Perio Test 1 Flashcards
(247 cards)
1
Q
ASA I
A
No systemic disease. Healthy. No organic, physiologic or psychiatric disturbance. Excludes the very young and the very old. Healthy with good exercise tolerance.
2
Q
ASA II
A
Mild systemic disease. No functional limitations. Has a well-controlled disease of one body system. Diabetes or hypertension without systemic effects. Cigarette smoking without COPD, mild obesity and pregnancy.
3
Q
ASA III
A
Severe systemic disease limiting activity, but not incapacitating. Some functional limitation. Has controlled disease of more than one body system or one major system. No immediate danger of death. Controlled CHF. Stable angina. Old heart attack. Poorly controlled hypertension. Morbid obesity. Chronic renal failure. Bronchospastic disease with intermittent symptoms.
4
Q
ASA IV
A
Severe systemic disease with constant threat to life. Has at least one severe disease that is poorly controlled or at end stage. Possible risk of death. Unstable angina. Systemic COPD. Symptomatic CHF. Hepatorenal failure.
5
Q
ASA V
A
Moribund patient not expected to survive the next 24 hours without surgery. Imminent risk of death. Multiorgan failure. Sepsis syndrom with hemodynamic instability. Hypothermia. Poorly controlled coagulopathy.
6
Q
ASA E
A
Patient requiring emergency surgery of any kind.
7
Q
What are smokers and pregnant women considered on the ASA classification?
A
ASA II.
8
Q
What is the most stable assesment for glucose?
A
Glycated hemoglobin.
9
Q
What are other glucose tests?
A
Fasting plasma glucose, postprandial plasma glucsose.
10
Q
What are the high risk areas in the mouth?
A
Floor of the mouth, lateral border of the tongue and ventral surface of the tongue.
11
Q
What is the prevalence of palato radicular grooves on all teeth and on lateral incisors?
A
All teeth 8.5%. On lateral incisors 4.4%
These teeth have questionable prognossis because they harbor bacteria and you often can’t get rid of them.
12
Q
What are the prevalence of Cervical enamel projections?
A
Mandibular molars: 28.6%
Maxillary molars 17.0%
Projections of enamel beyond the CEJ to the root. CT can’t properly attach to enamel surface so the area is susceptible to bacteria.
13
Q
What gives color to gingiva?
A
Vascualrity. Thickness and keratinization. Pigment containing cells.
14
Q
What happens to the color of ginigiva in disease?
A
White or red.
15
Q
What determines to the size of gingiva?
A
Cellular and intracellular elements.
16
Q
What happens to the size of gingiva in disease?
A
Increases and decreases, depending on the stage and the type of disease.
17
Q
What determines the contour/shape of the gingiva? What happens in disease?
A
Location of the proximal contact. Loses the knife edge and becomes blunted.
18
Q
What determines the consistency of gingiva?
A
Collagenous lamina propria.
19
Q
What determines the texture of gingiva? Is it an indicator of health?
A
Epithelial connections. Stippling. No.
20
Q
Biologic depth
A
Distance from the GM to the base of the pocket.
21
Q
Probing depth
A
Distance to which the probe penetrates into the pocket.
22
Q
In health, where does the probe stop? In disease?
A
Health: at the apical extent of the junctional epithelium.
Disease: Extends past the apical extent of the junctional epithelium.
23
Q
What factors influence probing depth?
A
Inflammation. Probing force. Calculus. Location. Angulation. Probe design.
24
Q
Clinical Attachment Level.
A
Distance between the base of the pocket and the CEJ.
25
What are the classes of mobility under the Miller Index?
Class 1: Mobility > normal.
Class 2: Less than 1 mm of mobility in any direction.
Class 3: More than 1 mm mobility, rotation and depressible.
26
How does bleeding frequencies predict disease?
If the patient had a bleeding frequency of greater than 75%, it predicts disease is only 24% of the time. It isn't that reliable of an indicatior. HOWEVER, the absence of BOP was a reliable sign of health.
27
What does suppuration on progbing mean?
A local PMN reaction to an ifection. High specificity and low sensitivity. Meaning, all disease sites don't suppurate, however if there is suppuration it isn't healthy. The predictive value is 40-50% for future attachment loss. ABSENCE OF SUPPURATION IS NOT A GOOD PREDICTOR OF STABILITY.
28
What is the best way to determine whether or not a site is losing attachments?
COMBINE INFORMATION such as probing depths and BOP.
29
What is the PSR?
Periodontal Screening and Recording. This is screening the sextants of the mouth and giving each sextant a single score to determine if our patients need a full blown perio exam.
30
What probe do you use for the PSR?
The WHO.
31
What do you record during the PSR?
The deepest pocket depth and other findings per sextant.
32
PSR Code 0
The probe's colored band remains completely visible. Ginigiva is healthy and no BOP. No calculus or defective margins. Only require appropriate preventative care.
33
PSR Code 1
The colored band is completely visible. No calculus or defective margins. Some BOP. Treatment includes subgingival plaque removal and oral hygiene instructions.
34
PSR Code 2
Probes band is completely visible. BOP. Supragingival or subgingival calculus and defective margins are found. Treatment is plaque and calculus removal, correction of margins and oral hygiene.
35
PSR Code 3
Colored band is partially submerged. INDICATION OF COMPREHENSIVE PERIO EXAM (CPE) and charting of the affected sextant to determine the necessary treatment plan. 2 or more sextants of code 3 mean a full mouth CPE.
36
PSR Code 4
The colored band completely disappears. Depth greater than 5.5. Comprehensive full mouth perio exam is needed.
37
What numbers do you report for a PSR exam?
For each sextant you forget the lower numbers and only use the highest number for each sextant. You only record and report the maximum code per sextant.
38
What does an asterisk mean in the PSR?
If you see the following abnormalities: Furcation involvement. Tooth mobility. Mucogingival problems. Gingival recession extending to the colored band of the probe or greater. Regardless of the PSR score, a patient with any of the above need a CPE.
39
How do you calculate the Clinical Attachment Level?
Probing depth + FGM
40
Grade I Furca
Incipient
41
Grade II Furca
Furcal bone loss, not through and through. You can feel the "roof"
42
Grade III Furca
Through and through, but not clinically visible.
43
Grade IV Furca
Through and through and visible clinically.
44
What do you align the bur with?
The long axis of the tooth.
| NO PENDULUM MOVEMENT.
45
What provides the majority of the resistance and retention form?
The internal form. An oclusal dovetail is used to resist proximal displacement.
46
What is the ideal degrees of taper?
~16 degrees. Bur alone doesn't provide enough.
47
When is a occlusal dovetail used and why?
Required for both additional resistance and retention form for 2 surface preparations such as MO or DO. It mechanically locks it in.
48
Draw, Line of Draw and Draw Variance
Line of draw is the path it takes. If the daw and line of draw aren't the same, then you have draw variance. This becomes a problem in the proximals because you block yourself out with the adjacent tooth.
49
What is the Entrant Angle?
The angle where the occlusal wall joins the proximal wall. It is the only occlusal angle which MUST be beveled. Formed at the point angle created by the primary bevel, secondary bevel and the occlusal surface. Beveled at a 45 degree angle using the 7901 bur.
50
The Occlusal Bevel
Not routinely placed because you need a gold margin angle of 30-45 degrees. Not placed unless the restoration will benefit.
51
What is the Full-tapered Slice Box?
The proximal surface is "sliced" with a "safe-sided" diamond disk. It is an aggressive reduction.
52
What is the modified bevel?
Used at UCSoDM. Performed with diamond points or finishing burs. There is a continuity of proximal bevel and gingival bevel.
53
What is the proper secondary bevel?
An exaggerated bevel angle. There is greater reduction at the occlusal than the gingival.
54
What is a common mistake when making the proximal bevel?
Failure to correctly remove the proximal tooth surface resulting in an undercut.
55
Where do you remove more tooth structure?
More tooth structure at the occlusal than the gingival.
56
What degree should the bevel be placed to permit a gold margin at the gingival bevel? What tools are used?
30-45 degrees. Gingival margin trimmer, needle, flame finishing or diamond bur.
57
Where do you place depth cuts and how do you know how deep?
Lingual incline of the buccal cusp and buccal incline of the lingual cusp. Depth determined by cusp being reduced, whether or not it is a functional cusp.
58
What should the buccal shoulder wall be parallel to?
The lingual occlusal wall of he inlay preparation. Tilting the bur too far toward the lingual will reduce retention form. The further away you are from parallel, the less the retention.
59
What are the dimensions of the buccal shoulder?
Should follow the flow of the cusps. The axial depth should be 1 to 1.5.
60
When are onlays indicated?
When you have a previous shallow restoration that ruins the occlusal structure of the tooth.
61
What is a provisional restoration?
An interim restoration placed in/on a tooth preparation during the fabrication of the final restoration.
62
What is the purpose of provisional restorations?
Pulp protection. Hard and soft tissue protection. Prevent tooth movement. Esthetics. Strength and rigidity to withstand functional forces.
63
What is IRM?
A powder and a liquid reinforced with zinc oxide and eugenol. 1:1 ratio. Mix on a paper or parchment pad. NO GLASS OR PLASTIC SLAB.
64
What is important to remember when preparing the matrix?
LUBRICATE the band, but NOT the preparation.
65
What is the consistency you want for your IRM?
It needs to be rolled into a ball with your gloved fingers without sticking.
66
Do you overfill IRM?
No. put powder on the tip of the condenser.
67
Do you use rotary instruments with IRM?
No. easy to destroy margins.
68
Lamina Dura
Cortical bones lining the walls of the socket. Also called bundle bone or cribriform plate. Presence or absence is not an indicator of disease, but presence is an indicator of health.
69
Alveolar Crest
The healthy distance from the CEJ to the Alveolar Crest is 1-2 mm. Greater than 2 mm means periodontal bone or attachment loss.
70
PDL Space
Radiolucent line that runs around the teeth that denotes the space. Can just be an artifact, isn't a reliable indicator of disease.
71
Trabeculation
The spiderweb. Isn't an indicator of periodontal disease, but it does react to excessive forces on teeth.
72
Sinuses
Seen in maxillary. Infections can cause problems due to proximity. Can arise both from the teeth and the sinus.
73
Interdental Septa
Dependent on the proximal contours of teeth. You want it to be within 1-2 mm of the CEJ. Can be used to determine what type of bone loss is occurring.
74
What percent of bone loss needs to be present to be visualized radiographically?
30-50 % of bone mineral needs to be destroyed.
75
How long before you can see the bone loss radiographically?
Clinical attachment loss precedes radiographic bone loss by 6-8 months.
76
How much do x-rays underestimate bone levels and defect depths by?
Approximately 1.4 mm.
77
Horizontal Bone Loss
When you connect the CEJ's of adjacent teeth, look to see if the alveolar crest lines are parallel.
78
Vertical Bone Loss
Alveolar crest is NOT parallel to the lines connecting the CEJs. Favorable for regenerative procedures.
79
Circumferential bone loss
Considered a type of vertical bone loss. Wraps around the tooth like a half moon. Isn't always visible on a radiograph.
80
Furcation defect
You can see a small dark space at the furcation area. Usually underestimate damage on radiographs. It is very hard to diagnose a furcation invasion. It takes a combination of clinical and radiographs. But even together, it is still very low percentage of diagnosis.
81
What is the Furcation Arrow?
A small triangular radiographic shadow across the mesial or distal roots of the maxillary molars. It is a helpful diagnosis indicating furcation involvement. (Grad II or III, but never I). Absence does NOT mean absence of furcation involvement. Presence is a good indicator absence is not a sign of health.
82
Bottom line, what is the best way to diagnose a furcation?
Radiographs, clinical probing and furcation sounding with anesthesia should all be used together to correctly diagnose furcation invasion.
83
Calculus
Even if calculus is not present on a radiograph, it does't mean it isn't in the patients mouth.
84
Defective restorations
Look for overhang. 32-90% have restoration overhangs. Overhanging amalgams are associated with bone loss. Removal of amalgam overhangs during periodontal initial therapy reduce gingival inflammation.
85
Molar Root Trunk Length
Distance from the CEJ until the point that roots divide. Takes longer to expose the furcation, the longer the root.
86
Maxillary Root Trunk Length
Short-3 mm
Medium-4 mm
Long- Greater than 5 mm
87
Mandibular Root trunk length
Short-2 mm
Medium-3mm
Long-Greater than 4 mm
88
Crown to Root Ratio
The larger the root, the more support you have.
89
Root proximity
The closer roots are to each other, the thinner the bone and the faster the progression of disease because you have less bone to lose.
90
What are the signs of trauma from occlusion?
Widened PDL. Decreased definition of the lamina dura. Bone loss. Altered trabeculation. Hypercementosis. Root fractures or cemental tears.
91
What are signs of implant failure?
Clinical mobility. Radiographic peri-implant radiolucencies. More than 0.2 mm of annual bone loss following the first year. Pain, infection, paresthesia or violation of the mandibular canal.
92
Why is panoramic radiography have a limited use in periodontics?
Underestimates small osseous defects. More accurate with moderate destruction, but overestimates severe bone loss.
93
What is subtraction radiography?
Requires two identical images that you overlap the densities and compare bone loss. Used mostly in research. Can detect a 0.5 mm change, but error happens when there is differences in the alignment of images.
94
What are the potential applications of subtraction radiography in periodontics?
Detection of bone loss in active periodontal disease and implants. Detection of bone apposition in regeneration. Detection of early bone changes that occur following a root fracture.
95
Computed Tomography
CT scan. Uses x-rays to generate detailed images of slices of the body. High radiation exposure.
96
Cone Beam Computed Tomography
A lot less exposure than conventional CT scan and a lot higher resolution. Used in implant cases.
97
What are the magnification of radiographs?
7% for periapicals and bitewings. 26% for panoramic radiograph. Panoramic has greater magnification and is not used for diagnosis.
98
Horizontal Bitewings.
Every 1-2 years. Used in adolescents to diagnose caries.
99
Vertical Bitewings
Every 2 years. Used over the age of 30. Use to diagnose periodontal disease and periapical pathology.
100
Panoramic radiograph.
Screening tool for all age groups. Single film survey.
101
What is the ALARA principle
As low as reasonably achievable.
102
What type of x-rays to you prescribe for an intraoral full mouth series for comprehensive periodontal evaluation for adults?
Vertical bitewings.
103
When do you use a panorex?
For periodontal screening, 3rd molar presence, implant diagnostics, impacted teeth, pathology evaluation.
104
What do you use for single site implant imaging?
Periapical or CBCT.
105
What do you use for multiple site implant imaging?
CBCT.
106
X-rays during pregnancy.
Most desirable to not have irradiation during pregnancy especially during the first trimester. The protective apron renders fetal radiation virtually immeasurable. Use x-rays selectively and only when necessary.
107
What are the limitations of radiographs?
2-D view of a 3-D structure. Does not show presence or absence of periodontal pockets (soft tissue). Only suggests morphology of bone deformities. No info on tooth mobility. Can't distinguish treated from untreated cases. Position and condition of facial or lingual structures is obscured. Does not demonstrate soft-tissue-to-hard-tissue relationships. Doesn't show success or failure of treatment. RADIOGRAPHS MUST BE SUPPLEMENTED BY CAREFUL CLINICAL EXAMINATION.
108
What is the primary factor in periodontal disease?
PLAQUE. Always present, but not sufficient to cause periodontist by itself. It needs contributing factors.
109
What is the composition of plaque?
80% water. Microbes. Host cells. Glycoproteins. Inorganic materials and polysaccharides.
110
What are the steps of plaque formation.
Scaffold of glycoproteins forms on the acquired pellicle. Initial colonizers begin colonization by attaching to the scaffold. Proliferation. Aggregation with other microbes. Alteration of composition.
111
What are some past beliefs of what caused periodontal disease?
Normal aging. Necrosis of infected bone. Systemic disease. Disharmony of occlusion. Calculus or hard toothbrushes.
112
Non-specific plaque hypothesis
Noxious products from plaque. It isn't a specific bacteria, but the amount of plaque. Volume overwhelms the host. Control accumulation and you control the disease. QUANTITY.
113
Specific Plaque Hypothesis
Only certain plaque is pathogenic. Specific organisms carry the pathogenicity and mediate the destruction of host tissues. QUALITY.
114
What hypothesis is most of our current treatment based off of?
Non-specific. Eliminate plaque=eliminate disease. However, we now believe there is more to the process than either hypothesis answered.
115
Describe the pathogenesis of periodontal disease.
Bacteria colonize the sulcus. Plaque QUANTITATIVELY increases. QUALITATIVE shift to G- anaerobes. Inflammatory mediators release resulting in inflammation.
116
What are the three phases of inflammation?
Vascular phase: Blood vessels proliferate increasing blood supply, capillary permeability and GCF.
Cellular phase: Movement of PMNs, Macs, T lymphs and B lymphs.
Humoral Phase: B lymphs differentiate into plasma cells and produce antibodies and cytokines.
117
What are the virulence factors of plaque?
Allow colonization, evasion and destruction. Leukotoxin. Epitheliotoxin. Pili/Fimbriae. Capsule/Slime layer. Tissue invasion. Enzymes. Endotoxin/LPS.
118
How do biofilms affect disease?
Create interacting bacterial communities that enhance protection and nutrition.
119
What are the virulence factors of Aggregatibacter actinomycetemcomitans? AKA AA
G-. Endotoxin/LPS. Non-motile. Capnophilic. Coccobacillus. Tissue invasion. Leukotoxin. Collagenase. Epitheliotoxin. Elicits host immune response.
PRESENT IN 97-100% of Localized Aggressive Periodontitis patients.
120
Porphyromonas gingivalis. AKA P. gingivalis.
Gram -. Endotoxin. LPS. NOn motile. Anaerobic bacillus. Leukotoxin. Collagenase. Proteases. Ammonia. Capsuule. Pili/fimbriae. Elicits host response.
121
What are the Red Complex bacteria?
P. gingivalis, Treponema denticola, and tannerella forsythia.
They have a very strong relationship with an increase in probing depth and BOP.
122
What microbe is associated with pregnancy?
Prevotella intermedia.
123
What other microbes are associated with periodontitis?
p. intermedia. Campylobacter rectus. Micromonas micra. Capnocytophaga sp. Fusobacterium nucleatum. Herpes viruses and cytomegalovirus.
124
What constitutes a susceptible host?
Genetics (IL-1 genotype). Altered Ab or Ig. PMN or macrophage dysfunction.
125
What is calculus?
A secondary factor. Always coated with plaque. It is a calcification of bacterial plaque. Porous. Attaches to tooth. Broadens the sphere of influence of plaque.
126
Supragingival plaque
Impedes OH (oral hygiene). Niche for bacteria. Forms rapidly. Heterogenous crystals. Mineralized by saliva.
127
Subgingival plaque
Hard. Tenacious. Niche for bacteria. Extends the radius of bacterial destruction. Slowly forming. Homogenous crystals. Mineralized by GCF.
128
Smoking
Dose dependent risk factor. Consumption, duration and lifetime exposure associated.
129
How does smoking affect LOA?
Increases loss of attachment by 2.05-4.75 times
130
How does smoking affect bone loss?
Increases by 3.25-7.28 times.
131
How does smoking affect calculus and PD?
Increases.
132
How does smoking affect periodontitis?
More prevalent and severe.
133
How does smoking affect fibroblasts?
Altered attachment.
134
How does smoking affect circulating Ab's?
Decreased. Protective response of Ab is lost.
135
How does smoking affect PMN chemotaxis and phagocytosis?
Decrease.
136
How does smoking affect gingival blood perfusion?
Decrease.
137
How does smokeless tobacco use affect the mouth?
Increase in gingival recession and attachment loss. Mechanical and chemical injury. Decrease gingival blood flow.
138
Traumatogenic Occlusion
Can be primary or secondary trauma. It doesn't initiate the diseases, but does play a secondary role in the progression of disease.
139
Traumatogenic toothbrushing.
LOA, gingival recession and loss of tooth structure. Hard brush and horizontal scrub motion are the bad guys.
140
Overhanging restorations
Occur in 32-90 percent of patients. Reduces ability to perform OH adequately. Not a problem if greater than 5 mm from the bone. Greater bone loss if greater than 20% of interproximal surface.
141
Open contacts and food impaction.
OC are correlated to FI and FI is correlated to PD but because OC is not correlated to PD. There are steps in between.
142
At what grade of Cervical Enamel Projections do you expect attachment loss?
Grade III.
| If there is furcation invasion, AL is associated.
143
What percent of molars have Cervical enamel projections?
Mand: 28.6%
Max: 17%
144
Where are enamel pearls most often found?
Maxillary 2nd and 3rd molars.
145
How do enamel pearls contribute to Periodontal disease?
No CT attachment to pearls. Associated with furcation invasions.
146
Palato-radicular grooves.
On 4.4% of maxillary laterals. "highway" for bacteria. Associated with increased GI, PD, Pl and mobility.
147
3rd molars
Periodontal healing impaired over age of 30. Greater incidence of intrabony defects greater than 4 mm distal to 2nd molars over the age of 26. Early removal is beneficial.
148
Marginal ridge discrepancies
MRD in posterior teeth is correlated with increased pd, loa, pi, gi and calculus. Health maintainable with good OH and treat with orthodontics.
149
Malocclusion
Increase in PI, GI and PD with non aligned surfaces. Health maintainable with good OH.
150
Root Pathology
Fractures or perforations. Endodontic stripping. Restorative pin placement.
151
Drug induced gingival enlargement
Severity related to plaque control. There is an increase in fibroblasts, collagen formation. To fix it, stop taking the meds.
152
What meds do you have a risk for DIGE?
Phytoin. Cyclosporin. Calcium Channel blockers.
153
What is the current disease model?
Bacteria, environment and host factors all work together to cause disease.
154
Plaque induced vs. Non-plaque induced gingival diseases.
Plaque induced is caused by plaque only and is modified by systemic factors, medication and malnutrition. Non-plaque induced originates from a specific bacteria, virus, fungus or is genetic. It can be gingival manifestations of systemic conditions, traumatic lesions and foreign body reactions.
155
Gingivitis associated with dental plaque only.
Most common form. Clinically there is variable color, size, shape, and consistence of the gingiva. Clinically there is erythema, edema, bleeding, ulceration. Rolled gingival margins, loss of stippling and change in composition of plaque.
156
Gingivitis associated with dental plaque and local factors.
Malocclusion, open bite/mouth breathing, oral habits, deviated septum. Clinically there is dry gingiva, shiny erythmatous surface. Rolled gingival margins. Gingival bleeding loss of stippling.
157
What are some systemic factors associated with the endocrine system that affect gingival disease?
Puberty, menstruation, pregnancy, diabetes. Leukemia. Clinically seen as erythema, bleeding and swelling. Leukemia is spontaneous bleeding.
158
Gingival diseases of specific viral origin.
Primary herpetic gingivostomatitis, recurrent oral herpes. Herpes zoster.
159
Gingival diseases of fungal origin
Candida species. Linear gingival erythema. Histoplasmosis.
160
Mucocutaneous disorders
Lichen planus, pemphigoid (bollous, mucous membrane), pemphigus vulgaris, erythema multiforme, lupus erythematosus, drug-induced lichenoid reactions.
161
Allergic reactions
dental restorative materials (mercury, nickel, acrylic), toothpastes, mouthrinses, food and food additives.
162
Early-onset periodontitis EOP
AgP: Aggressive Periodontitis
163
Prepubertal Periodontitis PPP
MSD: Manifestations of systemic disease
164
Localized Juvenile Periodontitis LJP
LAgP: Localized Aggressive Periodontitis
165
Generalized Juvenile Periodontitis GJP
GAgP: Generalized Aggressive Periodontitis.
166
Rapidly Progressive Periodontitis RPP
GAgP: Generalized Aggressive Periodontitis
167
Adult Periodontitis AP
CP: Chronic Periodontitis.
168
Localized vs. Generalized
Localized is less than 30 percent of the sites and generalized is greater. You look at the clinical attachment level.
169
Mild, Moderate and Severe
Mild is 1-2 mm, Moderate is 3-4 mm, Sever is greater than 5 mm.
170
How do you now characterize periodontitis?
Extent, severity, type.
171
Chronic Peiodontitis
Slow process, but not always. Most common and can see at any age. Can be localized or generalized. Increase in severity and prevalence with age. Local factors can make to disease more severe. Normal host immune response.
172
Aggressive Periodontitis
Localized or generalized. Prevalence in 0.9-17%. Rapid, severe periodontal destruction. Local factors often do not commensurate with disease severity. Pathogens are often different from CP. Abnormal host immune response. The primary diagnostic criteria are: Rapid progression. No relevant systemic disease. Familial aggregation.
173
Localized Aggressive Periodontitis
Initially presents BL around incisors and 1st molars. Familial distribution is possible. abnormal PMNS or macs. Generalized lack of local factors. Systemic infections are not common. AA.
174
Generalized Aggressive Periodontitis
Most/All of dentition. Rapid and sever horizontal bone destruction. Acute, fiery-re proliferative gingiva during active face. Abnormal PMNS or macs. SYSTEMIC MANISFESTATIONS: Depression, fever, malaise, infections.
175
NUG
Necrotizing Ulcerative Gingivitis. Punched out papilla. No chronic form. Inflammation, ulceration and necrosis. Pain, pseudomembrane, spontaneous bleeding, fetid odor. Associated with stress, smoking, poor oral hygiene, spirochetes, prevotella intermedia and compromised immunity.
176
NUP
Necrotizing Ulcerative Periodontitis. AIDS and other immunocompromised patients. Often follows NUG. AL with exposure of alveolar bone. Soft tissue necrosis. Rapid destruction of bone. Spontaneous bleeding and deep/aching bone pain. Low survival rate if you also have HIV.
177
Gingival Abcesses
Localized, painful. Rapid growth. No bone loss, limited to marginal gingivae or interdental papilla. 1-2 days. Rupture. Traumatic impaction.
178
Periodontal abcess
Purulent inflammation. Localized from impaired pocket drainage. May result from incomplete removal of calculus or Ab's. Radiographic bone loss. May become chronic and drain through a fistula.
179
Pericoronal Abcess
Localized and associated with an incompletely erupted tooth. Common in the mandibular 3rd molar area. Treatment is excision of the gingivae or extration of the tooth.
180
Endodontic Associated Periodontitis
Combined perio-endo lesions. Pain, percussion tenderness, increased probing depths, swelling, bleeding suppuration, sinus tract formation, mobility angular bone loss.
181
Functional or Physiologic Dentition
A dentition which has adequate number of teeth without the aid of prosthetic reconstruction to maintain the health, comfort, function and esthetics of the patient.
182
Importance of prognosis
How treatment modalities and resources are utilized. Keeps the patient's expectations realistic. Financial impact on the therapist.
183
Diagnostic Prognosis
An evaluation of the course of disease WITHOUT treatment.
184
Prosthetic/Restorative Prognosis
The forecast for success of the prosthodontic restoration given the anticipated results of the periodontal treatment and the periodontal health status obtained.
185
Therapeutic Prognosis
And evaluation of the course of the disease WITH treatment.
Assumptions: We perform the most appropriate and predictable therapy. Patient maintains good OH and complies with treatment recommendations.
186
Prognosis: GOOD
None to slight attachment/bone loss. Probing depths of 4 mm or less. No mobility to class I mobility. No furcation involvement.
187
Prognosis: FAIR
Slight to moderate attachment/bone loss. Probing depth of 4-6 mm. Class I mobility. Grade I to shallow grade II furcation
188
Prognosis: QUESTIONABLE
Moderate attachment loss. Probing depth 6-8 mm. Class I to Class II mobility. Grade II furcation with good access.
189
Prognosis: POOR
Moderate to severe attachment/bone loss. Probing depth 6-8 mm. Class II mobility. Poor root form. Grade II furcation with poor access or Grade III with good access.
190
Prognosis: HOPELESS
Severe attachement/bone loss. Grade III furcation with poor access. Class II to III mobility. Poor crown/root ratio. Root proximity problems.
191
Prognosis as a function of time.
Can be for overall dentition or individual teeth. Short term: 1-5 years. Long term: 5-10 years.
192
What factors influence the prognosis of functional dentition?
1. Plaque control and maintenance therapy.
2. Age. Better prognosis for the elderly because younger people have a longer time period that you need the teeth to last.
3. History of the disease and the rate of progression.
4. Systemic factors such as drugs and diabetes.
5. Contributing factors such as calculus, traumatogenic occlusion, malposed teeth/uneven marginal ridges, overhangs/ poor margins, frenum pull, smoking, strategic value of the tooth.
193
What factors influence the prognosis of the individual teeth.
1. Periodontal support or defect morphology.
2. Probing depth.
3. Furcations. Grade III is hopeless. The only way you can save them is if they have access to clean and prevent root carries.
4. Local anatomy. Tori/exostoses, external oblique ridge. Shallow vestibular depth.
5. Root sensitivity.
6. Caries.
7. Endo-perio lesions.
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What is the goal of periodontal therapy?
To create an oral environment that is conducive to maintaining the patient's dentition in health, comfort, function and esthetics.
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What is Non-Surgical Periodontal Therapy?
Includes plaque control. Supragingival and subgingival scaling and root planing. Chemical agents, systemic abx, local drug delivery. Host modulation.
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Why use NSPT?
Reduction of inflammation and improvement of clinical parameters. May decrease or eliminate the need for surgery.
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Modified Bass Technique
Gumline at 45 degree angle. Bristles should contact both gums and teeth. No technique has been proven to be superior.
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How far subgingivally do the bristles extend?
0.5-1.0 mm below the gingival margin. Recently found that plaque may advance as far as 0.8 mm into the pocket in 1 year.
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Are powered brushes as effective as manual brushes?
Improved plaque removal ranged from 1.5 times better than the manual on mid-tooth labial surfaces (anterior teeth) to 11.9 times better in the interproximal lingual surfaces (anterior teeth)
200
How well do our patients clean their dentition?
The oral hygiene efforts of most patients result in only an approximate 50% of reduction of plaque from baseline values during and after active therapy.
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How far subgingivally will an interdental brush clean?
As far as 2-2.5 mm below the gingival margin.
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Brush/floss compared to brush/interdental brush.
Brush removes plaque more consistently.
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Waxed vs. Unwaxed
No significant difference.
204
Powered flossers
Evidence of superiority, but there were no significant treatment differences between it and traditional floss. Traditional reduced 8.2-22.9% while powered reduced 19%.
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Rinses
Minimal penetration of pocket (0.2 mm) and minimal application of time.
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Chlorhexidine gluconate
Bisbiguanide compound. Most effective antiplaque agent. No systemic toxicity. Broad action for G- and + organisms. Staining and taste alterations are local side effects reported. Good because there is a prolonged persistence of antimicrobial action (substantivity). Adheres to the tooth and is released over a period of time. Used post oral surgery. Mentally and physcally handicapped. Those predisposed to oral infections. High risk caries patients. Recurrent oral ulcerations. Appliance wearers. Denture stomatitis. Oral malodor. Pre-operative rinsing and irrigation. Subgingival irrigation.
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Limitations of supragingival plaque control alone.
You need to remove subgingival plaque and calculus in order to see significant clinical improvement.
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Scaling
Instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus and stains.
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Root planing
A treatment designed to remove surface dentin that is rough, impregnated with calculus or contaminated with toxins or microorganisms.
210
Prophylaxis
SCALING. D1110. Can be used when gingivitis is present.
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Scaling and rootplaning.
Instrumentation of the crown and root surfaces to remove plaque and calculus. Indicated for patients with periodontal disease. THERAPEUTIC NOT PROPHYLATIC. Has to be some loss of attachment otherwise there would be no exposed root surface to plane. D4341/D4342
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Why do scaling and root planing?
Remove endotoxin. Remove plaque and calculus, disrupt the subgingival biofilm. Reduce inflammation and pocket depth.
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Probing depth less than 3 mm
89% plaque free.
214
Probing depth 3-5 mm
61% plaque free
215
Probing depth greater than 5 mm
11% plaque free.
216
Probing depth 1-3 mm
86% calc free
217
Probing depth 4-6 mm
43% calc free
218
Probing depth greater than 6 mm
32% calc free
219
What are my limitations?
In PDs averaging 6.2 mm the maximum depth free of plaque and calculus is 3.73. Limit of instrumentationion 6.21 mm
220
Hand vs sonic and ultrasonic scalers
Similar periodontal healing respons. Less time is spent with ultrasonic/sonic and produce less tooth surface loss, have better access to deep pockets and furcation areas but the tactile sensitivity is reduced.
221
Sc/RP on PD and AL.
Decreases inflammation and increases AL. Decrease and qualitative shift in bacteria. Healing is by the formation of a long junctional epithelium.
222
How much clinical improvement can we expect?
Initial PD 4-6 mm--->AG of 0.23 mm and Decrease in PD of 0.96 mm.
Initial PD of greater than 7 mm---> AG of .91 mm and Dec. PD of 2.2 mm.
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Furcation entrance diameter.
81% less than 1 mm. 58% less than 0.75 mm. We are using instruments loo large to enter the furcation and clean it.
224
Furcation instrumentation.
Ultrasonics are better when there is a smaller furcation. No difference in a larger furcation.
225
Subgingival Irrigation
Should reach entire pocket and maintained long enough at a sufficient concentration. The crevicular fluid outflow is very high. and the pocket fluid replacement rate is 40x/hr.
226
Limitations of irrigation.
1.8 mm depth at margin. Only .2 mm by rinsing alone. Lack of lateral spread.
227
Conclusions on irrigation
Microorganisms rebound in pocket within 1-8 weeks. Irrigation in conjunction with Sc/RP may or may not produce an additive effect. 50% is eliminated in 12.5 min. THERE IS STRONG EVIDENCE FOR LACK OF AN ADJUNCTIVE BENEFIT.
228
Systemic Abx plus Sc/RP
Impossible to eliminate all pathogens by mechanical therapy. Multiple bacterial reservoirs in the oral cavity increase the likelihood of reinfection. Quadrant by quadrant therapy allows reinfection of treated sites by untreated sites.
229
Systemic vs. Local
Advantages: Simple and easy to multiple sites. Eliminate pathogens on extra-dental sites. Reduces risk for future translocation.
Disadvantages: Can't get high GCF concentrations. Risk of adverse reaction. Increased selection of multiple abx resistant microorganisms.
230
Criteria of effective agents
reach site. Sustain high enough concentration for a long enough time. Kill or inhibit pathogens. Don't harm host.
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Amoxicillin
Broad spectrum penicillin.
Bacteriocidal: beta lactam inhibition of cell wall cross linking. Leading to cell death by osmotic lysis.
People are allergic.
Amoxicillin and Metronidazole for aggressive periodontitis.
Amoxicillin + Clavulanate for refractory periodontal disease.
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Tetracyclines
Broad. Bacteriostatic. Bind 30s ribosome. Effective against G+ aerobes and anaerobes. Several types that are cross reactive. High concentration in GCF. Long term use creates resistance
233
Metronidazole
Bacteriocidal. Uniquely effective against anaerobes. Not big effect against facultative and aerobic bugs.
Resistance is slow to develop except for P.g. in biofilms.
Adverse effect with alcohol. Could be teratogenic.
Used to treat NUG, pericoronitis, apical infections, alveolar osteitis and osteomyelitis.
234
Broad Specturm and Oral contraceptives
affect absorption.
235
Reality
Chronic: Short term benefit.
Aggressive: Better clinical response.
236
Who benefits most?
Deep pockets. Refractory patients. Systemically compromised patients. Acute periodontal. Aggresive periodontitis. Peri implantitis.
237
Actisite Tetracycline FIber
6 mm PD. Esthetic zone. May enhance scrp at non responding sites.
238
Atridox
10% doxycycline hyclade in gel. Refrigerate and removed 15 min prior to mixing. Inhibits proteases stimulated by smoking. Neutralize the neutrophil oxidative burst.
239
Perio chip.
2.5 mg chlorhexadine. gelatin matrix. controleld release. Don't use for abcesses. Attachment gain was greater for ScRP alone and there was greater recession for ScRP + Periochip. No statistical significance.
240
Arestin
minocycline HCL 1 mg. Polymer in powder form. No refrigeration. NO dressing. No mixing. 2 year shelf life.
241
Ideal Patient.
PD greater than 5 mm with persistent BOP. Not a surgical candidate. Refuses surgery. Smoker. Unregenerable site. Esthetic zone. MAINTENANCE PATIENT.
242
Arestin
ADDITIONAL PD REDUCTIONS
243
Periochip
ADDITIONAL CAL GAINS
244
Doxycycline gel
ADDITIONAL CAL GAIN
245
ABX Alone
NO EVIDENCE on the efficacy of local abx used as a monotherapy in patients with no scrp.
246
Periostat contraindications
pregnancy, nursing, allergy.
247
Periostate
Dose not promote resistance, does not alter existing flora. Stops the collagenases.
