Nield-Gehrig CH 11 Perry CH 7 Periodontal Diseases Nield-Gehrig CH 11 Perry CH 7

Objectives Define periodontal disease activity Compare and contrast chronic periodontitis and aggressive periodontitis Identify the five case types of periodontal disease Describe the clinical signs of periodontitis Describe the signs and symptoms of chronic periodontal disease Describe and define clinical signs of recurrent and refractory periodontitis Describe the impact of NUP and PMN dysfunction on the periodontium.

Periodontal Diseases Periodontal disease is an inclusive term describing any disease of the tissues surrounding the teeth, including gingival diseases and diseases o he supporting structures. Periodontitis is a set of periodontal diseases characterized by inflammation of the supporting tissues of the teeth, specifically the periodontal ligament, cementum, and alveolar bone.

Importance of disease classification Useful for diagnosis, prognosis, and care planning Classification of periodontal diseases are changing as new information evolves regarding causes, pathogenicity, and host factors Useful for legal documentation.

Periodontitis A bacteria infection Affects all parts of the periodontium Gingiva Periodontal ligament Bone and cementum Result of a complex interaction between the plaque biofilm and the body’s efforts of fight the infection #1 cause of tooth loss in adults Predisposing factors Smoking Uncontroled diabetis mellitus Genetic predisposition

Progression of Gingivitis to Periodontitis Systemic modifiers/risk factors – Host response primary in disease progression Conditions modify extent/severity of disease and rate of progression Classic signs of systemic involvement Increased pocketing Increased bone loss Ulcerations Fiery red tissue, sloughing or desquamation

AAP Case Type II Chronic Periodontitis – most common form , previously called adult periodontitis; most common in adults over 35 years of age---but can also occur in children and adolescents.

Chronic Periodontitis – AAP II Disease results from the inflammatory process originating in the gingiva (gingivitis) and extending into the supporting periodontal structures’ may have periods of activity and remission slow to moderate progression may have periods of rapid progression Characterized by: pocket formation and/or gingival recession leading to bone resorption Extent = number of sites involved Type IIA is Localized – 30% of sites or less Type IIB is Generalized – more than 30% of sites

Chronic Periodontitis Initiated and maintained by accumulation of bacterial plaque biofilm Host response plays critical role in pathogenesis of disease Prevalence and severity increase with age Progresses at slow to moderate rate, may have random bursts of rapid destruction Signs and symptoms: swelling, redness, BOP, periodontal pockets, bone loss, mobility, and/or suppuration Progression of disease may be modified by environmental, systemic, or local factors.

Recurrent and refractory chronic periodontitis Signs and symptoms of disease reappear after perio therapy – lack of good home care, or thorough treatment. Ask “does patient smoke?”

Treatment goals in chronic periodontitis Control plaque to level compatible with gingival health Alter or eliminate any contributing risk factors for periodontal disease Arrest disease progression (stop attachment and bone loss from worsening) Prevent the recurrence of periodontal disease

Early Periodontitis

Moderate Periodontitis

Advanced Periodontitis

Are You a Daily Flosser?

Remember the biofilm?

Aggressive Periodontitis Highly destructive, less common form of periodontitis Bacterial infection resulting in inflammation of the supporting structures of the teeth, characterized by rapid destruction of the PDL, rapid loss of supporting alveolar bone, high risk for tooth loss, and poor response to periodontal therapy

Aggressive Periodontitis Severity of destruction is often inconsistent with small amount of plaque present Immune deficiencies and genetic tendencies are possible modifying factors.

Localized Aggressive Periodontitis (AAP IIIA) Onset of disease around puberty, more common in females Characterized by localized bone loss in area of incisors and first molars. Rapid bone loss=3-4 times faster than in chronic periodontitis (AAP IIB) Unique microflora – actinobacillus actinomycetemcomitans* found in high frequency (90%) of lesions and in some patients - Porphyrmonas gingivalis

Localized Aggressive Periodontitis (AAP IIIA) A striking feature of LAP is the lack of clinical inflammation despite the presence of deep periodontal pockets and advanced bone loss. Pocket depths of 8-10 mm with furcation involvement are common Previously named localized juvenile periodontitis Without radiographs, often goes undetected b/c of minimal plaque.

Generalized Aggressive Periodontitis AAP IIIB Most common age of onset, persons younger than 30 Rapid destruction around most teeth Must have interproximal attachment loss on at least three permanent teeth other than first molars and incisors. Frequently associated with abnormal neutrophil function P.gingivalis, A. actinomycetemicomitans, and Tannerella forsythis (formerly Bacteroides forsythus) frequently are detected in the plaque that is present

Characteristics common to both types No obvious signs and symptoms of systemic disease (with generalized this should be verified) Rapid attachment loss and bone destruction Disease severity inconsistent with amount of plaque present Familial tendency

Treatment considerations in Aggressive Periodontitis Control of disease may not be possible, reasonable goal – slow disease progression Consultation with physician may be indicated in severe cases to rule out systemic diseases

Psychosomatic Factors and Stress Stressful life events increase susceptibility to and severity of periodontal disease Plasma corticosteroids become elevated, suppress immune response NUG is example of correlation between stress and periodontal disease

Tobacco use Nicotine and chemicals on rootsurface act as toxins for fibroblast attachment Environmental factor Nicotine is a vasoconstrictor, so inflammatory symptoms may be masked Local and systemic effects – primarily immunosuppression Tobacco users are at greater risk for developing periodontal disease at younger ages and respond poorly to treatment Smokeless tobacco users have higher risk for oral carcinoma, greater risk of periodontal disease, localized attachment loss at site of use

Tobacco use Signs and symptoms of smoking Thick fibrotic tissue with rolled margins More severe disease at young age with more rapid rate of destruction Pocketing greater on anterior and maxillary palatal surfaces Recession in both arches Wide embrasure spaces Level of oral hygiene may not correlate with severity of disease Often lack of marginal gingivitis (not always red or edematous) Significant bleeding/suppuration on probing Minimal reduction in pocket depths after scaling Repocketing within 1 year of surgical treatment

Nutritional disorders and periodontal disease Poor nutrition lowers immune response, increases susceptibility to perio US – malnutrition most common among elderly, low socioeconomic groups, anddicts to drugs and alcohol Good nutrition linked to overall health. The oral cavity reflects systemic health Protein deficiency – reduces host defenses and wound healing – Kwashiorkor or Marasmus – glossitis, angular chelitis, xerostomia, increased gingival inflammation, bone loss, NUG.

Alterations in sex hormones Diabetes Mellitus Neutrophil Abnormalities Endocrine disorders Hyperparathyroidism Alterations in sex hormones Diabetes Mellitus Neutrophil Abnormalities Neutropenias Cyclic neutropenia Neutrophil dysfunction Leukocyte adherence defect Chemotaxis defects

HIV – Related Periodontitis Compromised host allows periodontitis to progress much more quickly Lesions are not HIV specific, just exaggerated due to lack of host response CD4 < 200 – severe and extensive attachment loss, multiple infections HIV is modifier of existing periodontal disease

HIV – Related Periodontitis Oral signs and symptoms Bright red gingiva with spontaneous bleeding and suppuration May be painful NUP – necrotizing ulcerative periodontitis – rapid bone loss In non- HIV + patients, may be result of recurrent NUG Deep, osseous crater-like lesion Osseous lesions may extend to necrotizing ulcerative stomatitis May superficially resemble NUG Linear gingival erythema