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DENT 318 - Periodontology > Diagnosis of Periodontal Diseases > Flashcards

Diagnosis of Periodontal Diseases Flashcards

1
Q

6 characteristics common to all dental plaque-induced gingival diseases

A
  1. Signs and symptoms confined to gingiva
  2. Presence of plaque
  3. Clinical signs of inflammation
  4. Periodontium with NO LOSS of attachment OR a stable but reduced periodontium
  5. Reversibility of the disease
  6. Possible role as a precursor to attachment loss
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2
Q

4 clinical signs of inflammation of gingiva

A
  • Enlarged gingival contours due to edema or fibrosis
  • Color transition to a red and/or bluish-red
  • BOP
  • Increased gingival exudate
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3
Q

2 drug-influenced gingival diseases

A
  • Drug-influenced gingival enlargements
  • Drug-influenced gingivitis
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4
Q

Example of drug-induced gingivitis

A

Oral contraeptive-associated gingivitis (frank signs of gingival inflammation in the presence of relatively little plaque)

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5
Q

Example of a gingival disease modified by malnutrition

A

Ascorbic acid deficiency gingivitis or scurvy

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6
Q

Describe ascorbic acid deficiency gingivitis/ scurvy

A

Gingiva is bright red, swollen, ulcerated and tendency toward bleeding and alteration toward a spongy consistency

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7
Q

10 characteristics of plaque-induced gingivitis

A
  1. Plaque precent at gingival margin
  2. Disease begins at gingival margin
  3. Change in gingival color
  4. Change in gingival contour
  5. Sulcular temperature change
  6. Increased gingival exudate
  7. Bleeding upon provocation
  8. Absence of attachment loss
  9. Absence of bone loss
  10. Reversible with plaque removal
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8
Q

Color of normal gingiva

A

Pale pink

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9
Q

Color of gingiva with gingivitis

A

Reddish/bluish-red

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10
Q

Size of normal gingiva (describe papillary, marginal and sulcular)

A
  • Papillary gingiva fills interdental spaces
  • Marginal gingiva forms knife edge with tooth surface
  • Sulcus depth ≤ 3 mm
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11
Q

Size of gingiva with gingivitis

A

Swelling both coronally and bucco-lingually

Pseudopocket

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12
Q

Shape of normal gingiva

A

Scalloped - troughs in marginal areas rise to peaks in interdental areas

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13
Q

Shape of gingiva with gingivitis

A

Edema which blunts the marginal and papillary tissues leads to the loss of the knife edge adaptation. Marginal swelling leads to less accentuated scalloping

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14
Q

Consistency of normal gingiva

A

Firm

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15
Q

Consistency of gingiva with gingivitis

A

Soft; pressure-induced pitting due to edema

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16
Q

Clinically define pyogenic granuloma (pregnancy tumor)

A

Not a real tumor, but an exaggerated inflammatory response during pregnancy to plaque. Painless protuberant, exophytic mass that is attached by a sessile or pedunculated base from the interproximal space

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17
Q

Cause of pyogenic granuloma

A

Combination of the vascular response induced by progesterone and the matrix stimulatory effect of estradiol

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18
Q

Histological feature of pyogenic granuloma

A

Highily vascularized mass of granulation tissue

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19
Q

Most common area of mouth affected by pyogenic granuloma

A

Anterior papillae of the maxillary teeth

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20
Q

When do pyogenic granulomas regress?

A

Following parturition (not always)

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21
Q

3 main classes of medication implicated in drug-influenced gingival enlargement

A
  • Anticonvulsant
  • Immunosuppressant
  • Calcium channel blockers
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22
Q

2 examples of anticonvulsants implicated in drug-influence gingival enlargement

A

Phenytoin

Valproic acid

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23
Q

Example of immunosuppressant implicaed in drug-influenced gingival enlargement

A

Cyclosporine

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24
Q

Most common location for drug-influenced gingival enlargement

A

Anterior gingiva first observed at the interdental papilla

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25
Q

Age group with higher prevalence for drug-influenced gingival enlargement

A

Children

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26
Q

Time of onset of drug-ingluence gingival enlargement

A

Within 3 months

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27
Q

13 characteristics of drug-influenced gingival enlargement

A
  1. Variation in interpatient and intrapatient pattern
  2. Predilection for anterior gingiva
  3. Higher prevalence in children
  4. Onset within 3 months
  5. Change in gingival contour leading to modification of gingival size
  6. Enlargement first observed at the interdental papilla
  7. Change in gingval color
  8. Increased gingival exudate
  9. Bleeding upon provocation
  10. No evidence that attachment loss is a sequela, but can be superimposed on pre-existing periodontitis
  11. Pronounced inflammatory response of gingiva in relation to the plaque present
  12. Reducations in dental plaque can limit the severity of lesion
  13. Histological characteristics of the enlarged tissue may be similar to normal gingiva
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28
Q

3 examples of gingival diseases of specific bacterial origin

A
  • Neisseria gonorrhea-associated lesions
  • Treponema pallidum-associated lesions
  • Streptococcal species-associated lesions
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29
Q

Example of gingival disease of viral origin

A

Herpes virus infections

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30
Q

3 examples gingival diseases of fungal origin

A
  • Candida-species infections
  • Linear gingival erythema
  • Histoplasmosis (a granulomatous disease caused by the fungus Histoplasma capsulatum)
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31
Q

Example of gingival lesion of genetic origin

A

Hereditary gingival fibromatosis

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32
Q

2 examples of gingival manifestations of systemic conditions

A
  • Mucocutaneous disorders
  • Allergic reactions
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33
Q

3 types of traumatic lesions causing gingival lesions

A
  • Chemical injury
  • Physical injury
  • Thermal injury
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34
Q

8 non-plaque-induced gingival lesions

A
  1. Gingival diseases of specific bacterial origin
  2. GIngival diseases of viral origin
  3. Gingival diseases of fungal origin
  4. Gingival lesions of genetic origin
  5. Gingival manifestations of systemic conditions
  6. Traumatic lesions
  7. Foreign body reactions
  8. Not otherwise specified
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35
Q

3 ways that gingival lesions of specific bacterial origin may manifest

A
  • FIery red edematous painful ulcerations
  • Asymptomatic chancres or mucous patches
  • Atypical non-ulcerated, highly inflamed gingiva
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36
Q

3 main viruses known to cause gingivitis

A
  • HSV-1
  • HSV-2
  • Varicella-zoster virus
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37
Q

Describe how some viruses may manifest as gingival diseases

A

Usually enter human body in childhood and may give rise to oral mucosal disease followed by periods of latency and sometimes reactivation

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38
Q

Classic initial manifestation of HSV-1

A

Primary herpetic gingivostomatitis

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39
Q

Characteristic manifestation of primary herpetic gingivostomatitis

A

Painful severe gingivitis with ulcerations and edema accompanied by stomatitis. Characteristic feature is formation of vesicles which rupture, coalesce and leave fibrin-coated ulcers

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40
Q

When does healing occur for primary herpetic infection

A

Spontaneously without scarring in 10 - 14 days (but virus remains latent in ganglion cell)

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41
Q

Manifestation of recurrent intraoral herpes

A

Usually presents in the form of herpes labialis but recurrent intraoral herpes characteristically manifests as a cluster of small painful ulcers in the attached gingiva and hard palate (NOT on alveolar mucosa)

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42
Q

3 factors triggering reactivation of latent herpes virus

A

Trauma

UV light

Fever

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43
Q

Primary infection of varicella-zoster virus

A

Chickenpox

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44
Q

Location of latent VZV

A

Dorsal root ganglion

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45
Q

Latent reactivation of VZV from trigeminal ganglion

A

Herpes zoster (shingles) (20% of cases)

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46
Q

Primary VZV infection oral manifestation

A

Small ulcers usually on the tongue, palate and gingiva

NOTE: If the second and third branch of the trigeminal nerve is involved, skin lesions may also be associated

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47
Q

Characteristics of herpes zoster intraorally

A
  • Unilateral lesions following the infected nerve
  • Initial symptoms = pain and paresthesia which may be present before lesions occur
  • Lesions initiate as vesicles involving the gingiva
  • Vesicles rupture to leave fibrin-coated ulcurs which often coalesce to irregular forms
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48
Q

Potential manifestation of VZV in immunocompromised patients

A

Severe tissue destruction with tooth loss and necrosis of alveolar bone and high morbidity

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49
Q

When does infection by C. albicans typically occur? (4 conditions)

A

Infection is considered opportunistic and usually occurs as a consequence of reduced host defense, including immunodeficiency, reduced saliva secretion, smoking and treatment with corticosteroids

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50
Q

Oral manifestations of candidosis (1 typical and 4 other)

A
  • Erythema of attached gingiva often associated with a granular surface sometimes referred to as linear gingival erythema
  • Other = pseudomembranous candidosis, erythematous candidosis, plaque type candidosis, nodular candidosis
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51
Q

Describe pseudomembranous candidosis

A

Whitish patches which can be wiped off with a gauze leaving a slightly bleeding surface

No major symptoms

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52
Q

Describe erythematous candidosis

A

Erythematous lesions can be found anywhere in the oral mucosa. Intensely red lesions usually associated with pain, sometimes even severe

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53
Q

Describe plaque-type candidosis

A

Whitish plaque which cannot be removed

Usually asymptomatic

Lesion is clinically indistinguishable from oral leukoplakia

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54
Q

Describe nodular candidosis

A

Nodular candidal lesions are infrequent in the gingiva.

Slightly elevated nodules of white or reddish color

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55
Q

Define linear gingival erythema

A

LGE is regarded as a gingival manifestation of immunosuppression characterized by a distinct linear erythematous band limited to the free gingiva and a disproportion of inflammatory intensity for the amount of plaque present. No evidence of pocketing or attachment loss.

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56
Q

Key feature of linear gingival erythema

A

Lack of BOP

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57
Q

Microflora of lingear gingival erythema

A

Comprises both C. albicans and a number of periodontopathogens

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58
Q

Treatment for linear gingival erythema

A

Conventional therapy plus rinsing with 0.12% chlorhexidine gluconate twice daily –> significant improvement over 3 months

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59
Q

Define histoplasmosis

A

Granulomatous disease caused by Histoplasma capsulatum which is a soil saprophyte found mainly in feces from birds and cats

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60
Q

Course of infection of histoplasmosis in a normal host

A

Subclinical (usually must be immunocompromised for symptoms)

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61
Q

Clinical manifestations of histoplasmosis

A

Acute and chronic pulmonary histoplasmosis and a disseminated form mainly occurring in immunocompromised patients

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62
Q

Describe the oral lesions of histoplasmosis

A

May affect any area of the mucosa including the gingiva. Initiate as nodular and papillary and later become ulcerative and painful. Sometimes granulomatous and clinical appearance may resemble a malignant tumor

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63
Q

Treatment for histoplasmosis

A

Systemic antifungal therapy

64
Q

Define hereditary gingival fibromatosis

A

Gingival hyperplasia of genetic origin. May be an isolated disease entity of part of a syndrome. Uncommon condition

65
Q

6 clinical manifestations that may be associated with hereditary gingival fibromatosis in the setting of a syndrome

A
  • Hypertrichosis
  • Mental retardation
  • Epilepsy
  • Hearing loss
  • Growth retardation
  • Abnormalities of extremities
66
Q

Characteristics of hereditary gingival fibromatosis

A
  • Diffuse gingival enlargement, sometimes covering major parts of, or the total tooth surface
  • Typically presents as large masses of firm, dense, resilient, insensitive fibrous tissue covering the alveolar ridges and extends over the teeth resulting in extensive pseudopockets.
  • Color may be normal or erythematous
67
Q

Treatment for hereditary gingival fibromatosis

A

Surgical removal, but relapses are common

68
Q

5 mucocutaneous disorders that present gingival manifestations in the form of desquamative lesions or ulceration of the gingiva

A
  • Lichen planus
  • Pemphigoid
  • Pemphigus vulgaris
  • Erythema multiforme
  • Lupus erythematosus
69
Q

Most common characteristic oral manifestations of lichen planus

A

White papules with white striations which often form reticular patterns

70
Q

6 forms of lichen planus

A
  • Papular
  • Reticular
  • Plaque-like
  • Atrophic
  • Ulcerative
  • Bullous
71
Q

7 dental restorative materials that may cause an allergic reaction

A
  • Mercury
  • Nickel
  • Gold
  • Zinc
  • Chromium
  • Palladium
  • Acrylics
72
Q

Describe lesions associated with allergic reactions to dental restorative materials

A

Reddish or whitish, sometimes ulcerated lesions that have clinical similarities with oral lichen planus or leukoplakia which resolve after removal of the offending material

73
Q

Causative agents in toothpastes and mouthwashes that may cause allergic reactions

A

Flavor additives or preservatives

74
Q

Clinical manifestations of allergic reactions to toothpastes and moutwashes

A

Fiery red edematous gingivitis sometimes with ulcerations or whitening

May involve labial, buccal and tongue mucosa. Cheilitis may be seen

75
Q

Describe oral lesions associated with Crohn’s disease

A

Irregular long ulcerations with elevated borders with a cobblestone appearance. Granulomatous gingival hyperplasia.

76
Q

Type of leukemia most commonly associated with gingival changes

A

Acute myeloid leukemia

77
Q

5 clinical characteristics of leukemia-associated gingivitis

A
  • Pronounced inflammatory response of gingiva in relation to plaque present (NOTE: plaque not a prerequisite for oral lesions)
  • Change in gingival color (red to deep purple)
  • Change in gingival contour with possible modificatino of size (swollen, glazed, spongy)
  • Gingival enlargement first at interdental papilla –> maginal and attached gingiva
  • Gingival bleeding (may be one of initial signs and may indicate underlying thrombocytopenia)
78
Q

5 oral manifestations of leukemia

A
  • Cervical adenopathy
  • Petechiae
  • Mucosal ulcers
  • Gingival inflammation
  • Gingival enlargement
79
Q

4 causes of chemical injury to gingiva

A
  • Chlorhexidine-induced mucosal desquamation (pictured)
  • Aspirin burn
  • Cocaine burn
  • Slough due to dentifrice detergents
80
Q

3 causes of physical injury to gingiva

A
  • Oral hygiene agents, great brushing force and improper technique
  • Dental flossing
  • Self-inflicted (picking or scratching gingiva with a nail)
81
Q

Describe how physical trauma to gingiva may manifest

A
  • If limited, gingival response = hyperkeratosis
  • More violent trauma = superficial gingival lacerations to major loss of tissue resulting in gingival recession
82
Q

Describe how thermal injury may orally manifest

A
  • Most often occur on palate and labial mucosa
  • Area involved is painful and erythematous and may slough a coagulated surface
  • Vesicles may also occur and sometimes lesions present as ulceration, petechiae or erosion
83
Q

Definition of chronic periodontitis

A

An infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment and bone loss. Characterized by pocket formation and/or gingival recession. Most common form of periodontitis

84
Q

Role of plaque in chronic periodontitis

A

Initiator and sustainor

85
Q

4 primary clinical features of chronic periodontitis

A
  • Clinical attachment loss
  • Alveolar bone loss
  • Periodontal pocketing
  • Gingival inflammation
86
Q

5 secondary clinical features of chronic periodontitis

A
  • BOP
  • Increased tooth mobility
  • Enlargement or recession of gingiva
  • Drifting of teeth
  • Tooth loss
87
Q

Define localized chronic periodontitis

A

≤30% of sites are affected

88
Q

Define generalized chronic periodontitis

A

>30% of sites are affected

89
Q

Define slight/mild chronic periodontitis

A

1 - 2 mm clinical attachment loss

90
Q

Define moderate chronic periodontitis

A

3 - 4 mm clinical attachment loss

91
Q

Define severe chronic periodontitis

A

≥5 mm of clinical attachment loss

92
Q

5 histopathological characteristics of chronic periodontitis

A
  • Periodontal pocketing
  • Location of the JE apical to the CEJ
  • Loss of collagen fibers subjacent to the pocket epithelium
  • PMNs in the JE and pocket epithelium
  • Dense inflammatory cell infiltrate with plasma cells, lymphocytes and macrophages
93
Q

3 major features of aggressive periodontitis

A
  • Non-contributory medical history
  • Rapid attachment and bone loss
  • Familial aggregation
94
Q

What does diagnosis of aggressive periodontitis require

A

Exclusion of the presence of systemic diseases that may severely impair host defences and lead to premature tooth loss (ie. periodontal manifestation of systemic disease)

95
Q

5 secondary features of aggressive periodontitis

A
  • Amount of microbial deposits inconsistent with severity of periodontal destruction
  • Elevated proportions of aggregatibacter actinomycetemcomitans and porphyromonas gingivalis
  • Phagocyte abnormalities
  • Hyper-responsive macrophage phenotype, including elevated production of PGE2 and IL-1B in response to bacterial endotoxins
  • Progression of attachment loss and bone loss may be self arresting
96
Q

Define localized aggressive periodontitis

A
  • Localized to first molar/incisor presentation with interproximal attachment loss on at least 2 permanent teeth, one of which is a first molar and involving no more than 2 teeth other than first molars and incisors
  • NOTE: circumpubertal onset and robust serum antibody repsonse to infecting agents
97
Q

Define generalized aggressive periodontitis

A
  • Generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors
  • NOTE: usually affecting persons under 30 y-o but may be older, prnounced episodic naure and poor serum antibody response to infecting agents
98
Q

Define incidental attachment loss

A

Attachment loss that does not fit the specific diagnosis criteria established for AgP or chronic periodontitis

NOTE: patients with this clinical diagnosis should be considered as high risk for AgP or chronic periodontitis

99
Q

3 examples of incidental attachment loss

A
  • Recessions associated with trauma or tooth position
  • Attachment loss associated with impacted third molars
  • Attachment loss associated with removal of impacted third molars
100
Q

Oral manifestation of malignant neutropenia

A

Ulceration and necrosis of the marginal gingiva

101
Q

Oral manifestation of cyclic, chronic and familial benign neutropenia

A

Lesions are frequently severe with deep periodontal pockets and extensive generalized bone loss involving permanent dentition

102
Q

Oral manifestation of cyclic neutropenia (condition characterized by fluctuations in neutrophil counts with a periodicity of 14-36 days)

A

Oral ulceration, an exaggerated inflammatory response to plaque and aggressive periodontitis of early onset

Occasionally bone resorption may be seen in deciduous dentition

103
Q

Describe the oral manifestation of Chediak-Higashi syndrome

A

Neutrophil chemotaxis and bactericidal functions are abnormal –> generalized severe gingivitis, extensive alveolar bone loss and premature tooth loss

Patients are extremely susceptible to bacterial infections

104
Q

Periodontal features of histiocytosis syndrome (3)

A
  • Punched-out necrotic ulcers with considerable granulation tissue
  • Tissue necrosis
  • Bone loss

NOTE: May clinically resemble NUP lesions

105
Q

DIagnostic management of histiocytosis

A

Hematological and immunological investigations at an early stage. May be assisted by a biopsy of the granulation tissue associated with deep lesions

106
Q

What is periodontal disease in Down syndrome characterized by?

A

A generalized early periodontitis which commences in the deciduous dentition and continues into the adult dentition. Progression is very rapid.

107
Q

Describe the oral manifestation of hypophosphatasia

A

Decreased serum alkaline phosphatase and severe loss of alveolar bone and premature loss of the deciduous teeth, particularly anteriorly

108
Q

Describe the clinical manifestation of Papillon-Lefevre syndrome

A
  • Disease characterized by hyperkeratotic skin lesions
  • Palmar-plantar keratosis
  • Severe generalized periodontitis occuring commonly before puberty with early loss of deciduous and permanent teeth
109
Q

Two types of Ehlers-Danlos syndrome that have an increased susceptibility to periodontitis

A

Types IV and VIII

110
Q

Oral manifestations that Type VIII Ehlers-Danlos syndrome is particularly associated with

A
  • Fragile oral mucosa and blood vessels
  • Severe generlized periodontitis with the clinical appearance of early-onset periodontitis
111
Q

Define glycogen storage disease 1b

A

Autosomal recessive condition in which there is faulty carbohydrate metabolism and an association with low neutrophil numbers, impaired neutrophil function and periodontal disease

112
Q

Define infantile genetic agranulocytosis

A

Rare autosomal recessive disorder, which features severe neutropenia and has been associated with periodontitis resembling the early-onset form

113
Q

Define Cohen’s syndrome

A

Autosomal recessive disorder characterized by non-progressive mental and motor retardation, obesity, dysmorphia and neutropenia. More frequent and extensive alveolar bone loss

114
Q

Hallmark of necrotizing ulcerative gingivitis

A

Pain

115
Q

4 signs and symptoms of NUG

A
  • Pain
  • Lymphadenopathy
  • Fever
  • Malaise
116
Q

Predominant factor in the development of NUG

A

Immunosuppression

117
Q

4 risk factors for NUG

A
  • Smoking
  • Emotional stress
  • Alcohol Use
  • Inadequate sleep
118
Q

3 microorganisms involved in NUG

A
  • Fusiform bacteria
  • Prevotella intermedia
  • Spirochetes
119
Q

Describe the oral manifestation of NUG

A
  • Interdental gingival necrosis often describe as “punched out” ulcerated papillae and bleeding
  • Ulcers are covered by a yellowish-white or grayish slough or “pseudomembrane”
  • The zone between the marginal necrosis and the relatively unaffected gingiva usually exhibits a well-demarcated narrow erythematous zone, sometimes referred to as linear erythema
120
Q

5 constituents of the sloughed material from the ulcers in NUG

A
  • Fibrin
  • Necrotic tissue
  • Leukocytes
  • Erythrocytes
  • Masses of bacteria
121
Q

Define necrotizing ulcerative periodontitis

A

An infection characterized by necrosis of gingival tissues, periodontal ligament and alveolar bone. Most commonly observed in individuals with systemic conditions such as HIV infection, severe malnutrition and immunosuppression

122
Q

What may NUP be a sequela of?

A

Single or multiple episodes of NUG or may be the result of the occurence of necrotizing disease at a previously periodontitis-affected site

123
Q

Describe the lesions of NUP (4)

A
  • Same clinical appearance as NUG except sites demonstrate loss of clinical attachment and alveolar bone
  • Similar clinical, microbiologic and immunologic characteristics as NUG
  • Lesions are seldom associated with deep periodontal pockets because extensive gingival mecrosis often coincides with loss of crestal alveolar bone
  • Necrotic areas originating from neighboring interproximal spaces frequently merge to form a continuous necrotic area
124
Q

Define necrotizing stomatitis

A

Further progression of NUP beyond the mucogingival junction. Severe tissue destruction characteristic of this diseae is related to seriously compromized immune functions typically associated with HIV and malnutrition

125
Q

Etiology of NUP vs. PHS (primary herpetic gingivostomatitis)

A

Bacteria vs. Herpes simplex virus

126
Q

Age of affected persons in NUG vs. PHS

A

15 - 30 years vs. children frequently

127
Q

Site of NUG vs. PHS

A

Interdental papillae vs. gingiva and the entire dental mucosa

128
Q

Symptoms of NUG vs. PHS

A

Ulceration and necrosis and a yellowish-whitish plaque vs. multiple vesicles which burst –> small round fibrin-coated ulcers which tend to coalesce

129
Q

Duration of NUG vs. PHS

A

1 - 2 days if treated vs. 1 - 2 weeks

130
Q

Contagiousness of NUG vs. PHS

A

Not contagious vs. Contagious

131
Q

Immunity towards NUG vs. PHS

A

None vs. Partial

132
Q

Result of healing of NUG vs. PHS

A

Destruction of periodontal tissue remains vs. no permanent destruction

133
Q

6 contents of a periodontal abscess

A
  • Bacteria
  • Bacterial products
  • Inflammatory cells
  • Tissue breakdown products
  • Serum
  • Neutrophils in the central area
134
Q

Define a gingival abscess

A

Localized purulent infection that involves marginal gingiva or interdental papilla. Usually an acute inflammatory response to foreign substances forced into the gingiva. Early stages appear as a red swelling with a smooth shiny surface

135
Q

Define periodontal abscess

A

A Localized purulent infection within the tissues adjacent to the periodontal pocket that may lead to the destruction of periodontal ligament and alveolar bone. Calculus often detected on the root surface.

136
Q

Microorganisms that colonize the periodontal abscess

A

Gram-anaerobic rods (same microbiota than in deep periodontal pockets)

137
Q

Suggested main cause for tooth extraction during SPT

A

Periodontal abscesses

138
Q

6 clinical features of periodontal abscess

A
  • Smooth shiny swelling of the gingiva
  • Suppuration from either a fistula or the pocket
  • BOP
  • Increase in probing depth
  • Tooth may be mobile
  • Extrusion of the involved tooth
139
Q

Radiographic appearance of periodontal abscess

A
  • Discrete radiolucency along lateral border of root
  • May have normal apeparance of the interdental bone or some bone loss, ranging from widening of the PDL space to pronounced bone loss involving most of the affected tooth
140
Q

2 symptoms of periodontal abscess

A
  • Pain or tenderness
  • Sensitivity to percussion
141
Q

6 differential diagnoses of periodontal abscess

A
  • Periapical abscess
  • Vertical root fracture
  • Lateral periodontal cyst
  • Endo-perio abscesses
  • Tumors
  • Osteomyelitis
142
Q

4 factors associated with the formation of acute periodontal abscess

A
  • Marginal closure of a deep periodontal pocket and lack of proper drainage
  • Deep, tortuous pockets and deep concavities associated with furcation lesions
  • Systemc antibiotic treatment
  • Diabetes
143
Q

Explain how systemic antibiotic treatment may lead to periodontal abscess

A

In patients with untreated periodontitis, systemic antibiotics may lead to superinfection with opportunistic organisms resulting in development of an abscess

144
Q

Describe the mechanism of post-scaling periodontal abscess

A

Related to the presence of small fragments of remaining calculus that obstruct the pocket entrance or it can be caused by small fragments of calculus that have been forced in to the deep portion of the periodontal tissues during scaling

145
Q

Describe the mechanism of post-surgery periodontal abscess

A

The results of incomplete removal of subgingival calculus or the presence of foreign bodies in the periodontal tissues, such as sutures or periodontal pack

146
Q

Define pericoronal abscess

A

A localized purulent infection within the tissue surrounding the crown of a partially erupted tooth

147
Q

Describe the mechanism of periodontic-endodontic lesions

A

The inflammation from inflamed and necrotic pulps can spread through lateral canals and accessory foramina into the PDL. An apical endodontic lesion may also extend and drain along the periodontium

148
Q

4 localized tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis

A
  • Tooth anatomic factors
  • Dental restorations/appliances (overhangs, violation of biologic width)
  • Root fractures
  • Cervical root resorption and cemental tears
149
Q

6 tooth anatomic factors that modify or predispose to plaque-infuced gingival diseases/periodontitis

A
  • Cervical enamel projections and enamel pearls
  • Furcation anatomy and location
  • Tooth malposition
  • Root proximity
  • Open contacts
  • Grooves (i.e. palato-gingival grooves on maxillary incisors)
150
Q

6 mucogingival deformities and conditions around teeth

A
  • Gingival/soft tissue recession
  • Lack of keratinized gingiva
  • Decreased vestibular depth
  • Aberrant frenum/muscle position
  • Gingival excess
  • Abnormal color
151
Q

4 examples of gingival excess

A
  • Pseudopocket
  • Inconsistent gingival margin
  • Excessive gingival display
  • Gingival enlargement
152
Q

6 mucogingival deformities and conditions on edentulous ridges

A
  • Vertical and/or horizontal ridge deficiency
  • Lack of gingiva/keratinized tissue
  • Gingival/soft tissue enlargement
  • Aberrant frenum/muscle position
  • Decreased vestibular depth
  • Abnormal color
153
Q

Define occlusal trauma

A

Injury resulting in tissue changes within the attachment apparatus as a result of occlusal forces

154
Q

Define primary occlusal trauma

A

Injury resulting in tissue changes from excessive occlusal forces applied to a tooth of:

  • Normal bone levels
  • Normal attachment levels
  • AND excessive occlusal forces
155
Q

Define secondary occlusal trauma

A

Injury resulting in tissue changes from normal to excessive occlusal forces applied to a tooth with reduced support. It occurs in the presence of:

  1. Bone loss
  2. Attachment loss
  3. AND normal/excessive occlusal forces
156
Q

Describe how occlusal trauma can contribute to periodontitis

A
  • Trauma from occlusion alone cannot induce periodontal breakdown
  • It does however result in resorption of alveolar bone –> increased tooth mobility that is transient or permanent. This is a physiologic adaptation of PDL and alveolar bone to traumatizing forces
  • In teeth with progressive, plaque-associated periodontal disease, trauma can enhance the rate of progression of the disease

DENT 318 - Periodontology (4 decks)

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