IntroToPerio - Midterm05

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  1. RISK FACTORS affect Periodontal Diseases initiation and progression
    • Local Factors: Plaque retentive areas (calculus), anatomic factors (eg. groove, open contact, root proximity, fused root form), iatrogenic, occlusion.
    • Systemic Factors: Age, race, immunologic defects, endocrine dysfunctions, genetics, disease states. Harder to control.
  2. Host Defense:
    • Cytokines: IL-1b & TNF-a
    • Prostaglandins: PGE2
    • High in periodontal diseases. Markers. Cause breakdown.
  3. Genetic Disorders:
    • Familial & cyclic neutropenia
    • Down Syndrome
    • Leukocyte adhesion deficiency (LAD).
    • Papillon-Lefevre syndrome
  4. Systemic Disease:
    • Hematologic disorders
    • aquired neutropenia
    • leukemia
    • Endocrine Disorders:
    • diabetes
    • These can increase susceptibility to Periodontal Diseases
  5. Environmental Factors:
    • Microorganisms - P.gingivalis, B.Forsythus, & P. intermedia.
    • diet/nutrition,
    • stress - ANUG
    • pharmacologic agents,
    • Smoking.
  6. Pharmacologic Agents:
    • Cause Gingival overgrowth
    • Ca Channel Blockers
    • Immunosupressive drugs, eg. cyclosporin-A in transplant patients
    • Anti-convulsants, eg. dilantin
  7. Smoking
    • strong association with alveolar bone loss, tooth loss, and the severity of periodontal diseases.
    • clinical difference (vs non-smoker) in the prevalence of periodontitis, frequency of deep pockets and the mean attachment loss
    • Tissue is thick and fibrotic (vasculature constricts) – masks the affects of the plaque organisms
  8. Both Type-I & Type-II Diabetes are important systemic diseases that are risk factors for Periodontal Diseases.
  9. Open contacts are always a risk factor
    • does not cause perio disease, but does cause food accumulation which can lead to inflammation and increase risk for perio breakdown
    • important to restore to proper contacts
  10. Diabetes & Periodontium – mechanisms of action:
    • subgingival microflora
    • host defense
    • alterations in cytokines
  11. Diabetes – risk factor
    • prone to gingiva/periodontal abscess
    • prone to breakdown
  12. Oral Manifestations of Leukemia
    • Gingival enlargment
    • Gingival overgrowth (not hyperplasia, very vascular)
    • Gingival erythema.
    • Oral ulcers.
    • Gingival bleeding (spontaneous)
    • Prolonged healing after extraction.
    • Infections (prone to)
  13. POCKET DEPTHS
    • represent loss of attachment (CAL)
    • Determines the topography of the osseous lesions
    • bleeding denotes disease activity
    • helps diagnose an endodontic problem or a combined endo-perio or perio-endo problem.
  14. Probe with force up to __, with which the tip of the probe does not penetrate the junctional epithelium.
    Forces up to __ are used to reach the bone level and do bone sounding or mapping.
    • 30g
    • 50g
  15. Pocket measurements should be completed and recorded at every _______ visit, ________ visit and ________ visit.
    • maintenance
    • Phase I evaluation
    • diagnosis
  16. Osseous defects are described relative to _____ of the tooth, with the exception of _______, which is a defect that ________.
    • one side
    • the circumferential defect
    • transcends around a line angle
  17. NORMAL ARCHITECTURE
    The interproximal bone is coronally positioned to the buccal and lingual plates of bone and the alveolar bone follows the CEJs. It is a parabolic and scalloped form. If there is a thin biotype, then it is more scalloped and the teeth are triangular. If it is a thick biotype, then it is flat and the teeth are square.
  18. CLINICAL ATTACHMENT LOSS - CAL
    the actual amount of attachment loss, either due to recession or the formation of a periodontal pocket (apical migration of JE) and measured from the CEJ.
  19. Facial/lingual defects are classified as inconsistent margins, reverse architecture, dehiscences, furcations, etc.
  20. BLEEDING UPON PROBING
    • This is an indication that there is some disease activity present.
    • The bleeding is coming from the ulcerated sulcular epithelium, which is thin, non keratinized and present with no rete pegs. These histologic characteristics set this tissue up for easy breakdown from the inflammatory process.
  21. CAUSES of GINGIVAL HYPERPLASIA
    • Chronic Inflammation
    • Puberty Gingivitis
    • Pregnancy Gingivitis
    • Drug Induced
    • Hereditary – Gingival Fibromatosis
    • Blood Dyscrasias
  22. CAUSES of GINGIVAL RECESSION
    • Periodontal disease, particularly with a thin bio type and horizontal bone loss.
    • Structural problems, such as prominent roots and/or teeth in buccal version with or without a thin bio-type
    • Muco-gingival defects
    • Aggressive tooth brushing
    • Occlusal forces or orthodontic movement with thin bio-types
  23. PD MILLER CLASSIFICATION OF RECESSION DEFECTS (1985)
    • Marginal tissue recession vs MGJ; loss of interproximal bone or soft tissue.
    • Class I – Coronal. No. Root coverage is predictable.
    • Class II - Same or apical. No. Root coverage is predictable.
    • Class III - Same or apical. Apical to the CEJ, but coronal to the apical extent of the marginal tissue recession. Maybe partial root coverage.
    • Class IV - Same or apical. More apical to the extend of the marginal tissue recession. Not indicated for root coverage.
  24. If no ________, the graft will die because there is no blood supply.
    interproximal bone
  25. MOBILITY
    • Measured in terms of +1, +2, or +3 and marked inside the crown of the tooth on the chart.
    • Mobility can be a sign of significant attachment loss, trauma from occlusion (primary or secondary), infection, trauma, orthodontic movement, or a fractured root or tooth.
    • Mobility is a symptom, you must establish why there is mobility. Simply put, you must make a diagnosis.
  26. KEY CLINICAL TIP When patient presents mobility
    • probe
    • determine CAL.
    • If so, how much relative to the root form, length and shape.
    • If minimal, is it TFO? occlusal analysis
    • If negative, consider an infection, a fracture or possibly, pathology.
  27. FURCATIONS
    • In 28 teeth dentition
    • Max: 16 furcations – 3/molar and 2/1st bicuspid
    • Man: 8 furcations – 2/molar
    • The root trunk is the distance from the CEJ to
    • the beginning of the furcation. A long root
    • trunk is more favorable.
    • Plaque traps and susceptible to root caries
  28. HAMP classification for Violations of the furcation
    • Class I is an early lesion and loss of furcal bone. Horizontal loss of supporting tissues <=1/3 of the tooth width.
    • Class II is a moderate lesion with a horizontal and vertical component, but does not communicate with another furcal area of the tooth. Horizontal loss of supporting tissues exceeding 1/3 of tooth width, but not encompassing the total width of the furcation area.
    • Class III is an advanced lesion that communicates with another furcal area on the tooth. Total loss of the furcation tissues with “through and through” communication.
  29. EASLY & DRENNAN CLASSIFICATION FOR CHARTING FURCATIONS
    • Class I – Open Triangle
    • Class II – Closed Triangle
    • Class III – Shaded Triangle
  30. Class I & Class II furcations can be treated and
    • the bone regenerated with periodontal surgery
    • via bone grafting and the use of growth factors.
    • Class III furcations cannot be reversed. Teeth do not have to be extracted, but should never be used as a fixed abutment for a permanent bridge. At times, on lower molars, they can be bicuspidized or resected on all molars.
  31. The issue with a furcation violation is that routine plaque control procedures are difficult, but the major clinical problem with a furcation is root decay. Furcation violations are not always periodontal problems, but may also be indicative of a root canal problem due to accessory canals from the pulp chamber to the furcation area.
  32. MODIFYING FACTORS
    • Metabolic disease - Diabetes
    • Chemotherapy
    • Disease affecting Immune System (HIV, AIDS, etc)
    • Blood dyscrasia
    • Connective Tissue disease – Scleraderma
  33. SWELLINGS
    • Any type of swelling has to be evaluated.
    • Is the swelling in soft tissue or bony.
    • Determine the composition of a swelling is by needle probing the area.
    • A swelling may be the result of an abscess from an infection or a foreign body, neoplastic lesion, an inflammatory lesion, a traumatic transient lesion, a hematoma or a developmental lesion.
  34. The quickest and easiest way to determine the etiology of the fistula is to place a _________, without local anesthesia into the fistula and push it, until there is resistance and the point stops. Follow this with ______ of the area.
    • 30 gutta perch point
    • x-ray
  35. A periodontal pocket should be considered ________.
    a fistula
  36. MIGRATION OF TEETH
    • Teeth can migrate if there is no opposing tooth/no tooth next to it. Distal drifting possible, but rare.
    • Open anterior bites are usually due to an anterior tongue thrust
    • The problem is when you have pathologic migration, drifting of teeth, particularly anterior teeth, it is due to loss of support and/or excessive overload of force.
  37. PATHOLOGIC MIGRATION usually occurs in the _____ areas and teeth flare and open contacts result.
    In the maxillary arch this can cause an esthetic problem when a patient has a high or moderate smile line.
    The cause can be due to significant attachment loss, lost of posterior occlusion, anterior tongue thrust, poor prosthetic design or a combination of these factors. These cases will require some type of minor orthodontic therapy & stabilization
    incisor
  38. Always correct ______, prior to a periodontal surgical procedure.
    open contacts
  39. MODIFIED PLAQUE INDEX
    • 6 Teeth: four 1st molars + # 8 & # 24
    • Measure buccal on Max & lingual on Mand
    • Podchadley Index – ranges from 0 to 5 – 3 vertical components and middle column separated into 3 areas. (5 areas per tooth)
    • Formulate a %: Plaque Surfaces/30
    • If a tooth is missing, chose an adjacent tooth
  40. PLAQUE INDEX
    • 6 teeth (# 3, 8, 14, 19, 25 & 30)
    • “1”, w/ plaque and “0” w/o.
    • A tooth is inspected from the buccal and lingual and divided into 3 horizontal segments for a total of 5 surfaces per tooth or a total of 30 surfaces in total.
    • The Plaque Index is determined by placing the # of tooth surfaces with plaque over 30 to get a %.
  41. BLEEDING INDEX
    • Count the number of bleeding points per tooth with a maximum of 6 probings per tooth.
    • Formulate a % by dividing the # of bleedong points over the # of teeth examined times 6 areas per tooth.
    • More important than plaque index.
  42. GINGIVAL INDEX
    • Loe & Silness, 1963
    • used on all teeth or selected teeth and on all surfaces or selected surfaces.
    • qualitative changes in the gingival soft tissues.
    • does not consider pocket depth, degree of bone loss, or any quantitative change of the periodontium.
    • Each of the 4 gingival areas of a tooth are scored 0
    • (normal), 1 (mild inflammation), 2 (moderate), and 3
    • (severe-spontaneous bleeding)

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IntroToPerio - Midterm05
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2016-06-13 22:22:31
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