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Different perio probes
- Michigan O probe – 1,2,3,5,7,8,9,10, preclinic
- North Carolina probe – 1-15 without skipping numbers, used in clinic
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In normal healthy situation, the pocket should be from ___ to the __ – normally, JE is at ___. Pocket should be ___ max in normal.
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When the pocket depth has exceeded the MGJ, it is considered __________.
mucogingival defect
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HISTOLOGY & FIBER SYSTEMS
- Gingival collagen fiber system
- 1. Gingivodental Group, Circular & Transseptal
- Epithelium
- 1. Masticatory Mucosa – keratnized
- 2. Alveolar mucosa – non-kerratinized
- Connective Tissue
- 1. Masticatory Mucosa – Collagen fibers
- 2. Alveloar Mucosa - Elastic fibers
- Periosteum – Inner most layer of the connective tissue - Bound Down (2 layers)
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BIOLOGIC WIDTH CONCEPT
- a. Junctional Epithelium
- b. Collagen fibers from the attached gingiva, which attach to cementum on the facial and lingual; or Transseptal fibers that attach the cememtum of one tooth to the adjacent tooth’s cementum.
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Attachment of a tooth
- Begins with the biologic width
- Also includes the housing of the root by the bony socket - periodontal ligament & cementum of the root
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TYPES OF ATTACHMENT
- Long Junctional Epithelium
- Connective Tissue (fibers + cementum)
- True Attachment (bone , ligament + cementum)
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ATTACHMENT APPARATUS POSSIBLE RELATIONSHIPS OF THE ROOT
- Normal relationship – Cementum + Periodontal Ligament + Bone. The reason a tooth can be extracted.
- Ankylosis – Cementum + Bone. There is no ligament and the cementum and bone are fused. Has to cut the tooth out. Same mechanism for implant.
- Resorption – Normal relationship, but the cementum is resorbed and the tooth structure is destroyed. Etiology is unknown.
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Gingival bio-type
- thin = triangular teeth, bone is more scalloped -> very easy to get a black triangle -> esthetic challenge
- flat and thick = rectangular or square teeth
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Periodontal disease
- Etiology – retained plaque
- Results – inflammation, bleeding, pocketing, attachment (bone) loss
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Sulcular epithelium is thin, non-keratinized, and has no rete pegs
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Gingival Pseudo-pockets
- No migration of the junctional epithelium
- Usually due to gingival hyperplasia
- No loss of attachment
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STRUCTURAL PROBLEMS - MUCO-GINGIVAL DEFECTS
- Lack of attached keratinized tissue
- a. Probe passes MGJ – keratnized tissue unattached
- b. no keratinized tissue present
- Aberrant frenum is present & is pulling on the gingival margin
- Shallow vestibule
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MAJOR OBJECTIVES
- Don’t only treat symptoms
- Always try to establish a diagnosis by a careful diagnostic review, clinical exam, radiographic exam, occlusal exam and interview, in order to determine the etiology of the specific problem/s
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Dental plaque-induced GINGIVAL DISEASES
- Gingivitis associated with plaque w/ or w/o local contributing factors
- modified by systemic factors
- modified by medications
- modified by malnutrition
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Non-plaque-induced GINGIVAL DISEASES
- of specific bacterial origin
- of viral origin
- of fungal origin
- of genetic origin
- Gingival manifestations of systemic conditions
- Traumatic lesions
- Foreign body reactions
- Not otherwise specified
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Signs of Gingivitis
- a. Bleeding
- b. Change in tissue color
- c. Change in tissue consistency
- d. Retractable tissue
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GINGIVAL RESPONSE
- a. Fibrotic
- b. Edematous
- c. Both – Fibrotic & Edematous
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LOCAL CONTRIBUTING FACTORS which can make plaque control more difficult:
- a. Tooth anatomic factors (root grooves & furcation grooves)
- b. Dental restorations - iatrogenic
- c. Root fractures
- d. Cervical root resorption
- e. Calculus deposits
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Grooves on the roots of teeth
- a. Palatal of maxillary lateral and sometimes the central incisors
- b. Proximal surfaces of the max 1st bicuspids and the mesial roots of the lower 1st molar – furcation grooves
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CERVICAL ROOT RESORPTION
After gingival recession, the root cementum becomes exposed and becomes a plaque trap and potential area of decay.
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SYSTEMIC FACTORS
- Endocrine System
- a. Puberty
- b. Pregnancy
- c. Diabetes mellitus
- Blood Dyscrasias
- a. Leukemia
- b. Agranulocytosis
- c. Thrombocytopenia
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Drugs causing gingival enlargement
- a. Anticonvulsants – Dilantin
- b. Calcium Channel Blockers – Procardia
- c. Immunosuppressants - Cyclosporin
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Drugs influencing gingivitis
Oral contraceptives
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MALNUTRITION
Ascorbic Acid Deficiency - Scurvy
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VIRAL ORIGIN - Herpes virus Infections
- a. Primary Herpetic Gingivostomatitis - always on attached tissue
- b. Recurrent Oral Herpes - injection on the palate may induce it
- c. Varicella-Zoster Infections - shingles limit to one side; follows course of sensory nerve
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Fungal origin
Candida Infections
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CANDIDIASIS
- Also called Moniliasis or Thrush
- Caused by Candida Albicans - fungus
- Can also be a secondary infection - induced by VDO decrease
- 4 oral forms – pseudomembranous, hyperplastic, atrophic, & angular cheilosis
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HEREDITARY GINGIVAL FIBROMATOSIS
- Slow progressive enlargement
- Esthetic & functional problems
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MANIFESTATIONS OF SYSTEMIC CONDITIONS
- Mucocutaneous disorders
- 1. Erosive Lichen Planus
- 2. Pemphigoid
- 3. Pemphigus Vulgaris
- Allergic reactions
- 1. Dental restorative materials
- 2. Toothpastes - Mouthrinses
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TRAUMATIC LESIONS
- 1. Chemical injury
- 2. Physical injury
- 3. Thermal injury
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FOREIGN BODY REACTIONS
- Trapped toothpick
- Seed from a food product
- Shell from a peanut or seafood
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PERIODONTAL DISEASES
- 1. Chronic Periodontitis
- 2. Aggressive Periodontitis
- 3. Manifestation of a systemic disorder
- 4. Necrotizing Periodontal Disease
- 5. Abscesses of the Periodontium
- 6. Associated with Endodontic lesions
- 7. Developmental or Acquired Deformaties and Conditions
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PERIODONTITIS
- Chronic or Aggressive
- Inflammatory type disease
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In 1976 Page & Schroeder described periodontal disease based on histopathology of the diseased tissues.
- a. Initial lesion
- b. Early lesion
- c. Established lesion
- d. Advanced lesion
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CHRONIC PERIODONTITIS
- Localized - < 30% of sites involved
- Generalized - > 30% of sites involved
- Slight – 1 to 2 mm of CAL
- Moderate – 3 to 4 mm of CAL
- Severe - > or = to 5 mm of CAL
- Slow to moderate rate of progression
- Amount of destruction consistent with local factors
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AGGRESSIVE PERIODONTITIS
- Rapid attachment loss & bone loss – pocket formation
- Amount of plaque inconsistent with disease severity
- Genetic trait
- Healthy individual
- Occurs at puberty or ages 10 to 30 yrs
- Localized – 1st molars & incisors
- Generalized – >=3 teeth; 1st molars & incisors
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PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASES
- Hematologic Disorders
- a. Acquired neutropenia
- b. Leukemias
- Immune Compromised
- Genetic Disorders
- N.B. - Diagnosis depends upon the amount of local factors – Can be Chronic Periodontitis modified by the systemic condition or as stated above
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NECROTIZING PERIODONTAL DISEASES
- Necrotizing Ulcerative Gingivitis – NUG
- Necrotizing Ulcerative Periodontitis – NUP
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ACUTE NECROTIZING ULCERATIVE GINGIVITIS
- ANUG or Trench Mouth
- Marginal gingiva is affected
- Punched out gingival margins
- Painful – odor
- Pseudomembrane
- Fusospirochetes predominant
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ABSCESSES OF THE PERIODONTIUM
- Gingival abscess
- Periodontal abscess
- Pericoronal abscess or Pericoronitis
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GINGIVAL ABSCESS
- no loss of attachment
- starts in the gingival unit
- usually a result of trapping a foreign body in the gingival sulcus
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PERIODONTAL ABSCESS
- usually caused by a closed periodontal pocket
- resulting from loss of attachment
- a swelling or a fistula
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differentiate between a periapical abscess and a periodontal abscess.
- periapical abscess starts at the apex or apicies of the tooth and is caused by injury to the pulp – needs RCT
- A periodontal abscess occurs on the side of the tooth and is usually a closed pocket.
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PERIODONTITIS ASSOCIATED WITH ENDO
- Combined lesions
- a. Endo – Perio: good prognosis
- b. Perio – Endo (Retrograde Pulpitis): hopeless
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DEVELOPMENTAL OR ACQUIRED DEFORMITIES
- Localized tooth-related factors
- Mucogingival deformities and conditions around teeth
- Mucogingival deformities and conditions on edentulous ridges.
- Occlusal Trauma
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TOOTH-RELATED FACTORS
- Tooth anatomic factors
- Dental restorations
- Root fractures
- Cervical root resorption
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LOCALIZED TOOTH RELATED FACTORS - Root Proximity problem
- a. makes plaque control difficult
- b. restoring the tooth becomes a problem
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MG DEFECTS & SOFT TISSUE DEFORMITIES - TEETH
- Gingival recession
- Lack of keratinized tissue
- Decreased vestibular depth
- Aberrant frenum
- Gingival overgrowth
- Abnormal color
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MG DEFECTS & SOFT TISSUE - DEFORMITIESEDENTULOUS RIDGES
- Vertical-horizontal ridge deficency
- Lack of keratinized gingiva
- Aberrant muscle pull
- Decreased vestibular depth
- Abnormal color
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OCCLUSAL TRAUMA - TFO
- Primary Occlusal Trauma
- Secondary Occlusal Trauma
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SIGNS - TFO
- Clinical Signs – Mobility and/or Fremitus
- A. Primary Trauma from Occlusion
- a. Prematurity
- b. Parafunctional habit
- c. Poor prosthetic design
- B. Secondary Trauma from Occlusion
- C. Functional
- Radiographic Sign – Thickened PD ligament
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TFO CLASSIFICATION
- Primary
- 1. Clinical sign – Mobility and/or Fremitus
- 2. Cause - Overload of force
- 3. Treatment – Correct the force overload
- Secondary (to periodontal disease)
- 1. Clinical Sign – Mobility
- 2. Cause - Significant loss of attachment
- 3. Treatment - Do nothing or splint
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UPDATE BY AAP ON CLASSIFICATION
- Patients on maintenance w/ previous attachment loss
- If return with probing depths of <=3mm and no inflammation – healthy but reduced periodontium.
- If return with inflammation, and/or recession, and probing depths <= 3mm – reduced periodontium with inflammation.
- If return with inflammation, BOP, and/or recession, and probing depths > 3mm – periodontitis with severity guided by the following:
- Slight – 3-5 mm pocket, x-ray bone loss = 15% of root length & 1-2 mm of CAL
- Moderate – 5-7mm pocket, x-ray bone loss = 16-30% of root length & 3-4 mm of CAL
- Severe – >=7mm pocket, x-ray bone loss > 30% of root length & >=5mm of CAL
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