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Perio 2 > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

Loe and Silness Plaque Index

A

-assesses the amount of plaque at the gingival margin, examining the same anatomical units as the GI
-Plaque score range from {0} to {3}
-A probe is used to distinguish between scores {0} and {1}. Visible plaque is scored a {2} or {3}
-The Pl-I is computed for a tooth (4 surfaces), subject, or population
-It parallels the Gingival Index (GI) of Loe & Stilness
-First published by Silness & Loe
Problem with PI: very subjective, need a lot of training

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2
Q

Silness and Loe Gingival Index

A
  • The severity of inflammation is assessed in 4 distinct gingival areas: distofacial papilla, facial margin, mesiofacial papilla, lingual gingival margin.
  • Scores: 0 to 3; BLEEDING is considered. Presence of bleeding automatically leads to a score >=2
  • Useful for the calculation of prevalence and severity in population and individual
  • Score for tooth –> subject –> population
  • frequently used index in clinical trials
  • First published by Loe and Loe & Silness

increase PI, increase GI
If you have high GI but low PI – systemic issues?

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3
Q

PSR

A
  • Purpose: periodontal screening and recording is a rapid and effective way to screen patients for periodontal diseases and summarizes necessary information with minimum documentation
  • Endorsement: the ADA and the AAP support the use of PSR by dentists as a part of oral examinations
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4
Q

PSR Codes

A

0 - colored area visible, no calculus or defective margins, no BOP
1 - colored area visible, no calc/defective margins, + BOP
2 - colored area visible, + calc/defective margins, +/- BOP
3 - colored area partially visible, +/- calc/defective margins, +/- BOP
4 - colored area not visible, +/- Calc/defective margins, +/- BOP

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5
Q

PSR Benefits

A
  • Early Detection: PSR includes evaluation of all sites. For this reason, it is highly sensitive technique for detecting deviations from periodontal health and a uniquely appropriate screening tool for periodontal diseases that are, by nature, site specific and episodic
  • Speed: once learned, PSR takes only a few minutes to conduct for each patient
  • Simplicity: PSR is easy to administer and comprehend. The simplicity of the scoring system aids in monitoring a patient’s periodontal status
  • Cost-effectiveness: PSR utilizes a simple periodontal probe designed specifically for use with this screening system. It does not require the use of expensive equipment.
  • Recording Ease: Documentation for PSR requires the recording of six numerical scores, one for each sextant of the mouth. It does not require extensive charting or lengthy narrative explanation
  • Risk Management: Proper, consistent, and documented use of PSR shows that the dentist is evaluation a patient’s periodontal status
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6
Q

PSR Limitations

A
  • PSR is a screening system designed to DETECT periodontal disease. It is not intended to replace comprehensive periodontal examination when indicated.
  • Patients who have been treated for periodontal diseases and are in a maintenance phase of therapy required periodic COMPREHENSIVE periodontal examinations
  • in addition, PSR is designed primarily for use with ADULT patients and has limited utility in screening children and adolescents
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7
Q

Papilla Marginal Attached Index (PMA)

A
  • Background: “The number of units affected correlates with the severity of gingival inflammation”
    • – not talking about bleeding or redness
  • Facial gingival surface is divided in 3 scoring units P - M - A
  • Gingival units affected with gingivitis are counted. Presence or absence of inflammation is counted as {1} and {0}, respectively
  • Severity component can be considered
  • Score computed for tooth –> subject –> population
  • First published by Schour & Massler

incisors, canines, and premolars

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8
Q

NIDR Calculus Index

A

0 - calculus is absent
1 - supragingival calculus, but no subgingival calculus is present
2 - supragingival and subgingival, or subgingival calculus only is present

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9
Q

O’Leary Index

A

Percentage of tooth surfaces positive for plaque

  • what we use in clinic
  • disclose, rinse, then count red surfaces
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10
Q

Gingival Index Scores

A

[0=normal
1=mild inflam, slight color change, no bleeding, edema
2=BOP, moderate inflam, redness, edema 3=severe inflam, marked redness & edema, ulceration, spontaneous bleeding]

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11
Q

Plaque Index Scores

A

0 - No plaque
1 - a film of plaque adhering to the free gingival margin and adjacent area of the tooth. The plaque may be seen only by using the probe on the tooth surface
2 - moderate accumulation of soft deposits within the gingival pocket, or the tooth and gingival margin which can be seen with the naked eye
3 - abundance of soft matter within the gingival pocket and/or on the tooth and gingival margin

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12
Q

Reliability

A

an index to measure a condition in the same subject repeatedly and obtain the same score results each time

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13
Q

Validity

A

sensitivity and specificity of various diagnostic tools used to create an index

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14
Q

sensitivity

A

the probability that a test result will be positive when the test is administered to people who actually have the disease in question
- Pr(T+/D+) :: (+) –> (+)

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15
Q

specificity

A

the probability that a test will be negative when administered to people who are free of the disease in question
ex. no bleeding = healthy
exception = smokers – dont bleed as much
Specificity: Pr(T-/D-)
(-) —> (-)

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16
Q

Positive Predictive Value

A

the probability of disease in a subject with a positive test result
PVP =Pr(D+/T+)

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17
Q

Predictive Value Negative

A

The probability of not having the disease when the test is negative
PNV= Pr(D-/T-)

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18
Q

Gingival lesions of viral origin

A
  • herpes simplex viruses type 1 and 2
  • varicella-zoster virus

Herpes simplex 1 usually causes oral manifestation – main group

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19
Q

primary herpetic gingivostomatitis

A

through oral mucosal epithelium, virus penetrates a neural ending and travels to the trigeminal ganglion (comes back in stress/sickness/etc)

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20
Q

symptoms of primary herpetic gingivostomatitis

A
  • painful severe gingivitis with redness
  • ulcerations with SEROFIBRINOUS EXUDATE
  • edema accompanied by STOMATITIS
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21
Q

Characteristics of primary herpetic gingivostomatitis

A
  • incubation period is one week
  • formation of vesicles, which rupture, coalesce and leave fibrin-coated ulcers
  • healing within 10-14 days
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22
Q

areas where herpes virus can be found

A

gingivitis, necrotizing ulcerative diseases (NUG/NUP) and periodontitis

more primary infections occur at older ages in industrialized society

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23
Q

recurrent intraoral herpes infection

A

in 20-40% of individuals with primary infection

-vesicles will rupture and expose tissue

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24
Q

herpes labialis - recurrent HSV

A

-more than once a year
-recurrent herpes infection
-vermillion border and or the skin adjacent to it
-20-40% of individuals with primary infection
-trauma, UV light exposure, fever, menstruation (immune system down)
DIAGNOSIS:
intra oral lesions generally considered/mistaken for an APHTOUS ulceration (restricted to mouth)
differential diagnosis: aphthous ulcers do not affect keratinized mucosa
-ulcers in attached gingiva and hard palate

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25
Q

Gingival lesions of viral origin

A
  • lifethreatening in immunocompromised patients
  • if sampling is needed, aspiration from vesicle is the best way!!
    • hand instruments, not cavitron because want to protect against exposure
  • blood samples to determine increase Ab titer against virus [works better for primary infection]
  • histopathology is not specific
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26
Q

treatment of gingival lesions of viral origin

A

-careful plaque removal to limit bacterial superinfection of the ulcerations
[have to prevent infection to yourself]
-systemic uptake of an antiviral medication such as aciclovir
— in immunocompromised patients

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27
Q

herpes zoster

A

-gingival lesion of viral origin
-virocella-zoster virus causes varicella (chicken pox) [in later life = shingles]
-small ulcers usually on the tongue, palatal and gingiva
-latent in the DORSAL ROOT GANGLION
-skin lesions may be associated with intraoral lesions, or intraoral lesions may occur alone
-2nd and 3rd branch of the trigeminal ganglion
DIAGNOSIS: unilateral lesions associated with severe pain and paresthesia**

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28
Q

treatment of herpes zoster

A

soft diet, rest, atraumatic removal of plaque, and diluted chlorhexidine rinses
-this may be supplemented with antiviral drug therapy

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29
Q

Candidiasis

A
  • gingival lesion of fungal origin
  • candida species isolated from the mouth: C. albicans**, C. glabrata, C. krusei, C. tropicalis, C. parapsilosis, C. guilermondii

Oral carriage of C.albicans in healthy adults: 3-48%

  • reduced host defense {immunosuppressed individuals, infant and adult who has been on Ab treatment for some time}
  • C. albicans is frequently isolated from the SUBGINGIVAL flora of patients with severe periodontitis
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30
Q

Symptoms of Candidosis

A

Painless or slightly sensitive (burning)

  • red and white lesions
  • lesions can be scraped or separated from mucosa (culture or use color agent to test fungus)
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31
Q

patient susceptible to candidosis

A
  • cancer patients receiving high dose radiation or chemotherapy –IMMUNOSUPPRESION
  • patients who are using several different ANTIBIOTICS over a period of several weeks or months - lose regular oral flora
  • DIABETESpatients
  • MALNUTRITION
  • HIV
  • women who develop vaginal candidiasis
  • pregnancy and use of contraceptives
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32
Q

Diagnosis of Candidosis

A
  • a culture on nickersons medium at room temp (very old dentures = risk factor)
  • MICROSCOPIC EXAMINATION of a smear of the material scraped from the lesion and stained
  • culture can be misleading
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33
Q

treatment of candidosis

A

-use of the antimycotic/antifungal agents
[ex: nystatin given as a mouthrinse or systemically]
-flucanazole, nystatin, amphotericin B (IV)

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34
Q

clinical characteristics of candidosis

A

most clinical characteristic of gingival candidal infections is redness of the attached gingiva, often associated with granular surface

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35
Q

different types or oral mucosal manifestations of candidosis

A
  • pseudomembranous (Whitish patches that can be wiped off)
  • erythematous (red, associated with pain)
  • plaque type (whitish plaque that cannot be removed; need to differentiate from oral leukoplakia)
  • nodular (slightly elevated nodules of white or reddish color)
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36
Q

gingival lesions of systemic origin

A

Allergic and Traumatic reactions

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37
Q

allergic reactions

A 
type I (immediate type) - mediated by IgE
Type IV (delayed type) - mediated by T cells [12-48 hours following contact with allergen]
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38
Q

allergies to:

A

-dental restorative materials (type IV, contact allergy)
[mercury, nickel, gold, zinc, chromium, palladium, acrylics and others]
-oral hygiene products, chewing gum and food
[generally flavor additives or preservatives]

a diffuse fiery red edematous gingivitis sometimes with ulcerations or whitening

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39
Q

traumatic lesion

A

chemical
physical
thermal

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40
Q

chemical traumatic lesions

A
  • surface etching by various chemical products with toxic properties
  • ex. chlorhexidine-induced mucosal desquamation (sloughing with CT exposed), acetylsalicyclic acid burn, cocaine burn, alcohol content

incorrect use of caustics by the dentist

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41
Q

physical traumatic lesions

A
  • hyperkeratosis, a white leukoplakia-like, frictional keratosis
  • gingival laceration resulting in gingival recession
  • traumatic ulcerative gingival lesion (brushing and flossing technique)
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42
Q

thermal injury

A
  • minor burns from hot beverages
  • mostly seen on palatal and labial mucosa
  • painful, erythematous lesions
  • vesicles may develop
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43
Q

foreign body reactions

A
  • epithelial ulceration that allows entry of foreign material into gingival connective tissue
  • foreign body can be generally detected via X-rays
  • ex. amalgam tattoo, abrasives, toothpick etc.
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44
Q

Mucocutaneous disorders

A
  • lichen planus
  • pemphigoid
  • pemphigus vulgaris
  • lupus erthematosus
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45
Q

Lichen Planus

A

-oral involvement alone is common
- can be seen as skin lesion also
-premalignant potential (0.5-2%)
-characteristic skin lesions (wickham striae)
-various clinical appearances [papular, reticular, plaque-like = generally asymptomatic
atrophic, ulcerative, bullous = generally symptomatic]
-any area of the oral mucosa

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46
Q

histopathology of lichen planus

A
  • subepithelial band like accumulation of lymphocytes and macrophages characteristic of a type IV hypersensitivity reaction
  • fibrin in the basement membrane (Ag-Ab response)
  • deposits IgM, C3, C4 and C5
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47
Q

Oral Lichenoid Lesions

A

-an uncertain background

examples: lesions in contact with dental restorations
- lesions associated with various types of medications (NSAIDs, diuretics, beta blockers)
- a group of systemic disorders (liver disease)

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48
Q

treatment of lichen planus

A
  • take biopsy (handling is different than regular biopsy)
  • take sample for culture if questioning candida inf. (~ 38% of OLP causes have secondary inf)
  • a traumatic dental plaque control
  • topical corticosteroids to control pain, discomfort
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49
Q

pemphigoid

A

-a group of disorders in which autoantibodies towards components of the basement membrane result in DETACHMENT OF THE EPITHELIUM FROM THE CT
(a little more severe than lichen planus)

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50
Q

histopathology of pemphigoid

A
  • autoantibody reactions against hemidesmosomes and lamina lucida components
  • have sloughing of epithelium
  • complement mediated cell destructive processes may be involved in the pathogenesis
  • deposits C3, IgG and other Igs
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51
Q

Three types of pemphigoid

A
  • bullous
  • benign mucous membrane
  • cicatrical (specific with eye and oral cavity – scar formation in eye leading to blindness)

-female predominance > 50 years old

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52
Q

Nicholsky sign

A

associated with pemphigoid

-rubbing of the gingiva creates bulla formation

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53
Q

treatment of pemphigoid

A

plaque removal with daily use of chlorhexidine and/or topical corticosteroid

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54
Q

pemphigus vulgaris

A
  • formation of intraepithelial bullae in skin and mucous membranes
  • strong genetic background (jewish and mediterranean)
  • painful desquamative lesions, erosions or ulcerations
  • chronic course with recurrent bulla formation
  • typically in middle age or elderly
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55
Q

histology of pemphigus

A

ACANTHOLYSIS

  • due to destruction of desmosomes
  • pericellular epithelial deposits of IgG and C3
  • circulating autoantibodies against interepithelial adhesion molecules = more severe form

kumars slide:
canthus layer - another name for stratum spinosum
why? because it has intercellular bridges or ‘canthae’
-acantholysis - breakdown of the spinous bridges

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56
Q

Lupus Erythematosus

A

autoimmune CT disorders in which autoAbs form to various CELLULAR constituents
-central atrophic area with SMALL WHITE DOTS surrounded by irradiating fine WHITE STRIAE with a periphery of TELANGIECTASIA (vascular lesion formed by dilation of a group of small blood vessels – blanching)

  • lesions can be ulcerated and cannot be differentiated from leukoplakia or atrophic oral lichen planus
  • Together with characteristic skin lesions (BUTTERFLY)
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57
Q

histology of lupus erythematosus

A
  • degeneration of basal cells and increased width of the basement membrane
  • deposits of Igs, C3 and fibrin along the basement membrane
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58
Q

2 forms of lupus erythematosus

A

discoid forms - mild chronic which affects skin and mucous membrane

systemic forms of the disease (can be fatal)
-4% turn systemically

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59
Q

Necrotizing Ulcerative Gingivitis (NUG)

A

NUG = bacterial origin

  • adolescents or young adults, smokers and individuals often with psychological stress
  • PAIN, ulceration and necrosis of the INTERDENTAL PAPILLAE (very specific), bleeding
  • yellowish white plaque

duration: 1-2 days if treated
not contagious

  • differential diagnosis with primary herpetic gingivostomatitis
  • resolution of the disease is often required systemic Abs
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60
Q

predisposing factors of NUG

A
  • systemic diseases like ulcerative colitis, blood dyscrasias and nutritional deficiency states
  • abnormalities of white blood cell function
  • patients suffering from AIDS
  • associated with periodontal attachment loss
  • may progress to Noma or cancrum oris
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61
Q

Treatment of NUG

A
  • OHI
  • mechanical debridement
  • systemic Ab therapy
  • surgical correction of gingival destruction
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62
Q

Reactive processes of periodontal soft tissue

A
  • fibroma/fibrous hyperplasia
  • pyogenic granuloma
  • peripheral giant cell granuloma
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63
Q

reactive processes of periodontal hard tissue

A

-periapical cemental dysplasia

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64
Q

benign neoplasms of periodontal soft tissue

A

papillomas

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65
Q

malignant neoplasms of periodontal hard tissue

A

osteosarcoma

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66
Q

fibroma/fibrous hyperplasia

A
  • reactive processes of periodontal soft tissues
  • a focal fibrous hyperplasia causes by irritation
  • sessile, well-circumscribed smooth-surfaced nodules
  • cell poor, hyperplastic collagenous tissue
  • may show hyperkeratinization
  • very thick, fibrous tissue - VERY elastic = hard to cut
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67
Q

differential diagnosis of fibroma/fibrous hyperplasia

A

giant cell fibroma

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68
Q

pyogenic granuloma

A
  • reactive processes of periodontal soft tissues
  • ulcerated (may resemble purulence)
  • GINGIVAL MARGIN
  • reddish or bluish, sometimes lobulated, sessile or pedunculated. bleeding is common
  • highly vascular with chronic inflammatory cells
69
Q

differential diagnosis of pyogenic diagnosis

A

pregnancy tumor

70
Q

peripheral giant cell granuloma

A
  • reactive processes of periodontal soft tissues
  • ANYWHERE on the gingival mucosa
  • pedunculated (has a stalk), sessile (broad base), red or purple, commonly ulcerated
  • focal collection with a RICHLY CELLular and vascular stroma separated by collageneous SEPTA
  • probably originated from PDL
71
Q

differential diagnosis of peripheral giant cell granuloma

A

focal fibrous hyperplasia

72
Q

Periapical cemental dysplasia

A
  • reactive processes of periodontal hard tissues
  • fibrous-osseous cemental lesions
  • TOOTH is usually vital (whitening in xrays)
  • usually NO SYMPTOMS
  • periapical bone is replaced by cellular fibroblastic tissue through a CEMENTOBLASTIC PHASE
73
Q

differential diagnosis of periapical cemental dysplasia

A

cemento-ossifying fibroma and fibrous dysplasia

74
Q

Papillomas

A
  • benign neoplasms of periodontal soft tissues
  • four or five different types of papilloma are present
  • exophytic, pedunculated, or sessile lesions
  • reddish/normal or whitish/gray color
  • a granular/moruloid or filiform/digitated surface
  • human papilloma virus is commonly found
75
Q

osteosarcoma

A
  • malignant neoplasm of periodontal hard tissues
  • 7% of all osteosarcomas occur in the jaws
  • clinical and radiographic examinations are required
  • widening of PDL is common
76
Q

Primary TFO

A
  • excessive force (eg. high restoration)
    • bruxism, parafunctional habits
  • normal periodontium (PDL support = normal)
77
Q

Secondary TFO

A
  • Normal (or excessive forces)
  • applied to a weakened periodontium
    ie. periodontal disease –> teeth can no longer withstand normal forces
78
Q

Fremitus

A

Vibration that occurs in the alveolar bone when patient suffers from trauma from occlusion

  • teeth exhibit slight mobility rubbing against adjacent walls of their socket
  • volume with which has been ever so slightly expanded from inflammatory responses, bone resorption or both
  • to determine severity of periodontal disease pt is asked to bite down into max intercuspation and grind his or her teeth every so slightly. Fingers placed in labial vestibule against the alveolar bone can detect fremitus
79
Q

pathologic migration

A

a change in tooth position
that occurs when there is disruption of
forces that maintain teeth in a normal
relationship

  • displacement
80
Q

Clinical signs of TFO

A
  • these signs may represent injury or ADAPTION to injury
  • teeth ARE adaptable
  • progressive tooth mobility
  • fremitus
  • functional mobility
  • pathologic migration
  • infrabony pockets (controversial)
  • buttressing bone (controversial)
81
Q

possible radiographic signs of occlusal trauma

A
  • some of the changes may represent adaptation
  • some may be due to extension of inflammatory periodontal disease without occlusal trauma as a factor
  • widened PDL space and/or thickened radiolucent lamina dura
  • hypo or hyperfunction of trabecular bone
  • angular bone loss & furcations (controversial)
82
Q

Co-destruction theory

A

occlusal trauma may be a co-destructive factor that alters the severity and pattern of inflammatory periodontal disease

zone of irritation: plaque associated periodontal disease and bone loss
zone of co-destruction: below JE

2 lesions come together to cause different pattern

83
Q

Occlusal trauma is a _________ etiological factor for periodontal disease but… it can be a _________ etiological factor for peri-implant disease

A
  • secondary

- primary

84
Q

chronic periodontitis

A

common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues that is caused by the accumulation of perfuse amounts of dental plaque

  • slow or moderate progression of disease
85
Q

clinical features of chronic periodontitis

A
  • changes in gingival morphology (color, texture, volume)
    • redness, swelling
  • BOP
  • bad breathe = halitosis
  • Increased probing depth
  • Attachment Loss
  • Gingival Recession
  • alveolar bone loss (vertical or horizontal)
  • furcation involvement
  • increased tooth mobility
  • drifting of teeth
  • tooth loss
86
Q

overall characteristics of chronic periodontitis

A
  • prevalent in adults, but may be seen in children
  • tissue destruction commensurate with oral hygiene and plaque levels and local/systemic factors
  • specific subgingival species are implicated in disease
    • individual species vary among individuals
  • subgingival calculus is invariably present at disease sites
  • rate of progression is slow to moderate
    • rapid bursts of destruction can occur
  • host factors determine pathogenesis and progression
  • untreated diseased sites more likely to sustain further breakdown
87
Q

symptoms of chronic periodontitis

A
  • mostly painless
    • localized dull pain
    • gingival tenderness, “itching” gums
  • loose teeth
  • food impaction
  • drifted teeth/increased spacing
  • root sensitivity
  • bleeding gums
88
Q

extent and severity of chronic periodontitis

A
  • localized: 30% of sites
  • slight: 1-2mm ALoss
  • Moderate: 3-4 mm Aloss
  • Severe: >= 5mm Aloss
89
Q

typical diagnosis for chronic periodontitis

A

generalized slight with localized moderate chronic periodontitis

90
Q

risk factors for periodontitis

A
  • environmental, behavioral or biologic factors, which when present increase the likelihood that an individual will develop disease
    • longitudinal evidence
    • intervention can modify risk factor
      - smoking
      - diabetes
91
Q

risk determinants of chronic periodontitis

A

non-modifiable factors

age
gender

92
Q

risk indicators of chronic periodontitis

A

putative risk factors that have been identified in cross sectional studies but not confirmed longitudinally

HIV/AIDS
Osteoporosis
infrequent dental visits

93
Q

risk markers/predictors of chronic periodontitis

A

a characteristic associated with elevated risk for disease but may not be part of the casual chain

furcation involvement
calculus
history of attachment loss

94
Q

Gingivitis as a risk factor for chronic periodontitis

A
  • early studies - all gingivitis led to periodontitis
  • later - gingivitis and CP separate entities
  • gingivitis can be stable for years
  • bacterial plaque induces gingivitis, but host response determines if CP will develop
95
Q

Gingivitis as a risk factor (different studies)

A

Now- gingivitis and CP are different aspects of the same disease

  • chinese studies: gingival inflammation a risk for Aloss at any site
  • Norweigan study: tooth loss greater in sites with baseline severe gingival inflammation
  • Lang: absence of gingivitis = good indicator of periodontal health
96
Q

Diagnosis of Chronic Periodontitis

A 
probing depth
gingival recession
CAL = probing depth+ gingival recession
BOP (expressed as % of total sites available)
furcation involvement
mobility
fremitus - mobility of a tooth in occlusion
bony defects:
-horizontal vs. vertical 
1-wall, 2-wall, 3-wall bony defects
97
Q

goals of chronic periodontitis therapy

A
  • eliminate etiology
  • eliminate or reduce risk factors
  • prevent recurrence
98
Q

initial periodontal therapy for CP

A
  • removal of both sub and supragingival plaque
  • adequate oral hygiene
  • remove local and systemic risk factors
99
Q

rationale for periodontal therapy

A
  • periodontal treatment of CP is effective (<= 0.1 tooth loss/year)
  • non-compliant patients had double the rate of tooth loss (0.2 teeth/year)
  • untreated patients lost approximately 0.6 teeth/year
100
Q

outcomes of initial therapy

A
  • probing depth reduction after therapy:
    • gingival recession, gain of clinical attachment and pocket shrinkage
  • sites with initially shallow pockets tend to lose CAL (possible trauma)
    • critical probing depth (Lindhe) - probe depths less than which root planning will cause attachment loss (2.9 mm)
  • greater risk of additional attachment loss if presenting multiple sites with residual probing depth >= 6 mm after active treatment
    - bottomline - you cannot maintain 6 mm pockets; surgical therapy recommended
101
Q

Aggressive Periodontitis overall characteristics

A
  • non-contributory medical history
    • absence of significant systemic conditions
  • rapid attachment loss and bone loss
  • familial aggregation of cases - substantial genetic polymorphism
    - proposed for LAP = autosomal dominant
  • lack of consistency between bacterial deposits and severity of breakdown
  • asynchronous destruction during defined periods of life occur in bursts that are asynchronous for teeths/sites have to catch them in the bursts
  • clinical appearance can sometimes be deceiving - radiographs show bone loss
  • generally effects younger patients
  • less common than chronic periodontitis
102
Q

diagnosis - localized form AP

A
  • absence of systemic disease that may severely compromise host defense or lead to a premature exfoliation of teeth
  • circumpubertal onset
  • robust serum Ab response to infective agents (IgG2)
  • first molar/incisors
103
Q

diagnosis- generalized form AP

A
  • patients under 30 years of age
  • poor serum Ab response to infective agents
  • effecting other teeth besides first molars and incisors
104
Q

clinical outcome of LAP

A

severe destruction of periodontal tissues in short time

105
Q

possible reasons for destructive process of LAP

A
  • aggressive causative agents, or/and

- high level of susceptibility

106
Q

host defense mechanisms in gingival sulcus for LAP

A
  • intact epithelial barrier and attachment
  • salivary flushing action, agglutinins, Ab
  • sulcus fluid flushing action, opsonins, Ab, C
  • local Ab production
  • high levels of tissue turnover
  • presence of normal flora or beneficial species
  • emigrating PMNs and other leukocytes
107
Q

bacterial etiology of LAP

A

A. actinomycetemcomitans*** (90% of patients)
capnocytophaga sp.
eikenella corrodens
prevotella intermedia
anaerobic rods (campylobacter rectus)
Gram + (streptococcus, actinomyces, peptostreptococcus)

108
Q

AA in LAP

A
  • virulence factors
  • immune response against AA (serum and local Ab)
  • outcome of clinical therapy - treatment failure linked in reducing bacterial lead
    • AA is regarded as a true periodontal infectious agent, but this is still a little bit controversial!
109
Q

AAs virulence and pathogenic potential

A

leukotoxin** : kills PMNs and macrophages
endotoxin: activates cells to produce PG, IL-B, TNF-a
bacteriocin: may inhibit growth of “good” species
immunosuppressive factors: may inhibit IgG and IgM production
collagenases: degrade collagen fibers
chemotactic inhibition factors: inhibit PMN chemotaxis

110
Q

host response to LAP/bacterial pathogens

A
  • intense recruitment of PMNs
  • B cells and plasma cells dominate mononuclear infiltrate
  • plasma cells produce IgG, IgA, local IgG4 producing cells elevated
  • Ig levels in sulcus fluid higher than in peripheral blood
    • Ab levels against AA extremely high. However, GAP patients frequently have low titers
    • IgG2 seems to play a special role
  • Th:Ts ratio depressed as compared to healthy subjects, suggesting localized altered response
  • increased response to B cell mitogens
111
Q

Generalized Aggressive Periodontitis

A

SMOKING is a BIG problem (not true in LAP)

112
Q

summary of L/GAP

A
  • multifactorial diseases
  • result of imbalance between host genes and environment
  • exposure to pathogen and host’s inability to deal with it to avoid damage (necessary)
  • phenotype is determined by modifying environment (smoking) or genetic factors (IgG2)

1/3 of LAP will become GAP

113
Q

diagnosis of LAP and GAP (questions to answer)

A

-is there periodonitits?
[loss of clinical attachment and bone? is CAL associated with pocket or recession? other explanation for CAL than periodontitis? pattern localized or generalized? previous treatment for periodontitis?]
-match of plaque/calculus/local factors with periodontal destruction?
[other contributory factors?]
-systemic component (medical history?)?
-microbiologic diagnosis [AA Pg, both, neither?]
-other family members
-host defense
[crevicular PGE2 levels largely increased? other local inflammatory factors? If GAP: IgG2 titers against AA?]

  • last 3 dont do in normal office unless they are not responding to treatment
  • dont sample every pt for AA
114
Q

treatment principles for GAP/LAP

A
  • referrel to periodontist
  • elimination or suppression of microflora
  • address environmental factors
  • provide environment conducive to long-term maintenance
115
Q

risks to pulp vitality

A
  • deep caries
  • trauma
  • restorative procedures
  • infectious and non-infectious
116
Q

3 main pathways of perio-endo lesions

A

dentinal tubules
accessary canals
apical foramen

117
Q

dentinal tubules

A
  • contain odontoblastic processes that extends odontoblast @ pulpal dentin border to DEJ or CEJ
  • passage of microorganisms between pulp and periodontal tissues possible when dentinal tubules are exposed in areas of denuded cementum
  • more dense in cervical areas
  • loss of cementum = exposure
118
Q

accessary canals

A
  • multiple branches connecting root canal system with PDL
  • majority found in apical portion of root and molar furcation areas (perio endo problems much more common in molars than ant teeth because of increased amount of accessory canals)
  • multiple directions
119
Q

apical foramen

A
  • vascular and neuronal supply connection
  • principal & most direct route of communication from periodontium to pulp
  • total disintegration of pulp is CERTAIN if bacterial pulp involves apical foramen –> causes compromising blood supply –> necrosis of pulp –> inflamm response of periodontal tissues
120
Q

perio-endo interrelationship symptoms

A
  • pain (spontaneous & mastication)
  • percussion sensitive
  • mobility
  • radiographic signs
  • other clinical signs (no swelling, no increased probing depth)
121
Q

perio-endo interrelationships

A
  • microbial agents are the main cause of perio-endo lesions
  • formation of plaque on denuded root surfaces following perio disease
  • –> potential to induce pathological changes in pulp
  • process = reverse of the effects of necrotic pulp on PDL = reverse pulpitis
  • effects of perio lesions on pulp can result in atrophic & other degenerative changes like:
  • reduction in number of pulp cells
  • dystrophic mineralization
  • fibrosis
  • reparative dentin formation
  • inflammation & resorption
122
Q

root planning and scaling effects of perio

A
  • smear layer formed on root surface dissolves after a couple days
  • increased hydraulic conductance
  • decrease peripheral resistance to fluid flow at dentin
  • open tubules serve as pathway for diffusive transport of bacterial elements = localized inflammatory pulpal response
  • acid etching also removes smear layer
123
Q

primary endodontic lesion

A
  • acute exacerbation of a chronic apical lesion on a tooth with necrotic pulp (non-vital) may drain coronally through PDL to gingival sulcus
  • comes from accessary canals or apical foramen
  • mimics presence of periodontal abscess
  • reality: sinus tract originating from pulp that opens into PDL

Tx: root canal therapy (endodontic therapy if tooth still vital)

TOOTH CAN BE VITAL OR NON-VITAL
*** as long as tooth is vital - unlikely to produce irritants taht are sufficient to breakdown periodontium

124
Q

primary endodontic lesion leading to secondary periodontal lesion

A

TOOTH IS NON-VITAL
-causes:
untreated endo: plaque accumulation at gingival margin of sinus tract –> plaque induced periodontitis
root perforation (or misplaced pins and posts): may have acute symptoms, perio abscess formation (swelling, pain, exudates, pocket formation, tooth mobility) or chronic periodontitis without pain
root fractures: root canal treated tooth (endo therapy failure)

Tx: periodontal therapy

125
Q

primary periodontal lesion

A
  • caused primarily by periodontal pathogens
  • in process, chronic periodontitis progresses apically along root surface
  • THE TOOTH IS VITAL - reacts to testing!!
  • there is frequently an accumulation of plaque and presence of deep pockets may be detected

TX: OHI, fix any faulty restorations , PERIODONTAL THERAPY

126
Q

primary perio lesion into secondary endo lesion

A
  • if perio extends apically causes necrosis of pulp
  • enters through apical foramen
  • in single rooted tooth, prognosis = poor
  • multi-rooted: better prognosis because not all roots may be affected –> root resection
  • if blood supply circulating to pulp then pulp has a good chance of survival
  • bacteria originating from perio pocket are most likely source of root canal infection

-root canal therapy NOT indicated unless pulp vitality test results show change

127
Q

treatment of primary perio can lead to secondary endo lesion

A

-accessary canals and dentinal tubules open to oral enviro by scaling and root planning or surgical flap procedures –> microorganisms enter –> pulp inflam and necrosis

128
Q

TRUE combined lesions

A

-occurs less frequently
-formed when endo lesion progresses coronally, joining an infected perio pocket progressing apically
(initiate independently and coalesce)
-degree of attachment loss = LARGER
-prognosis = guarded (not good)
** particularly true in single rooted teeth
-root resection in molars

-radiographic of true combo similar to vertically fractured tooth

129
Q

periodontal therapy effects on the pulp

A
  • instruments: root exposure (recession), cementum and dentin removal, dentinal tubule exposure
  • pulp vitality unaffected
  • dentin hypersensitivity
130
Q

dentin hypersensitivity

A

(sharp pain, rapid onset)

  • various stimuli elicit response (hot, cold, sweet, acidic, touch, airflow)
  • peak at 1st week, then subside
  • may become chronic
  • few teeth in few patients becomes hypersensitive
131
Q

endodontic therapy things to consider

A
  • functional need for tooth?
  • is tooth restorable?
  • px suitable to lengthy, costly, invasive tx?

if no to any — extract!

132
Q

endodontic therapy effects on periodontium

A
  • perforations

- vertical fractures

133
Q

mechanism with which periodontitis could potentially influence systemic disease

A

acute-phase reaction cascade
-triggering factors –> local reaction –> mediators –> secondary systemic reaction

-all cells in local area have synthetic capabilities to release mediators that go into circulation

134
Q

triggering factors

A
  • infection
  • necrosis
  • surgery
  • neoplasia
  • radiation
135
Q

local reaction

A
  • macrophages
  • fibroblasts
  • endothelial and other cells
136
Q

mediators

A

(production and release of inflammatory cytokines)

  • TNF-a & IL -1 (signals of cell damage)
  • IL-6 (drives acquired immunity)
  • IFN-gamma (drives cell mediated immunity)
137
Q

secondary systemic reactions

A
  • fever and leukocytosis
  • complement activation
  • serum glucocorticoids increased
  • altered synthesis of acute phase proteins
138
Q

important acute phase proteins

A
  • complement components: opsonization, lysis, chemotaxis- CTX (increase with triggering event)
  • protease inhibitors: a2-macroglobulin (increase – have protective effect)
  • C-reactive protein (CRP): opsonization (increase)
  • fibrinogen: coagulation factor, CTX (increase)
  • plasminogen: degrades blood clots
139
Q

periodontitis as a risk factor for systemic disease

A

sources of risk:

  • 47.2% of americans >30 years old have periodontitis
  • periodontal pockets provide a significant area exposed to gm (-) biofilm
  • infected and inflamed tissues

as a result, there is a systemic exposure to:

  • bacteria & bacterial products
  • inflammatory cytokines
140
Q

what defines a risk factor?

A
  • consistency of association (but still varying strengths)
  • strength of association
  • correct time sequence (potential factor must precede the occurence of the disease)
  • specificity of association (if a given factor is related to other diseases, its association with the disease is less likely to be interpreted as causal)
  • degree of exposure : dose response effect (the risk of developing the disease should relate to the degree of exposure to the factor)
  • biological pausibility (association must make sense in light of known biological mechanisms and pathways)
  • support from experimental evidence (induction of the disease in ANIMALS exposed to the risk factor)
141
Q

periodontitis and systemic disease

A
  • artherosclerotic vascular disease (AVD)
  • adverse pregnancy outcomes
  • diabetic complications
  • respiratory infections
142
Q

periodontitis as a risk for AVD

A

artherosclerosis: a progressive diease in which large to medium sized muscular and large elastic arteries become occluded with fibro-lipid lesions termed atheromas
- coronary thrombosis and acute myocardial infarction are common complications of artherosclerosis

143
Q

pathway of periodontitis with AVD

A

periodontitis –> systemic inflammation and bacterial translocation –> acute phase reaction –> inflammatory response in arteries –> recruitment of macrophages (take up LDL & accumulate lipids –> phagocytose cells & then die –> development of plaque that narrows down lumen = lack of nutrients coming to that side of the heart.

lipid promotes coagulation —> platelet
-activation of thrombosis event

all leads to coronary heart disease

144
Q

AVD and periodontitis

A 
both diseases are more likely to occur in persons who are:
older
male
poor
not well educated
smokers
hypertensives
under stress
diabetic
-these observations suggest that the two diseases may share similar risk factors or common etiologic pathways
145
Q

AVD and perio studies

A

observational studies - positive

  • case control study - relation between poor oral health and MI
  • cohort study = NHANES 1 – relatively small increase in CHD with males with periodontitis
  • perio can influence atheroma formation
  • tooth loss increases MI
  • dose response relationship between periodontal bone loss and carotid arthersclerosis
  • decreasing perio probe depths –> decrease in CHD

observational studies - negative
- no results came with cohort study in first NHANES

146
Q

***biological rationale: pathways that explain the link between perio and cardiovascular disease (CVD)

A
  • effect of periodontal bacteria on platelets
  • invasion of endothelial cells and macrophages by periodontal bacteria
  • endocrine-like effects of pro-inflammatory mediators
147
Q

observations supporting biological plausibility

A
  • S. sanguis and P. gingivalis can induce thrombo-embolic events. mediated by collagen-like platelet aggregation associated proteins made by bacteria
  • DNA from perio pathogens was found in 19/27 artheromas
  • macrophages incubated in vitro with PG and LDL take up the bacteria and transform to form cells similar to those observed in the vessel intima during formation of atherosclerotic lesions
  • systemic pro-inflam mediators are up-regulated for endocrine-like effects in vascular tissues. studies show that CRP and fibrinogen are elevated in periodontally diseased subjects
148
Q

PATHWAY

A

periodontal inflammation and infection –> bacteria, endotoxin and cytokines released into systemic circulation

    - -> increase endothelial adhesion molecules --> monocyte and T cell recruitment, atheroma development and progression --> plaque rupture --> thrombosis --> clinical event (MI, stroke)
   - -> activation of peripheral monocytes: release IL1 TNF and IL6 which can increase endothelial adhesion molecules (same path as above), directly cause monocyte and t cell recruitment (same as path above), AND go to the liver --> acute phase response (CRP and Fibrinogen) --> increase coagulation --> thrombosis --> clinical event (MI, stroke)
149
Q

effect of periodontal therapy on CVD biomarkers (CRP)

A
  • periodontal pxs treated with Sc/Rp experiences significant reductions in serum CRP and IL6. px who had favorable response to Sc/Rp = 4 x more likely to exhibit decreaased CRP
  • other studies have not shown that
  • trend toward treatment-induced suppression of systemic inflam, but the effects of therapy are not consistent and the effects may not be sustainable over time
150
Q

effect of periodontal therapy on endothelial function

A
  • pxs who have a favorable response to non-surgival perio therapy exhibited a concomitant improvemen in endothelial function (flow-mediated arterial dilation)
  • several other studies have shown similar results
  • recent pilot study suggested that tx of mild to moderate periodontitis in otherwise healthy pxs may result in a significant decrease in carotid artery intimal-medial thickness
151
Q

effect of periodontal therapy on CV events

A
  • very few studies conducted - more focused on causation
  • a recent large multi-center pilot study was not conclusive because the subjects treated with periodontal therapy did not have a sustained improvement of their periodontal health
  • there is currently lack of strong evidence that tx of periodontitis reduces the risk of artherosclerotic vascular disease
152
Q

strength of evidence perio and AVD

A
  • consistency of study findings suggest observed association between perio and AVD is not a false finding
  • strength of reported associations is somewhat modest due to inconsistencies between studies
  • specificity - NO
  • time sequence - NO
  • degree of exposure - several studies suggest that there is a higher cumulative frequency of occurence of CHD with increasing periodontitis severity
153
Q

strength of evidence: AVD and perio: biological plausibility

A

-reasonable support for plausibility
ex:
-periodontal pathogens have been isolated from carotid artheromas
-P gingivalis can induce platelet aggregation
-systemic pro inflam mediators CRP and fibrinogen are elevated in subjects with periodontitis

154
Q

strength of evidence: AVD and perio: experimental evidence

A
  • animal models have supported the plausibility of a link between PG and AVD and identified biological pathways that might mediate this linkage
  • however, the models used were overly simplistic (mono-infections with a limited number of periodontal pathogens) human periodontitis is caused by polymicrobial biofilm
155
Q

PD and AVD: summary

AHA scientific statement

A
  • contribution of PD to AVD = biologically plausible but PD and AVD share multiple risk factors
  • observational studies support an ASSOCIATION between PD and AVD, independent of known confounders, but these studies do not support a CAUSAL relationship
  • although PD therapy can result in reduced systemic inflammation and improved endothelial function, there is not enough evidence to indicate that it can prevent AVD or modify its outcomes
156
Q

association with PD and adverse pregnancy outcomes

A
  • preterm low birth weight
    • preterm birth; <37 weeks
    • intrauterine growth restriction
    • combo
  • PLBW deliveries account for ~10% of annual births in developed countries and ~66% of overall infant mortalities
  • PTB often results in long-term disability
  • GU tract infection is a known risk ractor for PLBW; other types of infections may also play a role
157
Q

association with PD and PTB & Low birthweight

A
  • PD results in translocation of bacteria and endotoxin into systemic circulation
  • inflamed periodontal tissues produce significant quantities of inflammatory mediators including IL-1B, IL6, TNFa (increase MMPs causes weakening of membrane –> preterm labor) and PGE2 (PGE2 released from placental tissues and cause myometrial contractions–> preterm labor and low birth weight)
  • cytokines may have systemic effects
158
Q

Studies: PD and PLBW

A
  • pregnant hampster model
    - chronic exposure to PG –> fetal placental toxicity, increased TNFa and PGE2 –> decreased fetal weight
  • case-control study
    - mothers of PLWB had significantly more clinical attachment loss
  • study of 735 pregnant women
    - PTB rate significantly higher in subjects with moderate to severe PD
  • PTB study
    - mothers with severe PD were 4-7x more likely to deliver a preterm baby
159
Q

does periodontal therapy reduce the likelihood of PTB and PLBW?

A
  • randomized study of 351 pregnant women
    • 1/2 received Sc/Rp Tx, monthly scalings and OHI – greatly reduced incidence of PLBW
  • randomized study, 366 pregnant women
    • tx A) prophy + placebo B) Sc/Rp + placebo C) Sc/Rp + metronidazole D) untreated control
    • PTB: A) 4.9% B) 0.8% C) 3.3% D) 6.3%
  • not statistically significant results
  • randomized pilot study
    • treatment group of Sc/Rp and OHI had statistically significant 3.8 fold reduction in PTB rate
160
Q

strength of evidence for PD and adverse pregnancy outcomes

EFP/AAP Workshops

A
  • strength of observed association = modest
  • although periodontal therapy is safe and improves periodontal health in pregnant women, periodontal therapy doesn’t appear to significantly reduce overall rates of PTB and PLBW
161
Q

Diabetes mellitus - type 1

A
  • insulin dependent
  • destruction of pancreatic beta cells
  • hypo-production of insulin
  • usually occurs before age 30
162
Q

diabetes mellitus- type 2

A
  • non-insulin dependent
  • target tissues don’t respond to insulin
  • usually occurs later in life

most studies conducted on type 2

-poorly controlled diabetics of both types tend to have more PD attachment loss than non-diabetics

163
Q

does PD predispose to poor diabetic control?

A
  • longitudinal study
    - study 1: presence of 7 PD associated with a 6-fold higher risk of worsening glycemic control over 2 year period
    - study 2: subjects with severe PD are more likely to have elevated HbA1c levels than subjects in health or with moderate PD
164
Q

does PD therapy improve diabetic control?

A
  • longitudinal study
    • PD treatment with combo of Sc/Rp and oral tetracycline reduced pocket depth and PG — reduced HbA1c from 11 - 9.8%
  • meta-analysis study
    • mean change of HbA1c after Sc/Rp was only -0.40%
165
Q

strength of evidence for PD and diabetes

EFP/AAP Workshops

A
  • reduction of HbA1c by Sc/Rp (-0.4%) has a clinical impact similar to adding a second drug to the diabetes treatment regimen
  • randomized clinical trials with larger numbers of subjects and longer follow-ups needed
  • it would be sensible to provide guidelines for PD treatment of diabetic pxs to medical and dental professionals
166
Q

PD and risk of bacterial pneumonia

A
  • respiratory pathogens can colonize dental plaque and serve as a source of subsequent infection, resulting in hospital-acquired pneumonia
    • 50% of healthy subjects aspirate oropharyngeal contents during normal sleep
    • it is plausible that plaque can serve as a reservoir for bacteria that cause hospital-acquired pneumonia
  • an association between PD and hospital-acquired pneumonia is emerging, but further study is needed
  • oral hygiene is likely to become an important consideration for hospitalized pxs at risk for pneumonia
167
Q

PD and risk of COPD

A
  • individuals with poor oral hygiene have an increased risk of developing chronic respiratory disorders
  • pxs with a history of COPD have significantly more PD attachment loss than subjects without COPD
  • however, systemic reviews failed to detect conclusive evidence for an association between PD and COPD
168
Q

strength of evidence for PD and Pneumonia/ COPD

EFP/AAP Workshops

A
  • association between dental plaque and pneumonia appears to be stronger than for plaque and exacerbation of COPD
  • more studies of the association between PD and there 2 respiratory disease are needed

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