographic feature observed in localized aggressive periodontitis?

    <p>Vertical loss of alveolar bone around the first molars and incisors, beginning around puberty in otherwise healthy teenagers.</p> Signup and view all the answers

    Explain the possible reasons for the limitation of periodontal destruction to certain teeth in localized aggressive periodontitis.

    <p>Several factors may contribute to the localized nature of periodontitis, including the initial colonization of the first molars and incisors by Actinobacillus actinomycetemcomitans and the subsequent immune response, bacteria antagonistic to A. actinomycetemcomitans, a potential loss of leukotoxin-producing ability by A. actinomycetemcomitans, and a possible defect in cementum formation.</p> Signup and view all the answers

    Describe the radiographic findings typically observed in localized aggressive periodontitis.

    <p>The radiographic findings characteristic of localized aggressive periodontitis include vertical loss of alveolar bone around the first molars and incisors, &quot;arc-shaped&quot; loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar, a &quot;mirror-image&quot; pattern of bone loss, and horizontal bone loss at the interproximal surface of the incisors.</p> Signup and view all the answers

    The prevalence of generalized aggressive periodontitis is mainly limited to individuals under 30 years of age.

    <p>True</p> Signup and view all the answers

    What is the key characteristic of generalized aggressive periodontitis, highlighting its difference from localized aggressive periodontitis?

    <p>A poor antibody response to the pathogens</p> Signup and view all the answers

    Which of the following is a typical characteristic of generalized aggressive periodontitis?

    <p>Periods of rapid destruction followed by stages of quiescence</p> Signup and view all the answers

    Which of the following is NOT a common bacterial species found in the plaque of GAP patients?

    <p>Streptococcus mutans</p> Signup and view all the answers

    Generalized juvenile periodontitis is often considered a possible precursor to generalized aggressive periodontitis.

    <p>True</p> Signup and view all the answers

    Generalized aggressive periodontitis is often mistaken for severe periodontitis due to extensive destruction in relation to a patient's age.

    <p>True</p> Signup and view all the answers

    Generalized aggressive periodontitis is characterized by a slow rate of progression in bone and attachment loss.

    <p>False</p> Signup and view all the answers

    Why does GAP represent the most heterogeneous group of periodontitis?

    <p>GAP represents the most heterogeneous group of periodontitis because it encompasses a wide range of disease severity, from those with minimal bone loss to those experiencing significant destruction.</p> Signup and view all the answers

    What is the range of bone loss observed in GAP patients?

    <p>Both minimal and significant bone loss involving a range of teeth</p> Signup and view all the answers

    The quiescence stage of GAP demonstrates a pink and healthy gingiva, a stationary bone level, and the presence of deep pockets detected by probing.

    <p>True</p> Signup and view all the answers

    What is the key characteristic of the destructive stage in GAP?

    <p>The gingiva is acutely inflamed, proliferating, ulcerated, and fiery red</p> Signup and view all the answers

    What is a primary intervention for GAP patients to rule out potential systemic involvement?

    <p>Medical evaluations</p> Signup and view all the answers

    While GAP patients can experience spontaneous remission, they are also susceptible to continued disease progression despite conventional treatment.

    <p>True</p> Signup and view all the answers

    What is the primary microbiologic risk factor for localized aggressive periodontitis (LAP)?

    <p>Actinobacillus actinomycetemcomitans</p> Signup and view all the answers

    Actinobacillus actinomycetemcomitans is found in high frequency in LAP lesions.

    <p>True</p> Signup and view all the answers

    Elevated levels of Actinobacillus actinomycetemcomitans are often found at active disease sites.

    <p>True</p> Signup and view all the answers

    A successful reduction in the subgingival load of Actinobacillus actinomycetemcomitans during treatment leads to a successful clinical response in LAP.

    <p>True</p> Signup and view all the answers

    Actinobacillus actinomycetemcomitans produces virulence factors that contribute to the disease process.

    <p>True</p> Signup and view all the answers

    Electron microscopy has revealed bacterial invasion of connective tissue up to the bone surface.

    <p>True</p> Signup and view all the answers

    Which HLA antigens are consistently associated with aggressive periodontitis?

    <p>HLA A9 and HLA B15</p> Signup and view all the answers

    What are the common functional defects observed in the immune system of patients with aggressive periodontitis?

    <p>Both defects in chemotaxis and phagocytosis</p> Signup and view all the answers

    Hyperresponsiveness of monocytes to lipopolysaccharide (LPS) can lead to increased connective tissue or bone loss.

    <p>True</p> Signup and view all the answers

    A deficiency in the monocyte receptor for human immunoglobulin G2 (IgG2) antibodies has been observed in patients with aggressive periodontitis.

    <p>True</p> Signup and view all the answers

    Autoimmunity, characterized by host antibodies to collagen, deoxyribonucleic acid (DNA), and IgG, is a significant factor in the pathogenesis of aggressive periodontitis.

    <p>True</p> Signup and view all the answers

    Which of the following factors is often found to be altered in patients with aggressive periodontitis?

    <p>All of the above</p> Signup and view all the answers

    Study Notes

    Periodontitis

    • Periodontitis is a chronic multifactorial inflammatory disease
    • It's associated with dysbiotic plaque biofilms
    • Characterized by progressive destruction of the tooth-supporting apparatus
    • Is characterized by three factors:
      • Loss of periodontal-tissue support (manifested through clinical attachment loss (CAL) and radiographically assessed alveolar bone loss)
      • Presence of periodontal pocketing
      • Gingival bleeding

    Signs and Symptoms

    • Swollen or puffy gums
    • Bright red, dusky red, or purplish gums
    • Tender gums when touched
    • Gums that bleed easily
    • Pink-tinged toothbrush after brushing
    • Spitting out blood when brushing or flossing
    • Bad breath
    • Pus between teeth and gums

    Armitage 1999 Classification

    • Chronic Periodontitis (localized or generalized)
    • Aggressive Periodontitis (localized or generalized)
    • Periodontitis as a manifestation of systemic diseases
    • Necrotizing Periodontal Diseases
    • Periodontitis associated with endodontic lesions

    1999 (AAP) Classification

    • Categorizes chronic, aggressive, necrotizing, and endodontic-associated periodontitis forms.

    Chronic Periodontitis

    • Defined as an infectious disease
    • Causes inflammation within the supporting tissues of teeth
    • Characterized by progressive attachment loss and bone loss
    • The disease is site-specific
    • Slight (mild): ≤2 mm of clinical attachment loss
    • Moderate: 3-4 mm of clinical attachment loss
    • Severe: ≥5 mm of clinical attachment loss

    Clinical Diagnosis Detection

    • Characterized by chronic inflammatory changes in the marginal gingiva
    • Presence of periodontal pockets
    • Radiographic loss of alveolar-supporting bone (horizontal or vertical)
    • Localized periodontitis: ≤30% of sites demonstrate attachment and bone loss
    • Generalized periodontitis: ≥30% of sites demonstrate attachment and bone loss

    Clinical Diagnosis of Periodontitis

    • Clinical attachment loss
    • Gingival inflammation
    • Pain (localized or deep pain in the jaw)
    • Tooth mobility, diastema and tooth migration
    • Tooth mobility (can be reversible or irreversible)

    Bacterial Invasion

    • Bacterial invasion of the apical and lateral aspects of pocket wall (gram-negative: filaments, rods, and cocci).
    • There are periods of activation and remission in the inflammatory process as a result of host-bacteria interaction
    • The bacterial-leukocytes interaction leads to: intense epithelial desquamation, ulceration, hemorrhage, cementum fragmentation and necrosis, and prevents attachment of gingival fibroblasts.

    Mechanism of Collagen Destruction

    • Collagen fibers are destroyed by collagenases and enzymes secreted by host cells (fibroblasts, PMNs, macrophages)
    • Phagocytosis of collagen by fibroblasts
    • Collagen loss → apical proliferation of junctional epithelium along the root surface → detachment of the coronal portion of the junctional epithelium from the root → deeper pocket formation

    Histologically

    • Pocket epithelium thin and ulcerated
    • Inflammatory cell infiltration(PMNs, plasma cells)

    Diagnostic Aids

    • Probing the gingival margin along each tooth surface
    • Pocket presence or depth not detected by radiographic examination (bone loss detected by radiographic examination)

    Aggressive Periodontitis

    • Defined by primary and secondary features
    • Primary features: clinically healthy except for periodontitis, rapid attachment loss/bone destruction, familial aggregation
    • Secondary features: microbial deposits are inconsistent with the severity of tissue destruction, elevated proportions of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis, phagocyte abnormalities; hyperresponsive macrophages, including elevated PGE2 and IL-1B; progression of attachment/bone loss may be self-arresting

    Localized Aggressive Periodontitis

    • Lack of clinical inflammation despite advanced bone loss
    • Plaque forms thin biofilm on teeth, rarely calcifies
    • Rate of bone loss is ~3-4 times faster than in chronic periodontitis.

    Clinical Features of Localized Aggressive Periodontitis

    • Distolabial migration of maxillary incisors with concomitant diastema formation
    • Increasing mobility of first molars
    • Sensitivity of denuded root surfaces to thermal and tactile stimuli
    • Deep, dull, radiating pain during mastication
    • Possibly due to irritation of supporting structures.

    Radiographic Features of Localized Aggressive Periodontitis

    • Vertical loss of alveolar bone around first molars/incisors
    • "Arc-shaped" loss of alveolar bone, distal surface of second premolar to mesial surface of second molar (mirror image pattern)
    • Horizontal bone loss, thinner bone pattern at interproximal surface of incisors

    Etiology (Localized Aggressive Periodontitis)

    • Initial colonization of first molars/incisors by A. actinomycetemcomitans, destruction of periodontal tissues → stimulates adequate immune response

    • Bacteria antagonistic to A. actinomycetemcomitans may colonize periodontal tissues and inhibit further colonization of sites in the mouth

    • A. actinomycetemcomitans may lose its leukotoxin-producing ability → arresting disease progression

    • Defect in cementum formation may be responsible for lesion localization.

    Generalized Aggressive Periodontitis

    • Usually affects patients <30, may be older.
    • Poor antibody response to pathogens
    • Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors
    • Periods of advanced destruction followed by variable length quiescence (weeks to months or years)

    Systemic Involvement

    • Patients with GAP should have medical evaluations to rule out possible systemic involvement.
    • Disease may spontaneously arrest or continue to progress to tooth loss despite conventional treatment.

    Risk Factors

    • Microbiological factors
    • Immunologic factors
    • Genetic factors
    • Environmental factors (smoking)

    Microbiological Factors

    • Several microorganisms frequently detected
    • Actinobacillus actinomycetemcomitans implicated as primary pathogen associated with localized aggressive periodontitis

    Immunological Factors

    • HLA A9 and HLA B15 antigens are consistently associated.
    • Patients with aggressive periodontitis display functional defects in chemotaxis and phagocytosis of polymorphonuclear leukocytes (PMNs), and monocytes.
    • Hyperresponsiveness to LPS, leading to increased PGE2 production, contributing to tissue/bone loss

    Genetic Factors

    • Studies indicate a major gene role in aggressive periodontitis (transmitted through autosomal dominant mode of inheritance).

    Environmental Factors (e.g., Smoking)

    • Patients with generalized aggressive periodontitis who smoke exhibit more affected teeth and greater attachment loss compared to non-smoking patients

    Clinical Examination for Periodontal Health

    • Gingival inflammation and bleeding (color, contour, consistency, form, size, surface texture)
    • Pocketing or attachment loss
    • Furcation involvement
    • Gingival recession
    • Tooth mobility
    • Tooth migration
    • Alveolar bone loss
    • Discomfort and halitosis

    Probing Depth (PD) and Clinical Attachment Loss (CAL)

    • Probing depth depends on probe size, force, direction, tip, and tissue resistance
    • CAL is the measure of attachment loss from the cementoenamel junction to the base of the periodontal pocket

    Miller's Classification of Gingival Recession

    • Used to classify gingival recession based on the extent and severity of recession.
    • Classes I-IV, based on how far the recession extends beyond the mucogingival junction and the severity of interproximal tissue/tooth rotation loss.
    • Class I is mild, Class II is moderate, Class III is severe, and Class IV is the most severe type of gingival recession.

    Francesco Cairo et al (2011) Classification of Gingival Recession

    • Classification based on clinical attachment loss at buccal and interproximal sites (Type I, Type II, Type II)
      • Type 1: Gingival recession with no loss of interproximal attachment
      • Type 2: Gingival recession with less or equal interproximal attachment loss (compared to buccal attachment loss)
      • Type 3: Gingival recession with greater interproximal loss (compared to buccal attachment loss)

    Furcation Involvement

    • Goldman and Cohen classification (1-4)
    • Grade 1: incipient, suprabony pocket, soft tissue involvement
    • Grade 2: Cul-de-sac, bone destruction on one aspect, partial probe penetration
    • Grade 3: Through and through, interradicular bone absent
    • Grade 4: Complete bone destruction, tunnels present in the interradicular bone

    Mobility

    • Grade 1: slight mobility (<0.5 mm buccolingual excursion)
    • Grade 2: moderate mobility (0.5-1 mm buccolingual excursion)
    • Grade 3: advanced mobility (1.1-1.5 mm buccolingual excursion, possible socket depression)

    Radiographic Factors

    • Assess alveolar bone height, pattern of bone destruction, width of periodontal ligament.
    • Radiographs are supplementary to clinical probing and probing depth measurement.

    Pocket Classification

    • Classified as gingival/pseudo or periodontal/true
    • Supra bony: the pocket base is coronal to the alveolar crest
    • Infra bony: the pocket base is apical to the alveolar crest

    Classification of Pockets.

    • Simple pocket: involves one tooth surface
    • Compound pocket: More than one tooth surface, same base and orifice
    • Complex pocket: More than one tooth surface, different base and orifice

    Calculating the Patient's Individual Periodontal Risk Assessment (PRA)

    • Based on six parameters:
    • Low risk patient (all parameters in low-risk categories, or one in moderate-risk)
    • Moderate risk patient (at least two in the moderate category, at most one in high-risk category)
    • High risk patient (at least two in the high-risk category)

    Different Forms of Periodontitis

    • Based on pathophysiology
    • Necrotizing periodontitis
    • Periodontitis as a direct manifestation of systemic diseases
    • Periodontitis

    Difference Between Acute Periodontal Lesions and Other Periodontitis Lesions

    • Rapid-onset and rapid destruction
    • Pain or discomfort, prompting patients to seek urgent care

    Abscess of the Periodontium

    • A localized purulent inflammation of periodontal tissues
    • Classified into gingiva, pericoronal, periodontal abscesses
    • Causes: Microbial plaque, infection, trauma, foreign body impact
    • Diagnosis:History, clinical, radiographic findings (Widening of periodontal space to significant bone loss -early stages may not show on radiograph)
    • Treatment: Acute abscess: alleviate symptoms , control spread, & drainage
    • I: determine antibiotics, drainage through pocket, Gentle digital pressure, irrigation
    • II: scaling, root planing, antibiotics (penicillin allergy: clindamycin or alternative)
    • III: local anesthesia, incision, drainage, irrigate
    • IV: anesthesia, drainage, if swelling, or systemic signs = Systemic antibiotics

    Clinical Picture of Abscesses

    • Acute: Painful, red, edematous, smooth, ovoid swelling of gingival tissues
    • Chronic: Spreading infection, controlled by drainage/host response; few or no symptoms; periodontal pocket, inflammation, fistulous tract present.

    Diagnosis

    • Correlation of clinical, history & radiographic findings.
    • Radiographic examination may reveal bone loss or widening of the periodontal space or significant bone loss.

    Treatment Approaches for Abscesses

    • Acute: resolving the acute lesion
    • Chronic: scaling, root planing, or surgical therapy if deep defects are present

    Necrotizing Ulcerative Gingivitis (NUG)

    • Microbial disease, characterized by death and sloughing of gingival tissue
    • Untreated: may progress to necrotizing ulcerative periodontitis (NUP) & progressive, significant destruction of the periodontium/roots
    • Does not lead to pockets, involves marginal gingiva causing recession
    • Rare in edentulous (toothless) mouths

    Clinical Features of NUG

    • Non-specific acute inflammatory process
    • Pain
    • Ulceration and necrosis of interdental papillae (punched-out/covered by a slough or pseudomembrane)
    • Bleeding (either spontaneously or with manipulation)
    • Foul odor, bad metallic taste, increased salivation
    • Starts at the tip of interdental papilla, extends to marginal gingiva causing punched-out papilla
    • Later, affects attached gingiva & bone exposure
    • Adolescents or young adults

    Extraoral and Systemic Signs and Symptoms of NUG

    • Patients may have minimal systemic complications (mild to moderate stages)
    • Localized lymphadenopathy & slight elevation in temperature
    • Severe cases: high fever, increased pulse rate, leukocytosis, loss of appetite, general lassitude
    • Systemic reactions are worse in children

    Stages of NUG

    • Necrosis begins at the tip of the interdental papilla (grade 1) and may extend to other areas(grades 2-6) (93%, 19%, 21%, 1%, 6%, 1%)

    Predisposing Factors of NUG

    • Local: Deep periodontal pockets, pericoronal flaps, areas of the gingiva traumatized by malocclusion (e.g., behind maxillary incisors)
    • Systemic: Altered host response (e.g., ulcerative colitis, blood dyscrasias, nutritional deficiency, abnormalities in white blood cell function (e.g., AIDS), malnutrition, stress).

    Microbiology of NUG

    • Smear: spirochetes, fusiform bacilli, vibrios, filamentous organisms
    • Microscopically: pseudomembrane containing dead epithelial cells, inflammatory cells, fibrin meshwork & various microorganisms

    NUG Diagnosis

    • Clinical findings (necrosis, ulceration, bleeding, odor)

    NUG Fate if Untreated

    • Progresses to fulminating oro-facial infection (noma or cancrum oris)
    • Can involve other soft tissues and bone

    NUG Treatment

    • First Visit: comprehensive medical evaluation
    • Treatment Focuses on controlling the acute phase & managing residual condition (isolate, anesthetic, swab pseudo membrane, deep scaling - avoid subgingival scaling/curettage)
    • Second Visit (1-2 days later): pain diminishing, gingival margins becoming less erythematous, scaling if needed
    • Third Visit: 5 days later, symptom free or slightly painful, oral hygiene instructions, & follow up appointment to monitor response & compliance .

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