Presentation on theme: "Nield-Gehrig CH 11 Perry CH 7"— Presentation transcript:
1 Nield-Gehrig CH 11 Perry CH 7 Periodontal DiseasesNield-Gehrig CH Perry CH 7
2 Objectives Define periodontal disease activity Compare and contrast chronic periodontitis and aggressive periodontitisIdentify the five case types of periodontal diseaseDescribe the clinical signs of periodontitisDescribe the signs and symptoms of chronic periodontal diseaseDescribe and define clinical signs of recurrent and refractory periodontitisDescribe the impact of NUP and PMN dysfunction on the periodontium.
3 Periodontal DiseasesPeriodontal 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 planningClassification of periodontal diseases are changing as new information evolves regarding causes, pathogenicity, and host factorsUseful for legal documentation.
5 Periodontitis A bacteria infection Affects all parts of the periodontiumGingivaPeriodontal ligamentBone and cementumResult of a complex interaction between the plaque biofilm and the body’s efforts of fight the infection#1 cause of tooth loss in adultsPredisposing factorsSmokingUncontroled diabetis mellitusGenetic predisposition
6 Progression of Gingivitis to Periodontitis Systemic modifiers/risk factors – Host response primary in disease progressionConditions modify extent/severity of disease and rate of progressionClassic signs of systemic involvementIncreased pocketingIncreased bone lossUlcerationsFiery 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 progressionCharacterized by: pocket formation and/or gingival recession leading to bone resorptionExtent = number of sites involvedType IIA is Localized – 30% of sites or lessType IIB is Generalized – more than 30% of sites
9 Chronic Periodontitis Initiated and maintained by accumulation of bacterial plaque biofilmHost response plays critical role in pathogenesis of diseasePrevalence and severity increase with ageProgresses at slow to moderate rate, may have random bursts of rapid destructionSigns and symptoms: swelling, redness, BOP, periodontal pockets, bone loss, mobility, and/or suppurationProgression 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 healthAlter or eliminate any contributing risk factors for periodontal diseaseArrest disease progression (stop attachment and bone loss from worsening)Prevent the recurrence of periodontal disease
18 Aggressive Periodontitis Highly destructive, less common form of periodontitisBacterial 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 presentImmune deficiencies and genetic tendencies are possible modifying factors.
20 Localized Aggressive Periodontitis (AAP IIIA) Onset of disease around puberty, more common in femalesCharacterized 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 commonPreviously named localized juvenile periodontitisWithout radiographs, often goes undetected b/c of minimal plaque.
22 Generalized Aggressive Periodontitis AAP IIIB Most common age of onset, persons younger than 30Rapid destruction around most teethMust have interproximal attachment loss on at least three permanent teeth other than first molars and incisors.Frequently associated with abnormal neutrophil functionP.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 destructionDisease severity inconsistent with amount of plaque presentFamilial tendency
24 Treatment considerations in Aggressive Periodontitis Control of disease may not be possible, reasonable goal – slow disease progressionConsultation 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 diseasePlasma corticosteroids become elevated, suppress immune response NUG is example of correlation between stress and periodontal disease
26 Tobacco useNicotine and chemicals on rootsurface act as toxins for fibroblast attachmentEnvironmental factorNicotine is a vasoconstrictor, so inflammatory symptoms may be maskedLocal and systemic effects – primarily immunosuppressionTobacco users are at greater risk for developing periodontal disease at younger ages and respond poorly to treatmentSmokeless 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 marginsMore severe disease at young age with more rapid rate of destructionPocketing greater on anterior and maxillary palatal surfacesRecession in both archesWide embrasure spacesLevel of oral hygiene may not correlate with severity of diseaseOften lack of marginal gingivitis (not always red or edematous)Significant bleeding/suppuration on probingMinimal reduction in pocket depths after scalingRepocketing within 1 year of surgical treatment
28 Nutritional disorders and periodontal disease Poor nutrition lowers immune response, increases susceptibility to perioUS – malnutrition most common among elderly, low socioeconomic groups, anddicts to drugs and alcoholGood nutrition linked to overall health. The oral cavity reflects systemic healthProtein 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 disordersHyperparathyroidismAlterations in sex hormonesDiabetes MellitusNeutrophil AbnormalitiesNeutropeniasCyclic neutropeniaNeutrophil dysfunctionLeukocyte adherence defectChemotaxis defects
30 HIV – Related Periodontitis Compromised host allows periodontitis to progress much more quicklyLesions are not HIV specific, just exaggerated due to lack of host responseCD4 < 200 – severe and extensive attachment loss, multiple infectionsHIV is modifier of existing periodontal disease
31 HIV – Related Periodontitis Oral signs and symptomsBright red gingiva with spontaneous bleeding and suppurationMay be painfulNUP – necrotizing ulcerative periodontitis – rapid bone lossIn non- HIV + patients, may be result of recurrent NUGDeep, osseous crater-like lesionOsseous lesions may extend to necrotizing ulcerative stomatitisMay superficially resemble NUGLinear gingival erythema