Test 1 (Ch1-3) Flashcards
What are the types of gingivitis
Plaque induced due to systemic factors due to medications non plaque induced genetic origin gingival manifestations of systemic conditions
What are the systemic factors of gingivitis
endocrine and blood dycrasias or leukemia
What are the endocrine factors that effect the gingiva
Puberty, Pregnancy, Diabetes
What are the medications associated with gingivitis
Dylantin (Phenytoin sodium)
Nifedipine (Ca blocker)
cyclosporin (sand…)
What non plaque bacteria can cause gingivitis
N. gonorrhea, T. pallidum and Streptococcal (Betta-hemolytic)
What viral factors are involved in gingivitis
Herpes 1 and 2
Varicell-zoster infections
What are all the non-plaque induced gingivitis?
Bacterial,
Viral
Fungal
What are the 3 fungal infections associated with gingivitis
Hisoplasmosis
Candidia albicans
linear gingival erythema
What type of gingival manifestations of systemic conditions are there
Muccocutaneous disorders
Allergic reactions
Traumatic Lesions
Foreign Body Reactions
What are the causes of mucocutaneous disorders and Allergic reactions in gingivitis
Mucocutaneous disorders include Lichen planus pemphigoid erythema multiform lupus erythematosus
Allergic Reactions
Nickel
Acrylic
toothpastes
Treatment of gingivitis include use of a
electric tooth brush, water pick, chx rinse, flossing, toothpics
What does gingivitis look like
red blunted papilla
What are the 5 types of Acute periodontitis
Acute pericoronitis Acute Herpetic gingivostomatitis ANUG Acute Periodontal Abscess Acute Gingival Abscess
What is the Diagnosis of Acute periodontitis
S/S: pain > swelling and edema > lymphadenopathy > fever
What is the treatment of Acute periodontitis
control infection
How does acute periodontitis apeare
increased redness of soft tissues and altered contours- blunted bulbus
Increased bleeding on probing
Loss of CAL
Chronic Periodontitis is characterized as what
Localized where the % is 30%
How does Chronic periodontitis appear
Increased renew of soft tissues and altered contours, blunted/bulbus
increased bleeding on probing
loss of CAL
Increasing probing depths and CAL
Aggressive Periodontitis is characterized as
Localized Aggressive Periodontitis (Vertical bone loss)
Generalized Aggressive Periodontitis (Horizontal bone loss or jevenile.=)
Periodontitis as a manifestation of systemic Disease
Hematological - acquired neutropenia, leukemia
Genetic - familial and cyclic neutropenia, down syndrome, leukocyte adhesion deficiency syndrome, Papillon-Lefvre Syndrome, Chediak-Higashi Syndrome
What are the necrotizing Periodontal Diseases
NUG NUP
What is NUG
reversible not contagious age of onset is 15-30
What are the signs and symptoms of NUG
fetid oralis, pseudomembrane, necrosis (spirochetes), wet sticky appearance (fibrin meshwork), pain, sudden onset, spontaneous gingival bleeding, lymphadenopathy, fever.
how does NUG progress and what is the etology
anterior to posterior
stressed induced, smoking systemic diseases (AIDS,EBV)
What are the layers of NUG
Bacterial zone –> PMN rich zone –> necrosis–> spirochetes (lamina propia)
What cells are involved with NUG
PMN’s, macrophages (defect in chemotaxis or phagocytosis)
NUP is described as
irreversible attachment loss and bone loss
What are the signs and symptoms of NUP
punched out papilla fever lymphadenopathy pain multiple perio abscesses necrotizing stomatis necrosis and ulceration of marginal, papillary and attached gingiva
Ecology of NUP is
bacteria perio bugs and G- anaerobic enterics –> clostridium, klebsiella, enterococcus
fungi candida
viral EBV
other severe malnutrition, Aids, Immunocompromised
What is the treatment for NUG
debridement, abx amoxicillin, metronidazole, chi rinse, stress control SRP
What is the treatment for NUP
abx metronidazole, fluconazole, chx debridement, SRP, 2 month recall
Abscesses of the periodontium include what two types
Gingival abscess and Acute Periodontal abscess
Cellular components of gingivitis are
PMNs
T cells lymphocytes, macrophages
B-cells or Plasma cells
Cellular components of acute periodontitis include
osteoclasts MMP's Cytokines IL-1 IL-6 IL-8 TNF-a Leukotrines
How do you dtermine the extent of periodontitis
Slight 1-2 Cal
Moderate 3-4 Cal
Severe > 5 Cal
Diagnosis for Chronic periodontitis inclues
BOP exudate from pockets tooth mobility abscess formation Suprabony or infraboney pocket formation
How to treat chronic Periodontitis
don’t use abx,
you are likely to loose 3.5x more teeth if you don’t treat period.
What are the clinical ramifications to chronic perio
CAL .1-.3 mm/year on F and L surface, .3 mm/year IP
What does chronic periodontitis look like
Increased redness of soft tissues and altered contours- blunted/bulbus
increased bleeding on probing tooth mobility
loss of CAL
increasing probing depths and CAL
Suprabony or infrabony pocket formation
What is the red complex and what disease is it associated with
P gingivalis
T forsythia
T denticola
Agggressive peridontitis
What is the only type of treatment that can cure aggressive periodontitis
surgery
There is CAL clinical attachment loss in NUG
False there is not
what is the age range for aggressive periodontitis and NUG
15-30
What are the different names for NUG
Vincent’s stomatitis/infection, ulcerative Gingivitis, gangrenous stomatitis trench mouth
What causes the the wet sticky appearance in NUG
fibrin meshwork
NUP is reversible T or F
False attachment loss and bone loss
S/S for NUP include
punched out papilla low grade fever periodontal abscesses necrotizing stomatis- inter proximal bone exposure Aggressive loss of alveolar bone
What is the etiology of NUP
bacteria G- anaerobic enteric such as clostridium, klebsiella, enterococcus
What is the viral etiology of NUP
Candida
Viral is EBVs
other include severe malnutrition or immunocompromised AIDS
HIV/Aids and NUP
ulceration and necrosis of gingival tissue
rapid destruction and or exposure of alveolar bone
CD4+
What is the treatment for NUP
metronidazole fluconazole chlorhexidine soft tissue debridement SRP 2 month periodontal maintenance interval
What type of abscess are there in the periodontium
Gingival
Acute Periodontal abscess
Pericoronal abscess
Gingibal abscess S/S
localized pain
rapidly expansion
adjacent teeth painful to percussion
are gingival abscess limited to marginal gingiva or do they invade the bone
they are limited to gingival papilla and marginal gingiva
What are the causes etiology of gingival abscess
foreign body impaction w associated bacteria
Tx for gingival abscess are
drain
antibiotics
SRP
Possible surgery
Acute periodontal abscess
Swelling exudate deep pocket vital pulp fistula tooth mobility fever lymphadenopathy
What type of abscess is associated with multiple abscesses with DM and AIDS
Acute periodontal abscess
What bacteria cause acute periodontal abscess
G- anaerobic P. gingivalis P intermedia treponema spirochetes F. nucleatum P. micra T. forsythia Candida
What are the factors required for a acute periodontal abscess
blockage of perio pocket
subgingibal plaaque
plaque microbes with virulence factors (endotoxins and collagenase)
What is the his histopathology
infiltrate → hyperemia and thrombosis → lysis of collagen matrix in lamina propria and gingival fibers → ulceration and apical proliferation of JE → osteoclastic mediated bone resorption
What is the treatment for acute periodontal abscess
drainage
antibiotics local or systemic delivery
SRP possible surgery
SRP is scale and root planning
yup
pericoronal abscess treatmetn is what
control infection
extract 3rd molar
irrigation with peroxide or chx antibiotics extraction
can try to remove pericoronal tissues
what is the definition of abscess
dense localized collection of neutrophils with tissue necrosis
surrounded and walled off by immature connective tissue and proliferating capillaries
If a patient has periodontitis and needs end treatment what do you do
get the endo finished first.
What are some examples of developmental or acquired deformities and conditions of the periodontium
localized tooth related factors that modify or predispose to plaque inched gingival disease/periodontitis
mucogingival deformities
occlusal trauma
What are examples of localized tooth related factors that modify or predispose to plaque induced gingival disease/periodontitis
tooth anatomic factors
dental restoration
root fracture
cervical root resorption
Mucogingigival deformities
gingival/soft tissues recession lack of keratinized gingiva decreased vestibular depth aberrant frenum/muscle attachment gingival excess
Occlusal trauma
Primary occlusal trauma-grinding clenching
no bone loss no period but will have mobile teeth and widen PDL
Secondary Occlusal Tauma
normal or excessive forces are placed on a tooth with reduced periodontium
Chronic occlusal trauma more frequent than acute, does occlusal trauma cause periodontal pockets and attachment loss
NO
how can you see occlusal trauma on a radiograph
widened PDL space, disruption/loss of lamina dura, root resorption
What is a perio probe used for
measure attachment loss/pocket depth
what are the variables effecting probing depth
inflammation probe diameter Tapered vs Parallel Hand force Band width
Furcation probe measures
horizontal bone loss
BOP bleeding on probing
Positive BOP
active disease
presence of microbial biofilm/plaque
Ulcerative Sulcus/ pocket epithelium
how many data pocket depths are taken
6 points d->V
average width of the PDL in the adult is
.17
checking mobility we use instruments what are the different classes
Class 1 > .2mm but 1mm
Class 3 > 1mm + axial displacement (depressible no apical bone)
CAL probing depth + what
gingival margin level
Apical gingival margin means to do what
subtract ex PD is 6 and the GM is 4 mm apical
Biological width
junctional epithelium+ connective tissue attachment = around 2
CEJ to crest of alveolar bone is
1.5-2 mm
attachment epithelium + gingival fiber ligament is
Biological width
violations of the biologic width induce
inflammation
increasing probing depth
inconsistent resorption of alveolar bone
what do we see clinically with inflammation
vascular component of gingival inflammation
color edema swelling bleeding
What are the cell types involved with inflammation
Neutrophils basophils/mast cells monocytes/macrophages lymphocytes plasma cells
what is the job of the basophil
histamine causes vasodilation and increased vascular permeability platelet activating factor Heparin anticoagulant TNF-a SRS-As leukotriene C4 D4 E4
What are the jobs of monocytes and macrophages
secrete cytokines and lymphokines
What are the cytokines and lymphkines
IL-1 Osteoclastic activation beta lymphocyte activation and activation of CD8 lymphocytes
IL-6 osteoclastic activation
TNF-alpha inflammatory
INF interferon interferes with virus
Lipid mediators of inflammation prostaglandins, leukotrienes platelet activating factor
Lymphocytes = CD4 helper cells do what
key to the immune response
activates macrophages
activated CD8 cytotoxic T lymphocytes
Activates B lymphocytes to secrete immunoglobulin
Activates B lymphocytes to secrete immunoglobulin
Lymphocytes CD8 Cytotoxic T lymphocytes
destroy target cells by synthesis and release of cytotoxins Synthesis and release of
INF-y
Tumor Necrosis Factor alpha
Tumor Necrosis factor beta
Plasma cells
B lymphocyte is a precursor of plasma cells and both secrete IgG IgM IgE IgD IgA
IL-1
stimulates osteoclasts, fibroblasts macrophages
IL-6 stimulates
B and T clls
IL-8
attracts and activated PMS
TNF-a
activate osteoclasts
PGE2
vasodilation, pyrogenic, release mediator from mast cells, cell-mediated cytotoxicity
what is the average clinical attachment lost per year
.1-.3 per year for facial and lingual surfaces and .3 mm per year for inter proximal areas
In ten years a untreated patient may loose 3.5-5mm while those patients who receive treatment will loose one
what are the patterns of bone loss requires how much bone loss to show up on a radiograph
30-50%
Intrabony pockets are classified as walls remaining
3 walls being the best
Intradental craters
35% of maxillary intrabony defects
63% of mandibular intrabony defects most common in posterior teeth
How does a pocket form
apical migration of JE
loss of CT fiber attachment
how is a pseudo pocket formed
aka gingival pocket by excessive PD without loss of clinical attachment bc of increased bulk of gingiva
commonly found in edemas overgrowth or inflammatory hyperplasia
Periodontal pocket are formed by
excessive PD with loss of clinical attachment
associated with chronic aggressive periodontitis
