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

2. 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.

3. 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.

4. 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.

5. 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

6. 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

7. 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.

8. 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

9. 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.

10. 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?”

11. 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

12. Early
Periodontitis

13. Moderate Periodontitis

14. Advanced Periodontitis

15. Are You a Daily Flosser?

16. Remember the biofilm?

18. 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

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

20. 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

21. 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.

22. 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

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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.

29. 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

30. 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

31. 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