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Periodontics > Intrinsic Factors > Flashcards

Intrinsic Factors Flashcards

0
Q

What do intrinsic (systemic) factors modify?

A

the host’s response to components of microbial plaque and their by products

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1
Q

What is the major etiologic (initiating factor in periodontal disease?

A

bacterial plaque

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2
Q

“Risk factor” is defined as?

A

an attribute or exposure that increases the probability of occurrence of disease

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3
Q

What do risk factors determine?

A

the onset, progression, and response to treatment of periodontal disease

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4
Q

What are the reported Innate risk factors?

A

race, sex, genetic/inherited, congenital immunodeficieny, Down’s syndrome, phagocyte dysfunction, ehlers-danlos syndrome, papillon-lefevre syndrome

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5
Q

what are the reported acquired and enviornmental risk factors?

A

poor oral hygiene, age, medications, tobacco/smoking, acquired immune defects & inflammatory/endocrine diseases, nutritional deficiencies, stress

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6
Q

Describe the current model of periodontitis.

A
  1. Start with microbial challenge
  2. Antigens, LPS, and other virulent factors drive it to a HOST IMMUNO-INFLAM RESPONSE
  3. Normally host response release Antibodies and PMNs to go back to microbial challenge
  4. But if enviornmental/acquired and genetic risk factors occur then it drives host response to release cytokines, matrix metalo-proteinases, and prostanoids to drive it to BONE AND CT METABOLISM
  5. this is then driven to CLINICAL SIGNS OF DISEASE INITIATION AND PROGRESSION which then adds all the way back to microbial challenge
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7
Q

What % of the US population smokes

A

25%

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8
Q

_____% of periodontitis cases can be attributed to smoking ________ (dependent or independent) of all other risk factors

A

> 50%, independent

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9
Q

______ is the MAJOR preventable risk factor for periodontitis in the US

A

smoking

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10
Q

What is the risk for current and former smokers?

A

4x risk for current, 2x risk for former

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11
Q

There is a ____ response relationship between cigarettes smoked and the odds of periodontitis. What are the risk #s?

A

Dose; for equal to 31/day is 6x risk

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12
Q

former smoker risk _____ with years since quitting. What is the risk after 0-2 years, and >or equal to 11 years?

A

reduce; 3x risk; same risk as non-smokers

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13
Q

Association of cigarette smoking and adult periodontitis is independent of? (2)

A

plaque or calculus levels or the presence of specific pathogens

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14
Q

Concerning plaque/bacteria, smokers have…? (3)

A
  1. increased plaque (not rate of plaque accumulation)
  2. more virulent types of bacteria- b/c decreased oxygen levels supporting anaerobic infection
  3. bacteria that are more difficult to eradicate because of altered host defense mechanisms
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15
Q

Difference in smokers host response is? This causes? (5)

A

decreased white cell function;

  1. decreased ability to move through tissue and respond to infection
  2. WBC pool in tissues - so fail to reach sites of infection
  3. decreased ability to kill bacterial
  4. phagocytosis
  5. oxidative burst
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16
Q

Systemic effect of smoking? Examples? (4)

A

increases blood cell production of pro-inflam substances;

  1. IL 1 & IL6
  2. TNF alpha
  3. PGE2
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17
Q

Wound healing in smokers? Causes?(4)

A

impaired;

  1. nicotine decreases blood flow in gingival tissues
  2. the decreased blood flow decreases nutrient supply
  3. components of smoke increase pro-inflam cytokine production
  4. this increases tissue-destructive enzyme activity
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18
Q

______ ______ _____ has also been shown to be a risk to general health and well being

A

untreated moderate periodontal disease

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19
Q

Periodontal disease may increase risk for? (3)

A
  1. Cardiovascular disease
  2. preterm low birth weight infants
  3. diabetes
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20
Q

Diabetes in an UNCONTROLLED diabetic, the gingiva may be….? (3) What can also occur? (2)

A
  1. deep red
  2. edematous
  3. prone to repeated abscess formation;
  4. extensive, rapid periodontal destruction
  5. delayed wound healing
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21
Q

What is a diagnostic sign in an undiagnosed diabetic?

A

tendency to repeated periodontal abscess formation

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22
Q

Diabetics that are adequately controlled may be managed…?

A

as normal patients

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23
Q

Precautions to take with diabetic patients?

A
  1. do not jeopardize controlled ptn by excessive trauma or lenghty procedures
  2. surgery performed as atraumatically as possible and 2-3 hours AFTER meal or insulin administration
  3. consult with attending physician prior to perio therapy
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24
Q

In Addison’s disease, patients suffer from?

A

adrenocortical deficiency

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25
Q

What has been reported to occur in Addison’s disease? (3)

A
  1. pigmentation of skin in 98%
  2. pigmentation of mucous membranes in 82%
  3. greater incidence of periodontal disease
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26
Q

In Addison’s disease, what can trigger an adrenal crisis? What is essential for perio treatment?

A

infection, trauma (including surgery), and stress; close consultation with ptn’s physician

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27
Q

What endocrine imbalance conditions are intrinsic factors? (3)

A
  1. diabetes
  2. Addison’s disease
  3. Sex hormones: puberty gingivitis, pregnancy gingivitis, menstrual cycle, monopausal gingivostomatitis
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28
Q

Sex hormones are considered _____ or ______ factors

A

initiating or complicating

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29
Q

What is puberty gingivitis?

A

an exaggerated response of gingiva to local irritation

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30
Q

Puberty gingivitis is most common in?

A

females

31
Q

Occurrence and prevention of puberty gingivitis.

A

is NOT a universal occurrence during puberty; can be prevented with proper plaque control

32
Q

What is pregnancy gingivitis? What is the tissue response mediated by?

A

changes during pregnancy varying from mild gingivitis to so-called pregnancy tumors; effects of progesterone on the microvasculature of inflamed CT

33
Q

what are pregnancy tumors?

A

are localized, inflamed, hyperplastic lesions that arise in areas of irritation

34
Q

Similar phenomena like pregnancy gingivitis/pregnancy tumors is seen in?

A

use of oral contraceptives

35
Q

What is the prevention and treatment for pregnancy gingivitis? What is treatment for pregnancy tumors?

A

with good oral hygiene -> minimal perio changes during pregnancy; gingival changes diminish postpartum with good oral hygiene; pregnancy tumors will not completely resolve and will require surgical intervention

36
Q

What is the general rule of gingival changes during menstrual cycle?

A

they may occur, however gen rule is that cycle is not accompanied by notable gingival changes

37
Q

What is menopausal gingivostomatitis?

A

a RARE condition that occurs during the menopause or postmenopausal period

38
Q

What are the signs and symptoms of menopausal gingivostomatitis? (4)

A
  1. tissues are dry and shiny
  2. ptns complain of burning sensation throughout oral cavity
  3. extreme sensitivity to thermal changes
  4. abnormal taste sensations
39
Q

The signs and symptoms of menopausal gingiviostomatis is similar to?

A

desquamative gingivitis

40
Q

What is desquamative gingivitis characterized by? This gingival condition is prob a ____ ____/____rather than a _______, this is because…?

A

by desquamation or sloughing of gingival epithelium leaving an intensely red surface; clinical syndrom/sign rather an a disease; the sloughing is due to vesiculation

41
Q

the majority of desquamative gingivitis represent? 3 conditions? Desquamate lesions can also be caused by? (name?) All of these conditions make….?

A

the oral manifestation of the dermatoses; mucous membrane pemphigoid, pemphigus, and erosive lichen planus;

allergic reactions (allergic gingivostomatitis); make oral hygiene difficult

42
Q

_____ mechanisms are suspected in pemphigoid and pemphigus. the etiology of lichen planus is _____.

A

autoimmune; unclear

43
Q

What are the clinical features of mucous membrane pemphigoid? (3) The histologic features? (3)

A
  1. gingival erythema
  2. vescile formation
  3. epithelium separted from subepithelial tissues;
  4. devoid or minimal rete ridges
  5. may not be keratinized
  6. epithelium separates from underlying CT
44
Q

What are the clinical signs of Pemphigus? (1) Histological signs? (2)

A
  1. fiery red gingiva;
  2. vesicle formation and sloughing of superficial layer of gingiva occurs INTRA-EPITHELIALLY
  3. basal cell layer remains attached to CT component
45
Q

What are the clinical signs of Lichen planus? (2) Histological signs? (3)

A
  1. many forms
  2. spider web-like network of hyperkeratosis known as wickham’s striae;
  3. saw tooth like rete ridges
  4. hyperkeratosis
  5. inflam infiltrate visible subepithelialy
46
Q

Ingestion of ____ ____ such as _____, ____, and _____ in medicinal compounds and through industrial contact may produce a ____ _____ in the gingiva. This is associated w/?

A

heavy metals; lead, mercury, and bismuth;

linear pigmentation; local irritation in areas of inflam

47
Q

In medication influenced gingival overgrowth, medications cause……? The amount of associated ______ has been related to?

A

hypertrophy of CT elements of gingiva (primary collagen) so that the gingiva appears swollen or overgrown;

amount of associated hyperplasia related to accumulation of bacterial plaque

48
Q

What medications cause gingival overgrowth and what is each used for? (3)

A
  1. dilantin- treatment of convulsive disorder
  2. calcium channel blockers- cardiovascular disorders
  3. cyclosporin- immunosuppresion
49
Q

What drugs associated with dilantin hyperplasia?

A

diphenylhydantoin sodium (phenytoin) and Mysoline - used to treat epilepsy

50
Q

Dilantin hyperplasia associated with marked ____ _____? Where does it appear?

A

gingival hyperplasia; first appears in the interdental papillae, and in advanced cases may become completely covered

51
Q

In dilantin hyperplasia, what increases rate of gingival overgrowth? So what is essential?

A

poor oral hygiene; excellent OH

52
Q

What is an important clinical sign suggesting hematologic disorder?

A

abnormal bleeding that is difficult to control

53
Q

What hematologic disorders covered in lecture? (7)

A
  1. leukemia
  2. anemia
  3. thrombocytopenic purpura
  4. hereditary hemorrhagic telangiectasia
  5. sturge-weber syndrome
  6. infectious mononucleosis
  7. agranulocytosis
54
Q

Gingival lesions of acute leukemia consist of? (3) These lesions occur most frequenty in? less frequent in? and seldom in?

A

marked hyperplasia, ulcerations of gingiva and persistent bleeding;

acute monocytic leukemia;
acute and subacute lymphatic and myelogenous leukemia;
chronic leukemia

55
Q

What aids in alleviating severe oral changes in leukemia?

A

elimination of local irritants

56
Q

The most prominent oral changes observed in various types of anemia are? (3)

A
  1. marked pallor of gingiva
  2. severe glossitis
  3. uniform atrophy of fungiform and filiform papillae
57
Q

What occurs in the gingiva in thrombocytopenic purpura?

A
  1. SPONTANEOUS bleeding into skin or from mucous membranes

2. gingiva is swollen, soft and friable

58
Q

in thrombocytopenic purpura, the gingival bleeding tends to be directly related to?

A

number of circulating platelets and patients oral hygiene

59
Q

What is hereditary heorrhagic telangiectasia? What is it characterized by? Treatment?

A

relatively rare vascular anomaly, sometimes known as Rendu-Osler-Weber disease;

by multiple dilations of capillaries and venules in skin and mucous membranes, with a tendency toward hemorrhage;
lesions in areas of chronic trauma or potential trauma should be excised

60
Q

What is sturge-weber syndrome? What are there in the gingiva?

A

a congenital condition characterized by capillary angiomas;

there are telangiectasis, vascular hyperplasia, and enlargement of gingiva with associated resoption of alveolar bone

61
Q

What is infectious mononucleosis? Usually occurs in? What are its oral findings???

A

benign infectious disease of unknown etiology; in children and young adults;

  1. erythema or petechiae of mucosa (particulary soft palate)
  2. severe gingivitis
  3. may predispose to ANUG
62
Q

What is agranulocytosis? What is the most common cause? Clinical characteristics?

A

an acute disease characterized by extreme leukopenia and neutropenia; drug idiosyncrasy but may be idiopathic;

  1. ulceration in oral cavity and throat
  2. gingiva may be hemorrhagic and necrotic
  3. generally appears as acute disease but may appear in clinical episodes (cyclic neutropenia)
63
Q

The important consideration in undiagnosed hematologic disorders is?

A

to refer ptn for proper medical diagnosis and treatment

64
Q

patients that do not respond to normal thearpy in a reasonable period of time should be suspected of having…?

A

an underlying systemic condition

65
Q

patients who have diagnosed hematologic disorders should be treated…..?

A

judiciously and all therapy should be coordinated with patient’s physician

66
Q

In interaction of etiological factors, what systemic factors lead to periodontal disease? (7)

A
  1. hematologic
  2. nervous system
  3. drug manifestation
  4. endocrine
  5. debilitating disease
  6. nutrition
  7. heredity
67
Q

in interaction of eto factors, what are the local factors? (5)

A
  1. iatrogenic
  2. calculus
  3. traumatic injury
  4. chemical injury
  5. excessive occlusal force
68
Q

In interaction eto factors, what are the bacterial factors that lead to periodontal disease? (3)

A
  1. cytotoxins
  2. enzymes
  3. immunopathic mechanisms
69
Q

What are the steps in the progression to attachment loss? (6) At which steps does the host status and defense effect?

A
  1. plaque accumulation
  2. maturation of subgingival plaque
  3. presence and quality of certain bacteria
  4. inflammation
  5. CT destruction
  6. Attachment loss;

effects bacteria, inflam, and ct destruction (steps 3-5)

70
Q

What are the modifying influences in plaque accumulation? (5)

A
  1. OH
  2. tooth malposition
  3. tooth anatomy
  4. restorations
  5. gingival contours
71
Q

What are the modifying influences in presence and quality of certain bacteria? (7)

A
  1. maturation of marginal plaque
  2. host defenses
  3. pocket depth
  4. restorations
  5. subgingival enviornment
  6. calculus
  7. smoking
72
Q

what are the modifying influences in CT destrution? (4)

A
  1. genetic influences
  2. inflam
  3. particular bacteria
  4. smoking
73
Q

What were the steps in the 1970s model of periodontitis? (4/5)

A
  1. bacterial plaque
  2. calculus formation
  3. periodontal pocket formation & occlusal trauma
  4. bone loss
74
Q

In the progression of PD, what varies from patient to patient? (3) Why do these vary?

A
  1. severity of disease
  2. rate of progression
  3. response to therapy;

b/c PD is a complex interaction b/t an infection and a susceptible host

75
Q

What are the points in risk factors (4) vs risk markers (3)?

A

Risk factors:

  1. part of causal chain
  2. exposure of host to disease
  3. presence directly increases probability of disease
  4. removal decreases probability of disease

Risk marker:

  1. consequence of disease
  2. not part of causal chain
  3. alternative measures of the disease

Periodontics (4 decks)

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