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168 Cards in this Set
- Front
- Back
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Subjective s. Non-subjective
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Description of symptoms: Subjective
Signs (Intraoral exam): non-subjective |
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Radiographic evaluation
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DAY OF PRESENTATION
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Inflammation
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-a series of molecular and cellular responses designed to eliminate foreign agents and promote repair of damaged tissues
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Inflammation characterized by:
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-redness (rubor)
-pain (dolor) -heat (calor) -swelling (tumor) -loss of function (functio laseo) |
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Inflammation associated with..
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-flu like symptoms
-fever -chills -fatigue/loss of energy -headaches -loss of apetite -muscle stiffness |
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Factors of inflammation
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1. Nature of the inciting agent
2. Time of observation: -early acute lesions will be highly cellular -chronic lesions will be largely acellular and in the stages of fibrosis 3. Immune status of the host -previously immunized host will mount a vigorous response -immunocompromised individual-little to no response |
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Clinical onset and duration of inflammation
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-acute
-subacute -chronic |
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Acute response
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-Transudate and exudate
-neutrophil rich exudate |
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Transudate and Exudate
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-movement of fluid of low protein content, containing predominantly albumins and acute-phase proteins from the intravascular to extra-vascular space
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Neutrophil-rich exudate
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-fluid exudation stage is naturally followed by the influx of polymorphonuclear nuetrophillic leukocytes (PMNs)
-appear within hours: profound microbial kiling capacity -secretion of enzymes capable of digesting host tissue components -elicited most commonly in response to pyogenic microbial infections -accounts for histological appearance of suppuration -intact and disintegrating neutrophils within a background of fragmented and liquefied tissue elements |
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Acute Gingival diseases
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-acute gingival abscess
-acute herpetic gingivostomatitis -acute pericornitis -ANUG-acute necrotizing ulcerative gingivitis |
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Acute Gingival abscess
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-a localized, painful, rapidly expanding lesion
-sudden onset -limited to marginal gingiva or interdental papilla -red swelling with a smooth shining surface -within 24-48 hours it becomes fluctuant and pointed -a surfac eorifice may be visible from which a purulent exudate may be expressed |
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Etiology of Gingival Abscess
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-penetration of bacteria along with other solid matter into the tissues (ex. toothbrush bristle, small, hard particles - sesame, poppy seeds popcorn kernels) or other food particle penetrates the tissues
-often occurs in a previously disease-free area |
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Treatment of Acute Gingival abscess
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-treatment goal: reversal of acute phase and when possible, removal of offending agent
-treatment regimen: anesthesia, SRP to estalish drainage and remove microbial deposits and foreing material -may require incision and drainage with #15 blade. Express exudate with firm digital pressure -irrigate with saline. Pt to rinse with warm salt water q 2hrs. reassess at 24 hours -if lesion persists or access is poor,consider surgical intervention |
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Acute herpectic gingivostomatitis Palliative treatment
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-NSAIDS and viscous lidocaine or 1-2-3 mouth rinse
-dimetapp elixir 40 ml -kaopectate 80ml -distilled water 120 ml -use prn. shake well before use. rinse with 1 tsp for 1-2 minutes and expectorate |
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acute herpetic gingivostomatitis interventional
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-useful if within 3 days of onset
-acyclovir 15mg/kg five times daily for 7 days -NSAIDS -viscous lidocaine or 1-2-3 mouthrinse |
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ANUG
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-painful, ulcerated gingiva
-associated with impaired host response to microflora |
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ANUG treatment sequence overview
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-alleviation of acute inflammation: reduction of microbial load and removal of necrotic tissue
-treatment of chronic disease -alleviation of generalized symptoms -correction (address) systemic conditions |
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ANUG Med HX, H&N, Itraoral exam
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-skin lesions
-enlarged lymphodes -halitosis -fever -defer probing due to pain |
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ANUG treatment (1st visit)
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-1st visit: therapeutic goals are to reduce the microbial load and remove necrotic tissue
-dry affected area with cotton roll -apply topical anesthetic -gently swab affected areas with moistened cotton pellet to remove psuedomembrane and debris (use pellet in small area and then discard) -rinse with warm water or saline -remove superficial calculus using ultrasonic instrumentation |
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ANUG treatment 1st visit RX and instructions
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-anitiiots for moderate to severe cases with lymphadenopahty and or fever
-amoxicillin 500 mg q 6 hours for 10 days -PCN allergy: erythromycin 500 q 6 hrs or metronidazole 500 mg q 12 hours for 7 days -unless emergency exists, delay further therapy until patient is symptom free for 4 weeks to minimize exacerbating the acute symptoms -patient instructions: avoid tobacco, alcohol; rinse with a glassful of an equal mixture of 3% H2O2, and warm water q 2 hrs and/or twice daily with .12% chlorohexadine; rest; oral hygiene; no flossing during healing period; OTC analgesic prn |
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ANUG 2nd and 3rd visit
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-2nd visit : 24-48 hrs: reevaluation for improvement; scaling performed if necessary and sesnitivity permits
-3rd visit : 5 days after second visit -re-eval for improvement -pt should be essentialy free of symptoms -discontinue H2O2 but continue chlorohexidine rinse for 2-3 weeks -stress OHI, etiology, 3-6 month recalls -re-eval tissue at 1 month continue with other needs |
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"Chronic Lesions
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-chronic abscess
-cellulitis -can be difficult to manage -may range from low grade, well localized abscesses to severe life threatening facial space infections -appropriate therapy depends on understanding of cause, natural history (pathway), and management. |
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Odontogenic Infections
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-of indigenous bacterial origin
-polymicrobial -aerobic bacteria ~5% -anaerobic bacteria ~35% -mixed ~60% -antibiotics alone may help control the infection, but the infection will recur when antibiotic therapy is ended |
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Periapical odontogenic infections
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-pulpal necrosis and subsequent bacterial invasion into periapical tissues
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Periodontal Odontogenic infections
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-deep periodontal pocket allows inoculation of bacteria into the underlying soft tissue
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the chronic abscess
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-and infectious, suppurativ inflammatory event associated with a pyogenic organism
-most often an cute exacerbation of a chronic condition -occurs when a pyogenic stimulus is not readily eliminated -localized collection of pus caused by suppuration wihtin tissue, organ or confined space -produced by deep seeding of yoenic bacteria into tissues (in time the abscess may become walled off by connective tissue limiting further spread) |
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spread of abscess or infection
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-along lines of least resistance
-spread through cancellous bone until it encounters cortical plate -if plate is thin, erodes the bone and enters soft tissue |
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drainage of endodontic abscess into the sulcus
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-periodontal ligament fistulation
-extraosseous fistulation |
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spread of infection-manifestation
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-Determined by 2 major factors
1. thickness of the bone 2. relationship of perforation of the bone to the muscle attachments |
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Definition of Occlusion
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Contact relationships of teeth from neuromuscular control of the masticatory system. It relates to:
-TMJ -Muscles -Periodontium |
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Occlusal Relationships & Positions
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Centric Relation
Centric Occlusion Excursive Movements: -Laterotrusive (Workside side & Balancing side) -Protrusive |
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Forces on the Periodonium
When do they happen? |
Chewing (mastication)
Swallowing Minimally during speech Parafunctional habits (i.e. bruxism) Premature contacts |
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Adaptive Capacity of the Periodontium to Occlusal Forces
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The periodontium tries to accommodate to the forces exerted to the crown
The effect of these forces on the periodontium is influenced by their: -Magnitude - widening of PDL -Direction - tooth movement -Duration - longer time = increased injury -Frequency - constant versus intermittent |
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Occlusal Trauma Definition
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An injury to the attachment apparatus (periodontal ligament, alveolar bone, & cementum) as a result of excessive occlusal force
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Other Occlusal Terms
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Trauma from occlusion = tissue injury
Traumatizing occlusion Periodontal traumatism Occlusal overload Acute trauma from occlusion (abrupt change - ex: olive pit or iatrogenic) Chronic trauma from occlusion (gradual changes - ex: tooth wear, extrusion, bruxism, clenching) |
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Occlusal Trauma
(Clinically) |
Increasing mobility
Tooth migration Discomfort/tenderness Pain to percussion or upon biting |
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Occlusal Trauma
(Radiographically) |
Widened periodontal ligament
Alveolar bone and/or root resorption Discontinuity of the lamina dura -May not be seen initially -May be seen thickened if trauma persists Pathologic tooth migration (soft tissue cannot support occlusal forces and the teeth shift) |
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Normal Dimensions of the PDL
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.25mm average +/- 50%
0.17 - 0.32mm based on where you are looking at on the tooth |
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Histology of Occlusal Trauma
(Pressure side) |
-Disorganization
-Vascular dilation -Increased vascular permeability -Thrombosis -Hyaline degeneration of the collagen fibers -Frontal & undermining bone resorption cause by osteoclasts -Cementum resorption |
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Periodontal abscess
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-a localized accumulation of pus within a gingival wall of a periodontal pocket (also knows as a lateral or parietal abscess)
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Etiology of Periodontal Abscess
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1. severe chronic periodontitis
2. in the abscence of periodontal dises likely due to: -blunt trauma to tooth -root fracture -perforation fo the lateral wall of the root during endodontic or restorative therapy |
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Acute periodontal abscess
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-appears as an ovoid elevation of the gingiva along the lateral aspects of the root
-gingiva is edematous and red with a smooth shiny surface -area may be dome like and relatively firm or pointed and soft -pus may be expressed with gentle digital pressure -may be accompanied by throbbin, radiating pain, -tenderness to palpation -tooth mobility, extrusion -lymphadenopathy -other systemic effects such as fever and malaise |
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Chronic Periodontal Abscess
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-history of intermittent exudation
-pin point opening -usually asymptomatic -sometimes dull gnawing pain -slight extrusion of tooth may be noted -may have periods of acute exacerbations |
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Acute Abscess
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- mild to severe pain
-localized red, ovoid (swelling) -mobility, sligh extrusion, tenderness to percussion or biting -yes there is purulence -not usually a fistula |
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Chronic abscess
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-mild or no pain
-localized slight to no swelling -slight tooth extrusion -intermittent purulence -yes fistula |
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Diagnosis
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-health, dental history, review of symptoms, vitality/pulp testing
-radiographs, perio probing, periodontal pocket profile, prosthodontic considerations |
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The primary periodontal lesion
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-tooth generally vital
-generalized bone loss -plaque, calculus -soft tissue inflammation -broad based pocket formation -occlusal trauma |
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The primary pulpal lesion
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-sinus tract formation through the periodontium
-some degree of mobility -varying degree of bone loss -furcation bone loss -narrow pocket formation -swelling in the attached gingiva -soreness/pain on percussion -tooth may exhibit large restoration and/or caries |
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Treatment of Combined Lesion (endo/perio)
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-ENDODONTICS FIRST: resolves lesion to the point of periodontal involvement
-corrective Periodontal therapy second: eliminates bacteria of endodontic origin -prognosis depends on extent of periodontal involvement and tooth restorability |
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treatment of periodontal abscesses
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-acute periodontal abscess
-purpose of treatment is to alleviate pain, control spread of infection and establish DRAINAGE -drainage established though periodontal pocket or external incision |
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Treatment: DRAINAGE
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-after applicationof a topical or local (may be difficult), a flat instrument of probe is introduced into the pocket in an attempt to distend the pocket wall
-small curette is then used to penetrate the tissue andestablish drainage |
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External incision
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-when drainage cannot be easily established via the pocket or when the abscess can be seen pointing
-incision: a BP blade #12 or 15 is used to give a vertical incision through the most fluctuant part of the lesion- let gravity assist -blade should penetrate to firm tissue to reach purulent area -irrigate and spread tissue gently to facilitate drainage |
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additional treatment
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-if tooth is extruded, remove occlusal tooth structure to reduce slightly out of occlusion
-mouth rinses with warm salt water or chlorohexidine -systemic antibiotics, penicillin is treatment of choice IF there is a fever -for gingival abscess remove offending agent |
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treatment of chronic periodontal abscess
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-SRP, systemic antibitoics
-periodontal flap surgery if lesion persists or reoccurs -full thicknes flap is relfected -calculus/offending substances removed -bone recontoured, granulation tissue is removed and sutures placed -chlorohexidine rinse and antibiotics (fever) Rx |
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Root fracutures
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1. horizontal - may be restorable based on fracture location
2. oblique 3. vertical - usually hopeless prognosis-associated iwth abscess formation |
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Cellulitis
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-aerobic microorganisms (streptococci)
-acute -edematous -doughy to indurated in consistency -innocuous in early stages -dangerous in advanced, rapidly spreading stages |
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Abscess characteristics (compared to cellulitis)
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-Chronic or Acute
-localized moderate or severe pain -small -well cicumscribed borders -fluctuant (palpation) -purulence -less serious -anaerobic bacteria |
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Cellulitis characteristics (compared to abscess)
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-acute
-severe and generalized pain -large -diffuse borders -doughy to indurated -no purulence (usually) -greater degree of seriousness -aerobic bacteria |
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Treatment of pericoronitis associated with entrapment of food under the operculum
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-prognosis?
-gently flushing of the area with sterile saline -swabbing with antisetic after elevating flap from teh tooth with a scaler-debris removed -if fluctuant, incise and drain -may need to reflect/excise pericoronal flap -offending tooth may require extraction -antibiotics (fever) |
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Histology of Occlusal Trauma
(Tension side) |
-Increased vascular permeability
-Thrombosis -Collagen turnover (higher collagen turnover due to stress) -Bone & cementum apposition |
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Occlusal Trauma
(Primary vs. Secondary) |
Primary --> excessive occlusal forces to a tooth or teeth with normal supporting structures (no bone loss)
Secondary --> normal or excessive occlusal forces to a tooth or teeth with inadequate or reduced supporting structures (creates bone loss) |
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Occlusal Trauma
(Common Results) |
-Does not initiate gingival inflammation
-Does not initiate pocket formation -Does not aggravate gingivitis -Bone changes due to occlusal trauma, without existing inflammation, are reversible when the traumatizing forces are discontinued |
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Co-destructive Theory
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This hypothesis requires the production of a traumatic lesion immediately subjacent to an established marginal periodontitis
-Zone of irritation --> from gingival margin to gingival fibers (where plaque can stimulate inflammation) -Zone of co-destruction --> PDL, cementum, & alveolar bone (plaque + occlusal forces enhances attachment loss) |
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Animal Studies on Occlusal Trauma
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USA (Meitner 1975) --> questioned the hypothesis of co-destruction after evaluating the results of his studies in monkeys
Sweden (Lindhe 1974 & 1982) --> confirmed the hypothesis of co-destruction after evaluating studies in dogs |
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Co-destructive Theory
(Differences in studies between USA & Sweden) |
Differences attributed to:
-Variations int he animal models used -Differences in the initial periodontal lesion upon with trauma was produced -Type & magnitude of force applied |
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Occlusion in the Treatment of Periodontitis
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-Treatments for periodontitis and occlusal trauma are both directed toward the control of causal factors
-Until agreement is reached on the possible synergistic association between marginal inflammation & occlusal trauma, emphasis should be placed on the identification, diagnosis, & correction of both conditions |
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Tooth Mobility
(Miller index) |
I --> first distinguishable sign of movement greater than normal
II --> movement of tooth that allows the crown to move 1mm from its normal position in any direction III --> tooth moves more than 1mm in any direction. Also teeth that may be rotated or depressed in their alveoli |
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Diagnosis of Trauma from Occlusion
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-Requires evidence of active injury
-Continued or increasing hypermobility -Persistent discomfort and tenderness -Radiographic evidence of bone and/or root resorption -Other findings: wear facets, altered trabecular patterns, fremitus (tooth mobility or vibration that you feel when the patient is tapping their teeth together in MI - feel with finger on the facial of the maxillary incisors) |
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Occlusal Factors & Periodontal Disease
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Factors that may be related to increased periodontal breakdown that are not directly associated with occlusal trauma:
-Malocclusion -Tooth malposition -Loss of teeth -Caries & defective restorations -Soft tissue trauma -Parafunctional habits & bruxism |
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Occlusal Therapy
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Main objectives of periodontal therapy:
-Help control bacterial infection -Maintain existing support -Restore lost attachment, if possible While control of plaque is essential for any periodontal treatment, clinicians differ about the need to include occlusal therapy Includes: Occlusal adjustment, Occlusal bite plane, Splinting of teeth, & Orthodontics |
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Occlusal Adjustment Definition
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Reshaping of occluding surfaces of teeth by grinding to create harmonious contact relationships between the maxillary and the mandibular teeth
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Occlusal Adjustment
(Indications) |
-Occlusal contact relationships that cause trauma to the periodontium, joints, muscles, or soft tissues
-Interference to function (chewing, swallowing) -Interferences that aggravate parafunction -Need to establish a functional baseline for comprehensive restorative therapy, aid splint, therapy, stabilize results of orthodontics, orthognathic surgery, and TMJ surgery |
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Occlusal Adjustment
(Benefits) |
-Decreases magnitude & changes direction of forces on tooth
-Reduces mobility -Increase tooth stability & function -Aid in regaining lost alveolar bone caused by occlusal trauma -No control studies have proved that preventive occlusal adjustment helps control inflammatory periodontal disease |
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Occlusal Bite Plane Splints
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-Axial distribution of forces
-Ideal occlusal relationships -Stabilization of teeth -Non-invasive & reversible -Prevents tooth movement similarly to an orthodontic retainer (~8 hours/day) -Ideal for bruxism due to wear of stent and not teeth |
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Orthodontics
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Orthodontic movement should be performed only after the inflammatory process has been controlled
-Move teeth to more favorable occlusal position, so teeth have more occlusion in long axis and less lateral forces -Molar uprighting -Intrusion -Extrusion -Correction of traumatic crossbite |
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Splinting Benefits
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-Decreases magnitude and changes direction of forces due to distribution to adjacent teeth
-Tooth or teeth will have decreased mobility -Increase in tooth stability and function -Aid in regaining alveolar bone lost due to occlusal trauma only |
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When is the ideal time to perform occlusal therapy?
(In relation to periodontal treatment) |
Treat periodontal disease first --> then allow pt to heal from the scaling & root planing
Re-evaluate and then decide whether or not to do the occlusal adjustment (Do occlusal adjustment on the day of or after the surgery) Change the rules when pt is complaining of discomfort |
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Physical Routes for Endo-Perio
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-Apical foramina (retrograde periodontitis)
-Lateral or accessory canals -Dentinal tubules |
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Progression of Pathosis
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Normal tooth without any pulpal pathosis is richly vascularized and innervated --> with microbial challenges (i.e. caries), local tissue inflammation can occur in the pulp adjacent to the site of carious lesions, as well as in the apical regions --> Pulpal inflammation can lead to DECREASE in pulpal blood flow (PBF) caused by an INCREASE in intrapulpal pressure (IPP), causing pulpal necrosis --> Pulpal necrosis, if left untreated, can lead to chronic inflammation or periradicular tissues & abscess formation, leading to a draining sinus tract
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Classification of Endo-Perio Lesions
(A & B) |
A --> Primary pulpal infection can lead to chronic periradicular periodontis: periapical radiolucency (PARL) can develop & migrate cervically. Mand. molars can have accessory canals in lateral orientation or in the furcation. Accessory canals can lead the primary pulpal infection & cause secondary breakdown of periodontium.
B --> Primary periodontal infection can lead to extensive breakdown of alveolar crest bone. In these lesions, one would find generalized bone loss around a single tooth or often might involve multiple adjacent teeth. Because of the pulpal-periodontal continuum through main root canal foramina or through accessory canals, extensive perio infection can cause irritation in the pulp tissues (RARE) |
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Classification of Endo-Perio Lesions
(C & D) |
C --> Both primary pulpal & primary periodontal infection can occur simultaneously in an "independent" endodontic-periodontic lesion, exhibiting the characteristics of both
D --> Primary pulpal & primary periodontal infections can occur extensively in this "combined" endodontic-periodontic lesion |
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Retrograde Periodontitis
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Lesion that you see periapically (more like an endo lesion)
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Orthograde Periodontitis
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Conventional periodontitis (coming from cervical area of tooth - start losing tooth at the crest of the cortical bone)
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In a combined endo-perio lesion, which treatment is done first?
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ENDO first because you get rid of whatever infection is inside the tooth, and then you can treat the outside of the tooth
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Does periodontal treatment negatively affect the dental pulp?
Does endodontic treatment negatively affect eh periodontium? |
NO!!!!
Patients often develop sensitivity after Sc&RP, but there is no permanent irreversible condition due to scaling & root planing |
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Characterisitics of Primary Pulpal Lesions
(See Lecture & Know Chart) |
Patient symptom = Varies (Often severe pain)
Coronal integrity = Compromised Radiographic lesions = PARL (periapical radiolucency) Vitatity = Nonvital Periodontal probing = Narrow probing to apex |
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Characterisitics of Primary Periodontal Lesions
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Patient symptom = Mild discomfort (often mild pain)
Coronal integrity = Intact Radiographic lesions = Crestal bone loss Vitatity = Vital Periodontal probing = Generalized bone loss |
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Characterisitics of Independent Endodontic-Periodontic Lesions
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Patient symptom = Varies
Coronal integrity = Compromised Radiographic lesions = Separate PARL & crestal lesions Vitatity = Nonvital Periodontal probing = Generalized bone loss |
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Characterisitics of Combined Endodontic-Periodontic Lesions
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Patient symptom = Varies
Coronal integrity = Compromised Radiographic lesions = Continuous bony lesions from alveolar crest to apex Vitatity = Nonvital Periodontal probing = Generalized bone loss with narrow probing to apex |
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Goals of Periodontal Therapy
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-Arrest disease progression
-reduction of gingival inflammation: by reduction of probing depths and bleeding -removal or inhibition of primary etiologic (biofilm) and/or secondary factors (e.g. smoking, defective restorations) -regeneration of lost tooth-supporting structures |
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Phases of Periodontal Therapy
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-diagnosis and treatment planning
-address urgent care issues, if applicable -initial periodontal therapy -reevaluation of initial periodontal therapy -surgical therapy -reevaluation of surgical phase -periodontal maintenance (intervals to count as of initial periodontal therapy) |
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Definition and pupose of reevaluation
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-evaluation or assessment of tx
-determine the effectiveness of scaling and root planing and other procedures: plaque control, probing depth, CAL, BOP, tooth mobility, furcation involvement -consider re-instrumentation, if needed -consider entering surgical phase of periodontal therapy -make sure there is no calculus left behind |
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What is the ADA code to be used at UNC SOD for the reeval of intial therapy?
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Reeval: 0170
limited evaluation of problem focused evaluation NO charge for this procedure |
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Scaling and Root Planing
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-time interval: 4-8weeks
pocket reduction after root planing: -initial reduction (week 1) associated with gingival recession -secondary reduction (weeks 2-4) associated with gain in clinical attachment |
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Plaque control and BOP
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-plaque accumulation can be visible in 12 hours in some inividuals and easily seen in most individuals by 24-48 hours
-gingivitis can developin 10-21 days -gingivitis can be reversed in approximately 7 days |
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Tooth mobility: occlusal factors
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-abnormal tooth mobility decreases in approximately 30 days after SC&RP and occlusal adjustment
-longer time may be needed for definitive assessment |
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furcation involvement
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-normally expect a lesser response when evaluating furcated teeth
-due to dificult access to furcation areas, expect little or no chagnes after scaling and root planing |
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Histology Junctional epithelium
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-reepithelialization of gingival wounds occur within 1-2 weeks after SC&RP
-percentage of surfaces with residual calculus after SC&RP ranges from 17% to 69% |
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Histology Gingival Connective Tissue
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-at 2 weeks the granulation tissue is still immature and not yet replaced with collagen fibers
-it takes between 4 to 8 weeks to see more precisely oriented collagen bundle fibers |
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Outcome of therapy
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1. Gingival recession
2. reduction of PD and slight gain in CAL 3. Reduced BOP 4. Radiographic bone fill |
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What is the goal (percentage of sites with plaque) to consider that a patient is performing adequate plaque control?
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20%
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What is the meaning of BOP?
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-Inflammation
-30% chance of disease progression when there is bleeding -if no bleeding 100% predictor for stability- disease is not getting worse |
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Expectations of Tx Response probing depth and attachment changes
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-inital probing depth <3mm: will have .5mm PD reduction and -.5mm attachment change
-intial probing depth 3-6mm: will have 1-1.5mm PD reduction and -.5/+ .5mm attachment change -initial probing depth 7- >10 mm will have 2.5-5mm PD reduction and +.5/+2.0 mm attachment change |
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Microbiology
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-repopulation of pockets with large numbers of pathogenic spirochetes and motile rods takes 4-8 weeks
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Key points for Re-eval
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-After SC & RP connective tissue repari continues for 4-8weeks
-Subginigval microbial repopulation occurs within 2mo. after instrumentation of perio pockets in the absence of improved plaque control -longer than 2 mo. may be too long to wait for reeval because bacteria have already repopulated -Reeval- ideally at 4-8 weeks after last quadrant of ScRP -reeval of tooth mobiliy after occlusal therapy is 6-12 months |
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Decisions for future care
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-tx of most periodontal problems is in th hands of the general dentist
-advanced problems require specialized tx |
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Specialty care
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-PD >/= 5mm
-severe alveolar bone loss -tooth hypermobility -difficulty for scaling and root planing access -extensive multidisciplinary cases -severe medical compromise |
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Summary on cosideration for surgical needs
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-only with moderate or Severe periodontitis
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when should the dentist perform definitive and more involved restorative care in relation to periodontal therapy ?
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-periodontal areas should be stable
-this is very important |
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Sequence of Perio treatment phases
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-phase I
-reevaluation -Phase IV (maintenance) - either Phase II (perio surgery) or Phase III (restorative) -always enter code D0170(reevaluation) as part of the treatment plan -Maintenance should start right after to reevaluate your patient |
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Classes of Perio patients
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-first year
-class A -Class B -Class C |
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First year class perio patient recall intervals
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-routine therapy and uneventful healing, recall 3months
-difficult case with complicated prosthesis, furcation involvement, poor crown to root ratios, or questionable pt. cooperation (1-2 month recall) |
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Class A recall interval
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-excellent results well mainained for 1 yr or more. Displays good oral hygiene, minimal calculus, no occlusal problems, no complicated prostheses, no remaining pockets and not teeth wiht less than 50% alveolar bone loss (6 month to 1 year recall)
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Class B recall interval
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-generally good results maintained reasonably well for 1yr or more, but pt displays some poor prognostic factors (3-4 month , decide based on number & severity of negative factors)
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Factors that impact the prognosis of perio negatively
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-poor oral hygiene
-heavy calculus formation, -systemic disease predisposing to perio, remaining pockets -occlusal problems -complicated protheses -ortho therapy -recurrent decay -teeth with 50% bone loss -smoking -positive family or genetic factors ->20% BOP for pockets |
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Class C recall interval
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- generally poor results after perio therapy &/or several negative factors (1-3 months recall, decide based on number and severity of negative factor, consider re-treating some areas or extracting several involved teeth)
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Periodontal supplemental diagnostic tests
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-salivary components
-Gingival crevicular fluid (GCF) -Genetic test -Bacterial profile -gingival temperature -volatile sulfur compounds -imaging |
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Maintenance Recall Part I: Examination
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-approximate time 14mins
-pt greeting -medical history review/changes -head and neck exam -assessment or oral hygiene -gingival status/changes -probing depths/ attachment level -tooth mobility/occlusal analysis -dental caries -status or restorations, prosethsis over teeth and implants |
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Maintenance Recall Part I : Treatment
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-approx time 36 mins
-oral hygiene reinforcement -scaling and localized root planing as needed -polishing -consider fluoride treatment and locally delivered antimicrobials |
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Patient Compliance with maintenance therapy
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-only 16-17% of patients follow the recommended interval for recall
-~50% do not come regularly -patients in university-based programs have had a drop out rate (non-compliance) f 11%- 45%, in private practice complete compliance was seen in one third or less of patients |
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Maintenance Recall Part III: Report, cleanup, scheduling
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-Approx time 10 mins
-progress note -clean and disinfect operatory -schedule next perio maintenance visit -schedule further perio treatment if needed -schedule or refer for additional dental work |
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Exam needed for Caries or high risk for caries
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-Posterior bitewing exam and 12 to 18 month interval
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Exam for caries lacking high risk factors for caries
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-Posterior bitewing exam at 24 to 36 month interal
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Exam for periodontal disease with poor control
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-PA and/or bitewing xrays of problem areas with 12-24 months, FMS every 3-5 yrs
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Exam for history of periodontal disease with current good control
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-bitewing exam with 24-36 months, FMS every 5 yrs
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Exam for dental implants
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-PA or vertical bitewing radiographs at 6, 12, and 36 months after placement, then every 36 months unless clinical problems arise
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Exam for transfer periodontal or implant maintenance pts
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-FMS if a current is not available
-if FMS is approx 24 months old new radiographs of implants and preio problem areas should be taken |
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Increased Mobility possible Causes
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-increased inflammation
-poor oral hygiene -subgingival calculus -inadequate restorations -poorly designed prostheses -systemic disease modifying host response to plaque -occlusal trauma/discrepancies and interferences 0 |
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Gingival recession possible causees
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-toothbrush abrasion
-inadequate band of keratinized gingiva -frenum pull -orthodontic treatment |
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Increased mobility with no change in PD, CAL or radiographic bone loss possible causes
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-occlusal trauma caused by lateral movement occlusal interference, bruxism, high restoration
-poorly designed or worn-out prosthesis -poor crown to root ratio |
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Increased PD with no radiographic change possible causes
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-poor oral hygiene
-infrequent recall visits -sub-g calculus -mesial inclination into endentulous space -poorly fitting RPD -Failure of perio regeneration surgery -cracked/fractured tooth -root grooves -newly developed perio disease -drug induced gingival overgrowth |
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Increased PD with radiographic bone loss possible causes
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-poor oral hygiene
-sub-g calculus -inadequate or deteriorating restorations -infrequent recall visits -root grooves -inadequate surgical outcome -systemic disease modifying host response to plaque -cracked/fractured teeth -newly developed perio disease |
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Perio statistics
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-about 80% of population will have moderate progression of disease
-about 10% will have little or no disease at all regardless of country -about 10% will have sever perio disease - if you reside in a developed country with access to care you are more likely to not loose much bone or attachment, the opposite is true for undeveloped countries |
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Causes for tooth loss after complete active perio treatment
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-periodontitis
-caries -trauma -endo complications -root fracture |
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Teeth more prone to be lost with severe perio disease
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-maxillary 2nd molars
-maxillary 1st molars -trifurcation of the roots -maxillary bone is not as dense as mandible -more type 4 bone is maxilla |
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Teeth lease likely to be lost with sever perio disease
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-,mandibular anterior teeth including canines
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Gender and Smoking percentages
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-23.5% of men smoke
-17.9% of women smoke |
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Age and smoking percentages
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-21.8% of adults aged 18-24 yrs
-24.0% of adults ages 25-44yrs -21.9% of adults ages 45-62 yrs -9.5% of adults aged 65+ |
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Race/Ethnicity and smoking percentages
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-23.2% of american indians/alaska natives
-21.3% of blacks/non hispanics -14.5% of hispanics -22.1% of whites/non-hispanics |
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Education and smoking percentages
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-49.1% of adults with GED dipoloma
-33.6% of adults with 9-11 years of education -11.1% of adults with an undergrad college degree -5.6% of adults with grad college degree |
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Poverty status and smoking percentages
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-31.1% of adults who live below poverty level
-19.4% of adults who live at or above the poverty level |
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Smoking Epidemic
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-highest prevalence of smoking is clustered in the midwest and southeast
-lowest in the west |
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Smoking facts
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-43.4 million smokers in US
-approx 450,000 deaths/yr in US due to smoking -In Europe 29% of population are smokers -globally smoking kills 1:5men and 1:20 women over 30 -harmful to almost every organ in the body -associated with multiple disease -decreases quality and expectancy of life |
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Gas Phase of Smoking
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-carbon monoxide
-ammonia -formaldehyde -hydrogen cyanide |
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Known carcinogens
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-benzopyrene
-dimethylnitrosamine |
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Nicotine
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-highly addictive
-causes rise in blood pressure -increases HR and RR -causes peripheral vasoconstriction |
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How to assess smoking status
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-current smokers: pack-year=#of packs smoked per dayX # of years smoking
-Former smokers: ( how much they use to smoke, how may years they smoke, when they quite) |
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Effects of smoking on prevalence & severity of perio diseases
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- decreases gingival inflammation and BOP
-Increase prevalence and severity of perio distruction -Increased pocket depth, attachment loss, and bone loss -Increase rate of perio destruction -Increase prevalence of severe perio -increased tooth loss -increased prevalence with increased number of cigarettes smoked per day -decreased prevalence and severity with smoking cessation (5 yrs after quitting is when you start to see perio improvement) |
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Effects of smoking on the etiology and pathogenesis of perio disease Microbiology
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-no effect on rate of plaque accumulation
-Increased colonization of shallow perio pockets by perio pathogens -increased levels of perio pathogens in deep perio pockets |
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Effects of smoking on the etiology and pathogenesis of perio disease Immune-inflammatory response
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-altered neutrophil chemotaxis, phagocytosis, and oxidative burst
- increased TNF alpha and PGE2 in GCF -Increased neutrophil collagenase and elastase in GCF -increased production of PGE2 by monocytes in respones to LPS |
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Effects of smoking on the etiology and pathogenesis of perio disease physiology
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-decreased gingival blood flow with increased inflammation
-decreased GCF flow and BOP with increased inflammation -decreased sub-g temp -increased time needed to recover from local anesthesia |
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Effects of smoking on response to perio therapy Nonsurgical
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-decreased clinical response to root surface debridement
-decreased reduction in pocket depth -gain in clinical attachment levels -decreased negative impact of smoking with increased level of plaque control |
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Effects of smoking on response to perio therapy Surgery and implants
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-decreased pocket depth reduction and decreased gain in clinical attachment levels after access flap surgery
-increased deterioration of furcations after surgery -decreased gain in clinical attachment levels, decrease bone fill and increased recession and membrane exposure after GTR (perio regeneration technique) -decreased pocket depth reduction after bone graft procedure -increased risk for implant failure and perioimplantitis |
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Effects of smoking on response to perio therapy maintenance care
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-increased pocket depth and attachment loss during maintenance therapy
-increased disease recurrence -increased need for re-treatment -increased tooth loss in smokers after surgical therapy |
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Effects of smoking cesation on perio treatment outcomes
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-shift towards less pathogenic bacteria
-recovery of gingival micro-circulation -improved immuno-inflammatory responses |
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Reasons for changing in managing perio disease in smokers
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-smoking is major risk factor for perio disease
-may be responsible for greater than or equal to 50% of perio in US -Approx 10-15% of smoker adults have sever chronic perio |
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Helping patients quit smoking
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-Smoking cessation must be part of management
-interventions in dental practive do have a positive impact -brief intervention programs re beneficial |
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5A's
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-Ask
-Advise -Assess -Assist -Arrange |
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5R's
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-Relevance
-Risks -Rewards -Roadblocks, -Repetition |
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Methods for Smoking Cessation
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-set a quit date
-will power alone -self-help materials -brief intervention program in primary care -nicotine replacement therapy (NRT) -bupropion -other methods |
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evidence Based Dentistry
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-an approach to oral health care that requires the judicious integration of systematic assessments of clinically relevant scientific evidence, relating to pt's oral and medical condition and history with the dentists's clinical expertise and the pt's treatment needs and preferences
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Four components of Evidence Based dentistry
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-scientific evidence
-experience and judgement -patient preferences or values -clinical patient circumstances |
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levels of evidence
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From lowest to highest:
-in vitro studies -animal research -ideas, editorials, opinions -case reports -case control studies -cohort studies -randomized clinical trials -systematic reviews(meta-analysis) *better ability to control bias and demonstrate cause and effect |
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Evidence based practice
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-uses best evidence
-systematic appraisal of quality of evidence -objective, transparent, less biased -acceptance of levels of uncertainty |
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Traditional practice
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-unknown bias of evidence
-limited/incomplete appraisal of quality of evidence -subjective, opaque, potentially biased -black and white conclusions |
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Barriers to Change
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-Time
-access -complexity of information |
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ADA Accreditation Standards for Dental education programs
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-develop specific core competencies that focus on the need for graduates to become critical thinkers, problem solvers, consumers of current research, lifelong learners
-teach students to find, evaluate and incorporate current evidence into decision making |
