214 terms

Periodontics part I (Note cards)

When extensive SRP must be performed, the best approach would be
A series of appointments set up to scale and root plane a segment or quadrant of teeth at a time (thoroughly and completely)
In root planning, where should the ideal working stroke begin?
The apical edge of the junctional epithelium (the base of the pocket)
Which of the following presents the most difficulty in performing a thorough SRP?
Trifurcations of the maxillary molars
What is the best criterion to evaluate the success of SRP?
no evidence of bleeding upon probing
Some degree of curettage is done unintentionally when SRP are performed; this is called ____.
inadvertent curettage
Curretage accomplishes the removal of the chronically inflamed granulation tissue that forms in the lateral wall of the periodontal pocket
The main objective of root planning is?
To remove etiologic agents from the root surfaces
Maximum shrinkage after gingival curettage can be expected from tissue that is?
A curette designed to SRP anterior teeth with deep pockets will have a?
long, straight shank
Which teeth are most likely to have flutings, which make SRP diffult?
maxillary premolars
mandibular incisors
What is a problem on the mandibular incisors that makes SRP difficult?
root proximity
Contraindications for gingival curettage include?
acute periodontal disease
firm, fibrotic tissue
intrabony pockets
mucogingival involement
lateral wall of gingiva is extremely thin
toothbrush trauma (abrasion) usually occurs on the:
canines and premolars
Tooth brush trauma most frequently occurs on teeth that are ___.
most prominent in the dental arch
Dentin is abraded 25 times faster than enamel
cementum is abraded 35 times faster than enamel
How is hard tissue abrassion damage produced?
abrasive dentifrices
How is soft tissue abrassion produced?
usually by the toothbrush alone
Trauma from tooth brushing may result in?
-recession from marginal gingiva
-lacerations of soft tissue
-v-shaped notches in the cervical areas of teeth
-gingival clefts-which are narrow grooves that extend from the crest of the gingiva to the attached gingiva
The most accepted theory as to the cause of root sensitivity is the?
hydrodynamic theory
What is the hydrodynamic theory?
pain of root sensitivity results from indirect innervation caused by dentinal fluid movement in the tubules, which stimulates mechanoreceptors in the pulp
Active ingredients to treat hypersensitivity:
strontium chloride
potassium nitrate
sodium citrate
How do desenitizing agents work?
They act through the precipitation of crystalline salts on the dentin surface, which block dentinal tubules
The most important factor in the control of hypersensitive roots among patients with PD diease after gingival recession has exposed the cervical portion of the teeth is:
thorough daily plaque control
To desensitize, most likely the mechanism of action is the reduction in the diameter of the dentinal tubules so as to limit the displacement of fluid in them: This can be attained by:
-formation of smear layer produced by burnishing the exposed surface
-topical application of agents that form insoluble precipitates within the tubules
-impregnation of tubules with plastic resins
-sealing of the tubules with plastic resins
angular defects are classified on the basis of:
The number of osseous walls left surrounding the tooth
What is the most common pattern of bone loss?
vertical or angular defects
occur in an oblique direction, leaving a hollowed-out trough in the bone alongside the root; the base of the defect is located apical to the surrounding bone. In most instances, angular defects have accompanying intrabony periodontal pockets; intrabony pockets, however, always have an underlying angular defect
Osseous craters
concavities in the crest of the interdental bone confined within the facial and lingual walls. Craters have been found to make up about 1/3 of all defects and about 2/3 of all mandibular defects. They are more common in posterior segments than anterior segments. They are best treated with osseous surgery
loss of the buccal or lingual bone overlaying the root portion of the tooth, leaving the area covered by soft tissue only
intrabony defect
three-wall vertical defect that was originally caled an intrabony defect. The term was later expanded to designate all vertical defects
one-wall vertical defect
suprabony pockets
associated with horizontal bone loss, they are not intraosseous
When evaluating an osseous defect, the only way to determine the number of walls left surrounding the tooth is by:
exploratory surgery
-this is because a dense buccal and lingual plate of bone will tend to mask the defect, blocking it out on radiographs
Which type of pocket is formed by gingival enlargement without destruction of the underlying periodontal tissues
gingival pocket
Initially, the first group of cells to arrive at the site of injury are neutrophils. Later, ______ become more numerous. In certain parasitic infections, ____predominate. In viral infections, _____ rather than neutrophils usually predominate.
Macrophages, eosinophils, lymphocytes
What are the stages of acute imflammation?
1. vascular phase of inflammation
2. cellular phase of inflammation
What happens during Vascular phase of Inflammation?
1. vasoconstriction- immediately following tissue injury, there is a brief period of localized vasoconstriction
2. complement activation of mediator release
3. vasodilation
4. Increased vascular permeability
In the Vascular phase of inflammation, what is the complement activation of mediator release?
Tissue injury, or the presence of bacteria, activates complement. C3b molecules formed in this process bind to microbes and injured (opsonization). C3a and C5a (chemotaxins) trigger the release of histamine and serotonin from nearby mast cels. Tissue injury also triggers the formation of bradykinin and initiates the synthesis of prostoglandins and leukotrienes.
In the Vascular phase of inflammation, what happens during vasodilation?
Histamine, and other vasoactive mediators of inflammation, then cause relaxation of smooth muscle in arteriolar and capillary walls. Vessels dilate increasing blood flow to injured tissues. This manifests by redness (hypernia) and heat near the site of injury.
In the Vascular phase of inflammation, increased vascular permeability?
With vasodilation, the endothelial cells lining blood vessels contract slightly creating gaps between the cells that allow plasma to escape intp surrounding tissues. Plasma delivers antibodies and other antimicrobial substances to the site of injury. Fibrinogen from plasma also clots and serves as a temorary barrier to bacterial invasion.
What happens during the Cellular phase of inflammation?
1. Adhesion
2. Diapedesis and chemotaxis
3. phagocytosis
During the Cellular phase of inflammation; adhesion?
As blood vessels dilate, the velocity of blood flow slows allowing circulating WBC to accumulate on the inner surface of blood vessels. This process is called margination.
During the Cellular phase of inflammation; Diapedesis and chemotaxis:
The WBC then begin to squeeze between the contracted enothelial cells and migrate in an ameba-like fashion into the extravascular space (a process called diapedesis). Once in tissue, the WBC's are attracted by activated complement and and begin to migrate towards the site of injury or infection. WBC's (specifically PMN's) apparently have surface receptors for chemotactic agents. (C5a, TNF, IL-8, LtB4, IL-1, IFN-y) which causes them to move in the direction of increasing concentrations of the chemotactic substance (process is called chemotaxis). Intially, the first group to arrive at the site of injury are neutrophils (PMNs). Later, macrophages become more numerous. In certain parasitic infections, eosinophils predominate. In viral infections, lymphocytes rather than neutrophils usually predominate.
During the Cellular phase of inflammation; Phagocytosis?
When WBC (specifically PMNs) arrive at the site of tissue injury or microbial invasion they become very active and begin engulfing bacteria forming a phagosome which combines with lysosomal granules to form a phagolysosome, in which digestion of the engulfed particle occurs.
redness, caused by vasodilation from vessels dilating causing an increase in blood flow to injured tissues.
What cells line the blood vessels?
endothelial cells
With increases vascular permeability, what does plasma do?
gaps are created between the endothelial cells, and this allows plasma to escape into surrounding tissues. Plasma delivers antibodies and other antimicrobial substances to the site of injury.
Fibrinogen does what? Where does it come from?
It comes from plasma, and it clots and serves as a temporary barrier to bactieral invasion.
Adhesion is also called?
What happens during margination?
When blood vessels dilate or expand, blood flow slows down which allows circulating WBC to accumulate on the inner surface of the vessel wall
What happens during Diapedesis?
WBC squeeze between contracted endothelial cells and travel (migrate) in an ameba-like fasion into the extravascular space.
Which cells of the immune system possess receptors for the complement componene tof C3a, by which they participate in immediate inflammation?
Dermal dendrocytes (histocytes)
All cells in the immune system originate from what?
hematopoietic stem cell in the bone marrow.
The Hematopoietic stem cell in the bone marrow gives rise to two major lineages:
1. myeloid progenitor cell
2. lymphoid progenitor cell
These two progenitors give rise to the myeloid cells
dendrtic cells
These two progenitors give rise to lymphoid cells
T cells
B cells
Natural Killer cells (NK)
These cells make up the cellular components of the innate (non-specific) and adaptive (specific) immune systems.
What are cell receptors?
They are molecules on the cell surfaces that enable to cell to interact with other molecules or cells. Receptors reflect and dictate the function of cells.
Mast cells
important in immediate inflammation (anaphylaxis and allergic responses). They possess receptors for complement components (C3a and C5a) as well as receptors for the Fc portion of the antibody molecules IgE and IgG. They feature prominent cytoplasmic granules (lysosomes)-which store inflammatory mediators such as histamine and haparin.
cytoplasmic granules are also known as lysosomes, and they store:
stores inflammatory mediators such as histamine and heparin.
Two examples of inflammatory mediators
histamine and heparin
Dermal dendrocytes (histocytes)
distributed near blood vessels and possess receptors for the complement component C3a, by which they participate in immediate inflammation.
Peripheral dendritic cells (DCs)
are leukocytes of dendrites. Langerhans cells are DCs that reside in the suprabasilar portions of squamous epithelium. DCs are important in antigen processing and presentation of cells of the specific immune response.
Neutrophils and monocytes/macrophages are:
phagocytic leukocytes
predominant leukocyte in the blood. Do not need to differentiate substantially to function, they are suited for rapid responses. They posses receptors for metabolites of the complement molecule C3
are referred to as macrophages when they leave the blood. They present antigen to T-cells.
Together, macrophages and lymphocytes:
orcehstrate the chronic immune response
What are the three main types of lymphocytes?
-They are distinguished based on their receptors for anigens.
-Natural Killer Cells (NK)
recognize diverse antigens using a low-affinity transmembranous comples, the T-cell antigen receptor (TCR). T cells are subdivided based on whether they possess the co-receptor CD4 (T-helper cells) or CD8(T-cytotoxic cells)
help control extracellular antigens such as bacteria, fungal, yeast, and virions. B-cells recognize diverse antigens using the B-cell antigen receptor (BCR). After antigen exposure, some B-cells differentiate to form plasma cells which secrete IgM. Others differeniate into memory B-cells
Natural-Killer cells (NK)
recognize and kill certain tumor and virally infected cells
Cells that are part of the compliment component C3a:
mast cells (also part of the C5a)
dermal dendrocytes (histiocytes)
B-cells become:
plasma cells - secreting IgM
Memory Bcells
The main cells involved in chronic inflammation are?
lymphocytes and macrophages
Chronic inflammation
slow onset and persists for weeks. The symptoms are not as severe as with acute inflammation, but the condition is insidious and persistent, the main cells involved are lymphocytes and macrophages.
What aid of chemical mediator works with macrophages?
-Macrophages do an excellent job of engulfing or neutralizing or killing foreign antigens.
-lymphocytes and macrophages are interdependent in that the activation of one stimulates the actions of the other.
What is the predominant cell in chronic inflammation?
Characteristics of chronic inflammation:
-lymphocyte, macrophage, plasma cell infiltration
-Tissue destruction by inflammatory cells
-Attempts at repair with fibrosis and angiogenesis (new vessel formation)
When acute phase cannot be resolved: persistent injury or infection example:
When acute phase cannot be resolved: prolonged toxic agent exposure:
When acute phase cannot be resolved: Autoimmune disease states
Examples of macrophages scattered all over
-Kupffer cells
-sinus histiocytes
-alveolar macrophages
Macrophages circulate as monocytes and reach the site of injury within:
24-28 hours and transform
Macrophages become acvited by T-cells derived from:
-other products of inflammation
T and B lymphocytes are:
antigen-activared (via macrophages and dendtric cells)
-Release macrophage activating cytokines
Plasma cells are:
terminally differentiated B-cells that produce antibodies
Eosinophils are found esspecially at the sites of:
parasitic infection, or at allergic reaction (IgE mediated) sites
The ____ has emerged as a unique immune cell that could be activated by many non-immune processes, including acute stress:
Mast cell
Mast cells originate from?
pluripotent cells
Mast cells are frequently located at?
perivascular sites in the tissues, such as:
lungs, where they interact with external environment
When do Mast cells become activated?
When surface receptor-bound antigen-specific immunoglobulin E (IgE) encounters an antigen that the IgE recognizes. This triggers mast-cell degranulation, leading to the rapic release of inflammatory mediators, such as histamine, proteoglycans, and cytokines. Mast cells activation also stimulates the arrival of other inflammatory cells- a critical step in local inflammation
Mast cells are not only necessary for allgeric reactions, but recent findings indicate that they are involved in neuroinflammatory disease; esspecially those worsened by stress:
In these cases, mast cells appear to be activated through their Fc receptors by immunoglobulins other than IgE, as well as by anaphylatoxins, neuropeptides, and cytokines to secrete mediators selectively without over degranulation.
The mast cell content in human gingiva is ___.
high; the mast cell content of inflammed gingiva increases with severity of inflammation increases.
The anaphylactic repsonse is characterized by:
The degranulation of mast cells as a result of antigen-antibody complexes affixed to cell surfaces.
Prevotella intermedia was formerly known as:
bacteroides intermedius
Smoking has been identified as a significant variable to predict the response to PD treatment. Smoking has a negative effect on PD therapy.
Both statements are TRUE
What is one of te most significant risk factors currently available to predict the developement and progression of periodontitis?
Smokers have an increase in which type of bacteria?
Tannerella Forsythia; and more orange and red microbial complexes
Some autoimmune disesease have been associated with periodontal disease:
Crohn's disease
rhematoid arthritis
lupus erythematosis
CREST syndrome - scleroderma
Mediators produced as part of the host response that contribute tissue destruction include:
What are the Primary proteinases involved in the periodontal tissue destruction by degradation of extracellular matrix molecules?
Matrix metalloproteinases or MMPs
What are Matrix metalloproteinases or MMPs?
A family of proteolytic enzymes found in neutrophils , macrophages, fibroblasts, epithelial cells, osteoblasts, and osteoclasts that degrade extracellular matrix molecules such as collagen, gelatin, and elastin
Matrix metalloproteinases- eight or MMP-8 is:
released by infiltrating neutrophils
Matrix metalloproteinases-1 or MMP-1 is:
expressed by resident cells, including fibroblasts, monocytes/macrophages, and epithelial cells.
MMP-8 and MMP-1 are BOTH?
MMPs are also produced by periodontal pathogens ____ and ____.
P. gingivalis
A. actinomycetemcomitans
What are Cytokines responsible for?
Imporant signaling molecules released from cells. The properties of cytokines that relate to tissue destruction involve stimulation of bone resorption and induction of tissue-degrading proteinases.
Which cytokines have a central role in periodontal desctuction?
Interleukin-1 (IL-1)
Interleukin-8 (IL-8)
tumor necrosis factor alpha (TNFa)
Interleukin-1 (IL-1)
potent stimulant of osteoclasts proliferation (bone resoprtion), differentiation, and activation
Interleukin-8 (IL-8)
Is important in attracting inflammatory cells
tumor necrosis factor alpha (TNFa)
Similar affects of IL-1, but much less potent
ALSO it is important in activating macrophages
Prostoglandins are:
biochemically synthesized from the fatty acid, arachidonic acid of cells and membranes in response to cylooxygenases (COX-1 and COX-2).
Macrophages are recruited to the area of inflammation and are activated by binding to LPS, to produce ____.
(Prostoglandin E2, PGE2)
is upregulated by IL-1. TNF, and bacterial LPS and appears to be responsible for generating the prostoglandin (PG2) that is associated with inflammation.
The primary cells responsible for PGE2 production in the periodontium are ___ and ____.
macrophages and fibroblasts.
Induction of MMPs and osteoclastic bone resorption is induced by ____.
What is the least important diagnostic aid in recognizing the early stage of gingivitis?
stippling of the gingival tissue
-The presence of stippling is NOT diagnostic
-Inflammation, bleeding upon probing, and pocket depths are the MOST important diagnostic aids or signs of gingival or periodontal disease.
The normal tone or consistency of gingiva should be?
resilient and fibrotic in nature from the free-gingival groove apical to the MGJ.
No nutritonal deficiencies by themselves cause gingivitis or periodontitis. However, nutritonal deficiencies can affect the conditon of the periodontium.
Vitamin A deficiency
play an an important role in protecting against microbial invasion by maintaining epithelial integrity, A deficiency can impact the barrier function of epithelial cells
Vitamin D deficiency
essential for the absorption of calcium from the GI tract and the of the calcium-phosphorus balance. No human studies demonstrate a relationship between Vitamin D defiency and PD. Vitamin D deficiency can contribute to osteoporosis of alveolar bone in young dogs.
Vitamin B-complex deficiency
thiamin, riboflavin, niacin, pyridoxine, biotin, folic acid, and cobalamin. Deficiency of these as a group by contribute to gingivitis
Vitamin C deficiency
Severe deficiency results in Scurvy, bleeding, swollen gingiva and loosened teeth are common features of scurvy.
In a clinically healthy periodontitum, the microbial flora largely is composed of:
gram-positive facultative microorganisms
What are the predominant species of a healthy periodontium?
cocci and rods;
Bacteria found in the composition of plaque are?
gram-negative abaerobes
The host response of plaque bacteria is fundamentally an ___.
Inflammatory response
Decreases in the prevalence and numbers of which Three bacteria are associated with successful clinical treatment of disease?
P. gingivalis
T. forsythia
T. denticola
Endotoxins are the lipopolysaccaride component of the cell of:
gram-negative bacteria
lipopolysaccaride (LPS) containing gram negative cell wall extracts are capable of:
promoting bone resorption
inhibiting osteogenesis
chemotaxis of neutrophils
other events associated with PD
Free endotoxin is present in:
dental plaque and inflamed gingiva
Plaque accumulation has a _____ effect on the severity of gingivitis.
plaque bactera produces enzymes ____, ____, ___, ____, and ____ that may initiate periodontal disease
chondroitin sulfatase
produced by baceroides species
-catalyzes the degradation or hydrolysis of collagen
produced by streptococcus mitans and salivarius; may lead to the destruction of the amorphous ground substance
chondroitin sulfatase
produced by diphtheroids; may lead to the destruction of the amorphous ground substance
Antibodies or immunoglobulins are:
produced by plasma cells in response to oral bacteria or their by products.
What are the most numerous Antibodies or immunoglobulins? What do they do?
IgG; which act to neutralize bacterial toxins by enhancing phagocytosis.
The most likely source of of bacteria found in diseased periodontal tissue is __.
subgingival plaque
The likelihood that bacterial endotoxins play a major role in gingival inflammation is evidence by:
1. The reduction in inflammation by the removal of plaque
2. A reduction of the inflammatory state with antibiotic treatment
what is the predominant periodontal disease?
Which of the following clinical signs is characteristic of NUG?
"punched-out" papillae
Essential components of NUG:
-interdental gingival necrosis- described as "punch-out" papillae
-Variable features: fetid oris (offensive odor), lymphadenopathy, fever, malaise
What are the predominant organisms associated with NUG?
P. intermedia
Fusobacterium species
spirochetal microorganisms
NUG is usually associated with predisposing factors such as:
host factors
immunosuppression (HIV)
treatment of NUG or NUP:
-hydrogen peroxide (chlorhexidine)
-antiobiotic therapy: (Pen. V)
For treatment of Acute herpetic gingivostomatitis , which medication should be prescribed?
-If diagnosed within 3 days of onset, acyclovir suspension should be prescribed, 15 mg/kg fives times daily for 7 days
-All patients, including those presenting more than 3 days after onset, may recieve palliative care, including plaque removal, systemic NSAIDs, and topical anesthetics
-Patients should be informed that herpetic gingivostomatitis is contagious at certain stages; such as when vesicles are present
In a healthy sulcus, which bacteria are most abundant?
Streptococcus and Actinomyces species
-gram positive cocci and filamentous bacteria
Normal inhabitants of the oral cavity: gram-positive:
Normal inhabitants of the oral cavity: gram-negative :
_____ Consists of a variety of alpha-hemolytic streptococci, including: ____, ____, ____, and ___, ALL COMMON ORAL FLORA,
Viridans streptococci Consists of a variety of alpha-hemolytic streptococci, including: S. Salivarius , mutans, sanguis, and mitis, ALL COMMON ORAL FLORA
The oral cavity is usually sterile at birth, microorganisms appear abour ____ after birth.
10-12 hours after birth
After one year, the follwing bacteria are prsesent in a babies mouth?
-Streptococci: S. salivarius (most abundant), S. mutans and sanguis DO NOT APPEAR UNTIL TEETH ARE PRSENT.
By which age does the oral flora resemble an adult?
age 4-5
Early microbiolgic studies of localized agressive periodontitis (LAP) provided clear evidence of a strong association between disease and unique bacterial microbiota dominated by:
Actinobacillus actinomycetemcomitans (Aa) AKA Aggregatibacter actinomycetemcomitans
Refractory periodontitis patients
Do not respond to treatment and demonstrate continued clinical periodontal destruction
LAP characteristics:
localized agressive perio; onset around the time of puberty; localized almost exlusively to the incisors and first molars; familial pattern of occurence. Aa is the dominant bacteria in LAP
Diseases that clinically present as desquamative gingivitis include:
Linchen planus
pemphigus vulgaris
chronic ulcerative stomatitis
Linear IgA disease
Dermatitis herpetiform
Lupus erythematosus
Erythema muliforme
desquamative gingivitis
Clinical term charactertized by fiery red, glazed atrophic or eroded looking gingiva
-loss of stippling and the gingiva may desquemate easily with minimal trauma
-more common in middle-aged to elderly femailes
-painful affects on the buccal/labial gingiva
-spares the marginal gingiva, but can involve the whole thickness of the attached gingiva and its clinical appearance is not altered much by traditonal oral hygiene measures or periodontal therapy alone
What is the role of plaque in desquamative gingivitis?
It is vague
Periodontitis does not always begin with gingitvits
False, periodontitis ALWAYS BEGINS as gingivitis which usually is due to local irritation, primarily plaque, and the inflammation then spreads from the gingiva and soft tissues into the underlying structures.
Severe periodontal disease may be seen in patients with:
Chediak-Higashi syndrome
papillon-Lefevere syndrome
Down syndrome (increased levels of P.intermedia)
Lazy leukocyte syndrome
leukocyte adhesion deficiency (LAD)
Diseases that may be associated with increased severity of periodontal disease:
congenital heart disease
tetraology of fallot
Eisenmenger's syndrome
Ingestion of heavy metals; may result in chnages in the periodontium
A cuplike resorptive area at the crest of the alveolar bone in radiographic finding of:
Early periodontitis
Early periodontitis consits of:
localized erosion of the alveolar crest; blunting of the crest in anterior regions and a rounding of the junction betwen the crest and lamina cura in the posterior regions
Moderate periodontitis consist of:
The destruction of alveolar bone extends beyond early changes in the alveolar crest and may include buccal and lingual plate resorption, generalized horizontal erosion or localized vertical defects and possible clinical evidence of tooth mobilty.
Advanced periodontitis consits of:
The bone loss is so extensive that the remaining teeth show excessive mobility and drifting and are in jeapardy of being lost. There is usually extensive horizontal bone loss or extensive bony defects.
In health, the crest of alveolar bone is:
1-2mm below the CEJ of adjacent teeth
A reduction of only 0.5-1.0mm in the thickness of the cortical plate is sufficient to permit radiographic visualization of destruction of the inner cancellous trabeculae.
Diabetes DOES NOT CAUSE periodontal disease, but studies show:
it alters response of the periodontal tissues to bacterial plaque.
Characteristics of poorly controlled diabetics:
-enlarged gingiva
-sessile or pedunculated gingival polyps
-polypoid gingival proliferations
-abscess formation
-loosened teeth
Polymorphonuclear leukocyte deficiencies result in:
impaired chemotaxis
defective phagocytosis
impaired adherance
Chronic hyperglycemia adversely affects:
the synthesis, maturation, and maintenance of collagen and extracellular matrix. Numerous proteins and matrix molecules undergo a nonenzymatic glycosylation, resulting in accumulated glycation end products (AGEs). This increase in AGEs affects how collagen in normally repaired or replaced and may play a role in the progression of periodontal disease.
Which of the following is most significant in regard to the prognosis of a periodontally involved tooth?
Attachment loss (most critical)
ALSO mobility
Gingivitis is most often caused by:
Inadequate oral hygiene
The microbiota of chronic gingivitis consists of about equal proportions
gram positive: 56%
gram negative: 44%
faculatative: 59%
anaerobic: 41%
From health to disease
gram + shifts to gram -
cocci shifts to rods
nonmitile shifts to motile
facultative anaerobes shifts to obligate aerobes
fermenting shifts to proteolytic species
Components of the pellicle:
glycoproteins (mucins)
proline-rich proteins
phosphoproteins (stathetin)
histidine rich proteins
enzymes (alpha-amylase)
other molecules that function as adhesion sites for bacteria (receptors)
Bad breath is caused by
gram negative anaerobic bacteria associated with gingivitis and periodontitis cause bad breath by their proteolysis, which produced foul-smelling volatile sulfide compounds
Which of the following needs to be evident in order to make a diagnosis of periodontitis?
radiographic evidence of bone loss
What type of x-ray tends to be the most accurate in assessing alveolar bone resoprtion?
Bitewing x-rays, vertical bitewings
What percentage of the bone at the alveolar crest must be lost for a change in bone height to be reconginzed on radiographs?
Exudate is due to what?
presence of large numbers of neutrophils in the pocket
occlusal loading resulting in tooth flexure, mechanical microfractures, and tooth structure loss in the cervical area
loss of tooth structure by mechanical wear - horizontal tooth brushing with a hard tooth brush and abrasive dentifrice is the most common cause
The degree of gingival enlargemtn can be scored as follos: grade 0, grade I, grade II, and grade III. Enlargment confined to the interdental papilla would be scored as:
Grade 1
grade 0
no signs of gingival enlargement
grade I
enlargement confined to interdental papillae
grade II
enlargment involves papilla and marginal gingiva
grade III
enlarement covers three quarters or more of the crown
involving the marginal and attached gingivae and papillae
isolated sessile or pedunculated, tumor like enlargement
The most important plaque retentive factor is:
biologic width
Junctional epithelium and connective tissue attachment, average is 2mm (about .97mm for the JE and 1.07mm for the connective tissue attchment)
During pregnacy, there is an increase in levels of both progesterone and estrogen.

The so-called pregnancy tumor is not a neoplasm .
Both statements are TRUE
usually appears during the second or third month
What subgingival bacteria is increased during pregnacy?
Prevotella intermedia, these bacteria crave steroid hormones for their own metabolism
Gingival disease modified by systemtic factors include:
endocrine changes during pregnancy
blood dyscrasias (leukemia)
gingival diseases of specific bacterial origin
Neisseria gonorrhoeae
treponema pallidum
streptococcus species
gingival diseases of viral origin
herpesvirus infection
primary herpetic gingivostomatitis
Recurrent oral herpes
varicella zoster
gingival diseases of fungal origin
candidiasis (caused by Candida albicans)
gingival diseases of genetic origin
hereditary gingival fibromatosis
gingival diseases of systemic conditions
manifestations may appear as dequamative lesions, ulcerations of the gingiva or both
PMNs are the predominant immune cells in which stage of gingivitis?
stage I
Initial lesion (I)
Time: 2-4 days
Blood vessels: Vascular dilation, vasculitis
JE and SE: Infiltration of PMNs
Predominant immune cells:PMNs
Collagen: perivascular loss
Clinical findings: gingival fluid flow
Early lesion (II)
Time: 4-7 days
Blood vessels: Vascular proliferation
JE and SE: Infiltration of PMNs, rete pegs, atrophic areas
Predominant immune cells: lymphocytes
Collagen: increased loss around infiltrate
Clinical findings: Erythema bleeding on probing
Established lesion (III)
Time: 14-21 days
Blood vessels: Vascular proliferation + blood stasis
JE and SE: Same age stage II, more advanced
Predominant immune cells: plasma cells
Collagen: continued loss
Clinical findings: changes in color, size, texture
Advanced lesion (IV)
extenstion of the lesion into alveolar bone characterizes a fourth stage known as the advanced lesion or phase of periodontal breakdown. Microscopically, there is fibrosis of the gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage. In general, at this advanced stage, plasma cells continue to dominate the connective tissues, and neutrophils continue to dominate the JE and gingival crevice
Abnormalities in neutrophil function found in patients with ____ make the patient more suscpetible to agressive periodontitis.
Chediak-Higashi sydrome
Papillon-Lefevere syndrome
leukocyte adhesion deficiency type I (LAD-1)
leukocyte adhesion deficiency type 2 (LAD-2(
conditions in which the influences of periodontal infection are documented include:
Coronary heart disease
Diabetes mellitus
Acute bacterial pneumonia
Periodontal disease is the ___ complication of diabetes
sixth; others are retinopathy, nephropathy, neuropathy, macrovascular disease, altered wound healing
The frequency of maintenance visits for a patient who has had previous PD treatment should be dependent on two factors:
1. on the appearance and clinical condition of the gingival tissue
2. on the ability and performance of homecare
bleeding during circumfrential probing indicates:
that crevicular eptihelium is ulcerated due to active periodontal disease
Puberty is often accompanied by an exagerated response of the gingiva to plaque
Gonadotropic hormones during puberty may lead to increased levels of:
P. intermedia