Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
115 Cards in this Set
- Front
- Back
|
What is the difference between coaggrigation and adherence?
|
Adherence refers to the physical mechanism of attachement via fimbrae etc. and coaggrigation refers to the propagation by symbiotic growth.
|
|
|
What is another name for subgingival plaque?
|
Serumal plaque because it uses oral derived and serum sources of Ca ions. The serumal is darker pigmented due to Heme
|
|
|
What pattern does plaque follow?
|
It is usually symmetrical. What you see on one side of the mouth is what you are likely to find on the other.
|
|
|
Does calculus cause the irritation that leads to periodontal disease?
|
No. It is not the calculus, but the bacteria that are the irritants that lead to periodontal disease.
|
|
|
What is calculus?
|
Mineralized plaque
|
|
|
Which type of plaque forms first?
|
Supra gingival from Ca ions in the saliva.
|
|
|
How does calculus attach?
|
Ca ions bind carboprotein complexes in plaque, then phosphates come out of saliva and CAPO4 moves from extracellular to intracellular. The calculus begins to form from the tooth side of the plaque and moves outward.
|
|
|
What is calculus made from?
|
¾ is made up of Ca3PO4(2) (Calcium Phosphate)
|
|
|
What are 4 types of Calcium phosphate from most common in calculus to least common?
|
Hydroxyapatite, Magnesium withlockite, octacalcium phosphate, and brushite.
|
|
|
How does calculus grow?
|
You start with CaPO4 saturation, then you get heterogeneous nucleation to form islands that coalesce and form rings with cyclical spacing. It grows in mass not like enamel with rods or prisms.
|
|
|
Where is the advancing disease front of calculus formation?
|
Near the apices. The calculus at the top just gives a history of past calculus formation
|
|
|
Where should you start when removing these calculus rings?
|
You should always start at the bottom and work up. The blood and fluids might make it very difficult to see what is going on if you wait.
|
|
|
What one thing has improved dental treatments of calculus deposits more than any other?
|
Cavitrons…we should use the heavy tips for the removal of these tenacious deposits.
|
|
|
What is the most effective treatment for reducing inflammation associated with chronic periodontal disease?
|
SRP to remove calculus.
|
|
|
What are some possible iatrogenic issues?
|
Restorative Margins, Open contacts/food impaction, Pontic form, RPD design, Post-orthodontic problems, and root fractures.
|
|
|
What can lead to overhangs in the margin on amalgam restorations?
|
Failure to wedge
|
|
|
Is it better to be over contoured or undercontoured?
|
It is better to be undercontoured. Too large of a bulge can cause irritation
|
|
|
What can cause food impaction?
|
If there is no contact between the teeth and less than 1 mm/ slightly open contacts. If the space is more than 2mm then the food will exit laterally.
|
|
|
What can food impaction cause?
|
Accelerated periodontal and carious lesions.
|
|
|
What can be done to hide papillary recession on anterior teeth?
|
You could lengthen the contact point gingivally to cover the whole.
|
|
|
What is the most important key to distributing the stress correctly on an RPD?
|
The rest seat. The clasping arrangement also dictates torque
|
|
|
Does crowding cause periodontal disease or aid in its progression?
|
No. There is no cause and effect relationship.
|
|
|
What might equal periodontal pockets located on opposite sides of a tooth root in a patient that doesn’t have pockets in the balance of the mouth suggest?
|
Root fracture.
|
|
|
What is a common cause of root fracture?
|
Build-up posts. We have to be careful when altering the stress loads in the teeth.
|
|
|
What are some habits that might affect periodontal status?
|
soft tissue trauma (recession due to brushing), Bruxing, Clenching, factitious habits, medications, and chemical irritation.
|
|
|
Does Clenching or Bruxing cause more periodontal issues?
|
Clenching does. It is virtually bruxing without the movement.
|
|
|
What happens to the PDL with occlusal trauma?
|
The PDL gets wider.
|
|
|
Can occlusal trauma cause periodontal disease?
|
No, but it can be accelerated if gum disease is already going on.
|
|
|
What are some examples of factitious habits?
|
Floss notches and pipe chewer
|
|
|
How long on average do bruxers have their teeth in contact?
|
17 min per night compared with 2 min per day for a non-bruxer
|
|
|
Which has worse outcomes, Bruxing or clenching?
|
Clenching
|
|
|
How does occlusal trauma affect perio disease?
|
A pre-existing gum disease is accelerated by occlusal trauma
|
|
|
What 4 things need to be controlled to solve occlusal related trauma?
|
Duration, direction, frequency and intensity of force
|
|
|
What medications cause gingival hyperplasia?
|
Dilantin (anticonvulsants), Cyclosporine (Immunosuppressants), Calcium Channel Blockers (a class of antihypertensives)
|
|
|
What is the largest single risk factor for periodontal disease?
|
Smoking
|
|
|
What are the effects of smoking?
|
Decreased gingival blood flow, Cotinine and nicotine root contamination, Increased humoral destructive mediators, Cytotoxic to fibroblasts, Decreases chemotaxis of macrophages and PMNs, and Encourages growth of gram neg flora, some species more resistant to therapeutic control especially AA and B. Forsythus
|
|
|
What can unerupted teeth cause?
|
Erosion of tooth roots or leave defects in bone upon removal
|
|
|
What are enamel projections?
|
Areas that should be cementum but are enamel. 8-28% of teeth, most common in mand. 2nd molars, then max. 2nd molars
|
|
|
What kind of issue are root grooves?
|
Home care issues when disease exposes the concavity of the root. Most common in max. 1st bicuspids on the mesial surfaces
|
|
|
What effects do caries at proximal contacts have?
|
Encourages food impaction and periodontitis development
|
|
|
How does active caries influence gingival health?
|
Bacteria accumulate and complicate perio health
|
|
|
What problems can occur with a misplaced frenum insertion?
|
May interfere with normal oral hygiene, deflect gingival margin during function, receive traumatic injury or encourage food impaction
|
|
|
What does the roll test check?
|
Keratinized versus attached gingival
|
|
|
Can future outcome be predicted based on original diagnosis?
|
No
|
|
|
What group of people have depressed clinical signs of disease?
|
Smokers, because of reduced blood flow
|
|
|
What are the two mechanisms for defending gingival?
|
Saliva and Gingival crevicular fluid
|
|
|
What does saliva do?
|
Cleanses exposed oral surfaces, buffers bacterial acids, and controls bacterial activity through lysozyme, lactoferrin, myeloperoxidase, IgA, Parotid Amylase, Antiproteases and glycoproteins
|
|
|
What are the characteristics of gingival crevicular fluid?
|
Contains crevicular leukocytes (PMNs), has outward flow, and concentrates some antibiotics like tetracycline
|
|
|
What are the stages of gingivitis?
|
Initial lesion 2-4 days, Early lesion 4-7 days, and Established lesion 14-21 days
|
|
|
What is periodontitis often referred to as?
|
As an Advanced gingival lesion. This is confusing b/c periodontitis is defined as loss of attachment while gingivitis is confined to the gingival.
|
|
|
What are some characteristics of an initial lesion?
|
Mostly subclinical , increased intercellular spacing but not ulceration, Edema from dilation and inflammation adjoining the vessel, chemically mediated bacterial destructuion by PMNs
|
|
|
What facilitates vessel widening in an initial lesion?
|
Loss of perivascular connective tissue
|
|
|
What are the clinical signs of initial gingivitis?
|
GCF flow and edema
|
|
|
When is the maximum PMN migration?
|
6-12 days
|
|
|
What are the clinical signs of early gingival lesions?
|
Erythema, BOP, and ulceration
|
|
|
What are some characteristics of early lesions?
|
Rete peg formation, vessel proliferation below epithelial attachment, pocket wall relaxes creating space between sulcus wall and tooth, immunological cells – PMNs, and T-lymphocytes in CT at basement membrane sulcular epithelium
|
|
|
What are the clinical signs fo established gingivitis?
|
GCF flow rate related to intensity of inflammation,
|
|
|
What are some characteristics of established gingivitis?
|
Bluish discoloration, glistening surface, loss of gingival adaption to the tooth, Plasma cells preponderant, B-lymphocytes, IgG components. Defensive cell lines rather than repair cell lines
|
|
|
What happens to the gingival fiber apparatus as it is converted to a gelatinous mass of inflammatory cells?
|
It becomes flaccid
|
|
|
What can happen to the CT of chronically inflamed gingival?
|
They may become fibrotic as collagen is being produced to wall off the lesion.
|
|
|
Which shrinks more with SRP flaccid or fibrotic?
|
Flaccid tissues
|
|
|
How is gingival inflammation described?
|
Duration – acute, chronic, or recurrent. Area involved – Localized or generalized. Tissues involved – papillary, Marginal, or diffuse (inflammation extends to the mucogingival junction)
|
|
|
Why is most gingivitis first seen in the papillary area?
|
Plaque control is poorer interproximally
|
|
|
What is marginal gingivitis?
|
Gingivitis that has the involvement of the marginal gingival tissues, which includes the papillary tissues. So both papillary and marginal tissues are involved in marginal gingivitis
|
|
|
What is involved in papillary gingivitis?
|
Only the papillary tissue not the marginal tissue
|
|
|
What is diffuse gingival inflammation?
|
Inflammation involves the papilla, marginal tissues and extends through the attached gingival to the alveolar mucosa
|
|
|
What are two ways that you might see gingival pigmentation?
|
You might get impactioin of amalgam filings that were deposited during crown prep or heavy metals such as bismuth can be deposited during heavy drug use.
|
|
|
What type of gingival enlargement is characteristic of anticonvulsants?
|
More fibrous
|
|
|
What type of gingival enlargement is associated with channel blockers or immunosuppressant drugs?
|
More mushy and flaccid.
|
|
|
What can be used to gauge the intensity of inflammation in the gingival?
|
The severity of bleeding and the ease of provoking it.
|
|
|
What might be the cause of bluish discoloration of the gingival adjacent the pocket?
|
Calculus
|
|
|
What happens to the gingival of smokers?
|
The gingival blood flow is slowed for about 4 hrs each time they smoke. This might cause gingival palor that might be mistaken for health.
|
|
|
Do initial, early or established lesions progress to periodontitis?
|
Not always.
|
|
|
What differentiates gingivitis from periodontitis?
|
Attachment loss
|
|
|
What is the difference between a sulcus and a Pocket?
|
A pocket bleeds on probing and a sulcus doesn’t.
|
|
|
What is a gingival/psuedopocket?
|
Coronal movement of the gingival margin without attachment loss.
|
|
|
What is a periodontal pocket?
|
Apical movement of the epithelial attachement due to the loss of the attachement apparatus.
|
|
|
What are the 3 types of pocket formation?
|
Pseudopockets/gingival pockets, Suprabony pockets (epithelial attachemt is coronal to crest of bone with horizontal bone loss), and Infrabony pockets (epithelial attachment is apical to the crest of the bone with vertical bone loss).
|
|
|
What steps of true pocket formation?
|
Gingival inflammation, epithelial attachement cells experience widening of cell to cell junctions, degeneration of gingival fibers apical to attachment, PMN’s invade coronal portion of attachment and at 60% volume the attachment detaches and sulcus deepens, and epithelial cells migrate apically.
|
|
|
What are the subgingival zones in periodontal pockets coronal to apical?
|
Calculus, attached plaque, unattached plaque, JE, Partially lysed CT fibers, and intact CT fibers.
|
|
|
What zone to P gingivalis and AA generally reside in?
|
the Junctional Epithelium
|
|
|
Is chronic periodontis a generalized condition?
|
No. It is site specific and occurs at different rates in different areas.
|
|
|
What are 7 different areas with in the periodontal pocket?
|
Quiescence, bacterial accumulation, emergence of leukocytes, leukocyte-bacterial interaction, epithelial desquamation, ulceration w/exposed CT, and areas of hemorrhage.
|
|
|
What process results in gum recession?
|
The fusion of sulcular epithelium as it migrates laterally with the oral epithelium
|
|
|
What causes gingival recession?
|
It isn’t natural and is usually associated with soft tissue trauma from excessive brushing or from infection.
|
|
|
What are the cemental changes associated with periodontal disease?
|
Bacteria found on the roots, Bacteria can penetrate the cementum, bacterial growth lead to breakdown of cementum surface and necrotic cementum, bacteria produce endotoxins that produce root toxicity that is antigenic to the soft tissues and so recession can occur.
|
|
|
What is the primary treatment to remove the bacteria laden cementum?
|
SRP and surgical exposure. The cavitron can remove 90% of the bacteria.
|
|
|
What is used as a gauge for required therapy?
|
Pocket depth
|
|
|
What dictates the prognosis of periodontal disease?
|
Attachement level
|
|
|
What is the normal distance between the apical end of the JE and the alveolar bone?
|
Usually about 1 mm.
|
|
|
What path does the gingival inflammation take?
|
It follows the vaculature via the interdentinal artery or the supraperiosteal.
|
|
|
How is the biological width maintained when the JE moves apically?
|
Demineralization of alveolar crest
|
|
|
What are the 4 types of bone loss?
|
Cell mediated(osteoclast induction), non-cell mediated (chemical), Negative bone balance(osteopenia, osteoporosis), and direct bacterial induction
|
|
|
How far away will plaque have an effect?
|
A radius of 2.5 mm or more.
|
|
|
In the study of tea laborers how many had rapid progression of periodontal disease and how many didn’t?
|
8% had rapid progression, 81% had moderate progression, and 11% had minimal or no progression.
|
|
|
What is the normal rate of bon loss per year facially and proximally if disease is untreated?
|
.2mm facially and .3 mm proximally.
|
|
|
What is the most common defect in chronic periodontitis?
|
The osseous crater.
|
|
|
What are the 3 types of vertical osseos defects/craters?
|
3 wall, 2 wall, and 1 wall.
|
|
|
Which teeth are lost first most often?
|
Max 2nd molars, mandibular 2nd molars, Max First molars, Mand 1st molars, Max lateral and Mand central incisors and then maxillary first bicuspids.
|
|
|
Which teeth are often left as the lone ones in the mouth?
|
K9’s and 2nd premolars.
|
|
|
What are the 7 characteristics of chronic periodontitis?
|
Supra and subgingival plaque, Marginal inflammation, Pocket formation, Recessiion, Bone loss (crater initially), attachement loss, and site specific.
|
|
|
What did the goodson et. al. study in 1982 look at?
|
Trends in attachment levels in untreated subjects over a years time. 83.8% of sights didn’t change. 5.7% of sites significantly deeper. 11.5% of sites became significantly shallower. Results suggest a dynamic condition of disease exacerbation and remission as well as periods of inactivity may be characteristic of periodontal disease
|
|
|
What are the different progression models?
|
Chronic progression (site specific), Asynchronus burst (rits both chronic and aggressive disease), Synchronus burst (true of more aggressive disease)
|
|
|
What are the classifications of aggressive periodontitis?
|
Generalized and localized
|
|
|
What are the characteristics of aggressive periodontitis?
|
Onset under 30 yrs, otherwise clinically healthy pt, rapid attachment loss and bone destruction, amount of micerobial deposits inconsistent with chronic disease severity, alterations in host’s immune response, familial aggregation of diseased individuals, predilection for black and Mediterranean races, incidence .1-.5%
|
|
|
What are common but not universal characteristics of aggressive periodontitis?
|
Sites infected with AA, Abnormalities in phagocyte function, hyperresponsive macrophages, producing increased PGE2 and IL-1B, in some cases, self-arresting disease progression
|
|
|
How has terminology of localized aggressive periodontitis?
|
1923 – Gottlib “cementopathis, 1938 – Wannamacher “parodontitis marginalis progressive” “periodontosis”, 1967 – Chaput “juvenile periodontitis” 1971 – Baer disease seen around 1st molar, 1989 – World workshop “localized juvenile periodontitis” on of several “early onset periodontitis”, 1999 – International Workshop on periodontal Nomenlature “localized aggressive periodontitis
|
|
|
How does aggressive periodontitis present?
|
Circumpubertal onset of disease, localized 1st molar or incisor disease with proximal attachment loss on at least two permanent teeth, one of which is a first molar, robust serum antibody response to infecting agent, strong relationship with AA, organisms are found in CT instead of an organized biofilm
|
|
|
What findings are seen in advancing disease?
|
1. Distolabial migration of the max incisors with concomitant diastema formation 2. Increasing mobility of the 1st molars 3. Sensitivity of denuded root surfaces to thermal and tactile stimuli 4. Deep, dull, radiating pain during mastication, probably because of irritation of the supporting structures 5. Periodontal abscesses may form 6 regional lymph node enlargement may occur
|
|
|
What are possible disease limiting factors?
|
1. Opsonic Antibodies limit infection by enhancing cellular destruction of AA 2. Bacterial competitive inhibition reduces AA site infection 3. AA loses its leukotoxin production capability as it replicates (reason unknown) 4. Cemental formation defect facilitates breakdown but is limited to only certain teeth
|
|
|
What are characteristics of generalized aggressive periodontitis?
|
Affects persons under 30, attachment loss affecting at least three teeth other than 1st molars and incisors, pronounced episodic nature of periodontal destruction, poor serum antibody resoponse to infecting agents, may be autoimmune related, intensified by smoking, bone loss of 25-69% can occur in as little as 9 weeks
|
|
|
What does an active generalized aggressive periodontitis infection look like?
|
Severe acutely inflamed tissue often proliferating ulcerated and fiery red, bleeding may occur spontaneously or with slight stimulation. Suppuration may be an important feature. AA, P. Gingivalis, T. Forsythus singly or mixed infection.
|
|
|
What does the quiescent phase of generalized aggressive periodontitis look like?
|
Gingival tissues appear pink, free of inflammationand occasionally with some degree of stippling. Despite mild clinical appearance, deep pockets can be demonstrated by probing
|
|
|
What three diseases are develop with genetic leukocyte adhesion defects?
|
Otitis media, upper respiratory disease, prepubertal periodontitis
|
|
|
In prepubertal aggressive periodontitis what usually parallels the degree of disease, localized or generalized?
|
The severity of immunological defects
|
