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CPEBLS Stage 1 > Soames Oral Pathology Chapter 7 > Flashcards

Soames Oral Pathology Chapter 7 Flashcards

1
Q

Gingivitis is used to designate?

A

Designate inflammatory lesions that are confined to the marginal gingiva.

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2
Q

Periodontitis is used to designate?

A

Inflammatory lesions that extend to include destruction of connective tissue attachment of the tooth and loss of alveolar bone.

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3
Q

Chronic inflammatory periodontal disease of varying severity affects practically?

A

All dentate individuals.

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4
Q

Gingivitis is common in ____ even by the age of 3 years, and early periodontitis may be detected in ____.

A

Children; teenagers

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5
Q

Extent and severity of disease increase with age in general regarding chronic inflammatory periodontal.disease

A

True

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6
Q

Prevalence of pocketing/loss of attachment increases with age.

A

True

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7
Q

The proportion of teeth affected by periodontitis decreases with age.

A

False, increases with age.

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8
Q

Early periodontitis involves some of the teeth in the minority of adults.

A

False, majority of adults.

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9
Q

Advanced periodontal disease affects a major percentage of the population.

A

False, only a small percentage

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10
Q

Tooth loss as a result of periodontal destruction is common before the age of 50 years.

A

False, it is uncommon.

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11
Q

Most forms of periodontitis in adults are considered to be manifestations of the same disease, but other rarer types occur in younger patients.

A

True

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12
Q

What is the essential aetiological agent in chronic periodontal disease?

A

Dental plaque

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13
Q

Epidemiological studies in many parts of the world have demonstrated no association between dental plaque and prevalence and severity of periodontal disease.

A

False, there is a strong positive association between dental plaque and prevalence and severity of periodontal disease

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14
Q

Clinical experiments in man and other animals have demonstrated that withdrawal of oral hygiene in healthy mouths results in the accumulation of dental plaque and this is paralleled by the onset of ______.

A

Gingivitis

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15
Q

List classifications of gingivitis

A
  • Associated with dental plaque only
  • Modified by systemic factors
  • Modified by medication
  • Modified by malnutrition
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16
Q

List classifications of chronic periodontitis

A
  • Localised

- Generalised

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17
Q

List classifications of aggressive periodontitis

A
  • Localised

- Generalised

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18
Q

List classifications of periodontitis in systemic diseases

A
  • Immunocompromised patients

- Genetic disorders

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19
Q

A number of topically applied antimicrobial agents have been shown to inhibit _____ ______ and prevent the onset of ______.

A

Plaque formation; gingivitis

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20
Q

Bacteria isolated from human dental plaque are capable of inducing ____ ______ when introduced into the mouths of gnotobiotic animals.

A

Periodontal disease.

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21
Q

Gnotobiotic animals

A

Animals raised clear of any bacteria

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22
Q

Several species of pathogenic bacteria have been isolated from ____ _____ that have the capacity to invade tissues and evoke destructive inflammatory changes.

A

Periodontal pockets.

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23
Q

There is increasing evidence that there are differences in bacterial flora associated with ________ and various stages of disease.

A

Healthy gingival crevices

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24
Q

Healthy periodontal tissues of humans are associated with a scanty flora located almost entirely ______ on the tooth surface.

A

Supragingivally

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25
Q

Microbial accumulations are _____ cells in thickness and comprise mainly gram-positive bacteria.

A

1-20 cells

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26
Q

Predominating gram-positive bacteria?

A

Streptococcus and Actinomyces

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27
Q

In developing gingivitis, the total mass of plaque is ____ and the microbial cell layer often extend to ________ cells in thickness

A

Increased, 100-300 cells

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28
Q

Actinomyces species predominate but the proportion of _____ and ____ organisms increases.

A

Spirochaetes; capnophilic

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29
Q

As gingivitis becomes established, there is a substantial increase in the proportion of _________.

A

Obligate anaerobic gram-negative bacteria.

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30
Q

Examples of obligate anaerobic gram-negative bacteria

A
  • Porphyromonas gingivalis

- Prevotella intermedia

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31
Q

Obligate anaerobic gram-negative bacteria are mostly located?

A

Subgingivally

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32
Q

Microbial examination of subgingival plaque in periodontitis has revealed a complex flora rich in?

A
  • Gram-negative rods
  • Motile forms
  • Spirochaetes
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33
Q

Which other bacteria are prevalent and consistently isolated from subgingival plaque in periodontitis?

A
  • Actinobacillus actinomycetemcomitans
  • Porphyromonas gingivalis
  • Bacteroides forsythus
  • Prevotella intermedia
  • Prevotella nigrescens
  • Fusobacterium nucleatum
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34
Q

List key points of microbiology of periodontal disease

A
  • Gram-positive cocci decrease as gingivitis progresses in periodontitis
  • Gram-negative anaerobic bacilli increase as disease progresses
  • Motile forms increase as disease progresses
  • Periodontal disease involves interactions of mixtures of bacteria forming complexes in plaque
  • Certain species (periodontal pathogens) are prevalent in destructive lesions
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35
Q

Main species in healthy gingiva?

A

Streptococcus + actinomyces

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36
Q

% Aerobic/anaerobic (facultative anaerobes) in healthy gingiva

A

75/25

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37
Q

% Gram positive/ gram-negative in healthy gingiva

A

90/10

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38
Q

Motile/non-motile in healthy gingiva

A

Very few motile forms; motile:non-motile = 1:40

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39
Q

Main species in chronic gingivitis

A
  • Actinomyces
  • Streptococcus
  • Porphyromonas
  • Prevotella
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40
Q

% Aerobic/anaerobic (facultative anaerobes) in chronic gingivitis

A

60/40

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41
Q

% Gram positive/ gram-negative in chronic gingivitis

A

65/35

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42
Q

Motile/non-motile in chronic gingivitis

A

Number of motile rods and spirochaetes increases with disease

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43
Q

Main species in chronic periodontitis

A
  • Actinobacilles
  • Porphyromonas
  • Bacteroides
  • Prevotella
  • Fusobacterium
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44
Q

% Aerobic/anaerobic (facultative anaerobes) in chronic periodontitis

A

20/80

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45
Q

% Gram-positive/ gram-negative in chronic periodontitis

A

25/75

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46
Q

Motile/non-motile in chronic periodontitis

A

Abundant motile rods and spirochaetes; motile; non-motile; 1:1

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47
Q

Local factors that increase risk of periodontal disease

A
  • Pre-existing anatomy of the teeth, gingiva, and alveolar bone,
  • Alignment and occlusal relationships of teeth
  • Approximal restorations that may affect the accumulation and growth of plaque or interfere with its removal.
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48
Q

List systemic factors that may be associated with increased incidence or severity of periodontal disease

A
  • Diabetes mellitus
  • Nutrition
  • Blood diseases
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49
Q

How can diabetes be a risk factor for periodontal disease?

A

Vascular changes and defects in cellular defence mechanisms

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50
Q

How can pregnancy and sex hormones be a risk factor for periodontal disease?

A
  • Pre-existing gingivitis increases in pregnancy fro the second to the eighth month of gestation and then decreases.
  • Healthy gingiva are not affected.
  • Hormonal changes modify tissue response to dental plaque
  • Increased levels of sex hormones or their metabolites are found in inflamed gingiva.
  • Aggravation of gingivitis during pregnancy is related mainly to progesterone which affects function and permeability of gingival microvasculature
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51
Q

Localised gingival hyperplasia also occurs during?

A

Pregnancy, known as pregnancy epulis

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52
Q

Increased levels of gingivitis occurring around _____ and in some women taking _______ may also be related to concentration of circulating sex hormones.

A

Puberty; oral contraceptives

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53
Q

Pregnancy and sex hormones are not risk factors for?

A

Periodontitis

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54
Q

How does blood diseases increase risk of periodontal disease?

A
  • Acute leukaemia may be accompanied by a generalized enlargement of the gingiva due mainly to infiltration and packing of the tissues by leukaemic cells
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55
Q

Oral signs of generalized enlargement of gingiva can be related to?

A
  • Pacytopaenia
  • Mucosal pallor
  • Necrotizing ulceration (particularly of the oropharynx)
  • Petechial haemorrhages
  • Gingival bleeding
  • Gingival ulceration
  • Candidosis and recrudescence of herpetic infections are also common.
  • Alveolar bone loss
  • Severe periodontal destruction have been reported caused by leukaemic infiltration
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56
Q

Severe gingival inflammation, ulceration and advanced bone destruction may be seen in certain chronic types of neutropenia, such as?

A

Cyclic neutropenia

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57
Q

Functional disorders of neutrophils have also been implicated in ?

A

Juvenile periodontitis

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58
Q

List drugs that affect gingival hyperplasia

A

Anti-epileptics e.g. phenytoin

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59
Q

Which drugs affect equivocal reduction in disease activity?

A

Immunosuppressants e.g. Azathioprine, corticosteroids

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60
Q

Which drugs affect gingival hyperplasia?

A

Immunosuppressants e.g. cyclosporin

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61
Q

Which drugs can affect equivocal reduction in disease activity?

A

Non-steroidal anti-inflammatory drugs e.g. indomethacin, ibuprofen

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62
Q

Which drugs can affect gingival hyperplasia?

A

Calcium channel blockers e.g. Nifedipine, verapamil

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63
Q

Which drugs can affect exacerbation of pre-existing gingivitis?

A

Sex hormones e.g. oestrogen, progesterone

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64
Q

Periodontal status of many HIV-positive patients is similar to the general population.

A

True

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65
Q

Tobacco smoking is an important risk factor for development and progression of periodontal disease.

A

True

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66
Q

Smoking impairs what in periodontal disease?

A

Impairs phagocytic function of polymorphoneutrophils and impairs healing. Composition of subgingival plaque may also be affected and favour the overgrowth of potential periodontal pathogens

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67
Q

List factors that can increase microbial plaque?

A
  • Direct injury
  • Toxic products
  • Enzymes
  • Antigenic challenge
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68
Q

List factors that increase host defences?

A
  • Salivary factors
  • Crevicular fluid
  • Epithelial barrier
  • Migrating neutrophils
  • Immune response
  • Potential for tissue regeneration and repair
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69
Q

What is chronic periodontal disease?

A

A dynamic process reflecting changes in the balance of the host-parasite relationship with time.

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70
Q

In healthy, non-inflamed gingiva, there is continuous migration of _______ through the junctional epithelium into the gingival sulcus.

A

Polymorphonuclear neutrophil leucocytes (PMN)

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71
Q

The migration of PMN is part of the normal host defences to the low level of bacterial challenge to the gingiva which is likely to occur even in?

A

Healthy mouths

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72
Q

Initial lesion of gingivitis involves _______ and cannot be detected clinically.

A

Microscopic area of tissue

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73
Q

Gingivitis is essentially an acute inflammatory response characterized by dilatation which manifests as?

A

An increase in the flow of crevicular fluid.

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74
Q

Crevicular fluid contains?

A

All classes of plasma proteins, notably immunoglobulins and complement, which in addition to the activity of the PMNs, may play a role in controlling the initial bacterial challenge.

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75
Q

List key points in initial gingivitis

A
  • Microscopic area around base of gingival sulcus
  • Acute inflammatory changes include: cellular exudate (enhanced migration of PMN); fluid exudate (increased crevicular fluid flow)
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76
Q

Describe the full pathogenesis of gingivitis

A
  1. Bacterial products activate junctional epithelium and endothelial cells to release cytokines e.g. IL-1 and IL-8 (enhance recruitment and migration of PMN)
  2. PMN recruitment and migration are enhanced by activation of serum proteins released as result of increased vascular permeability.
  3. Enhanced expression of adhesion molecules by endothelial cells mediated by cytokine activity recruits macrophages and lymphocytes into the area
  4. Activation of macrophages and lymphocytes leads to production of complex arrays of pro- and anti- inflammatory cytokines
  5. Cytokine activity induces B cells to differentiate into antibody-producing plasma cells
  6. Pro-inflammatory cytokines, e.g. IL-1 and IL-6 enhance production and activation of metalloproteinases leading to tissue destruction.
  7. Progression, stabilization or regression of gingivitis reflects the changing balances between plaque products, their interaction with host cells and the production of pro- and anti-inflammatory cytokines.
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77
Q

Increasing level of bacterial challenge imapirs function of the junctional epithelium to?

A

Maintain its attachment to enamel, and as the attachment is lost there is progressive deepening of the gingival sulcus resulting in the formation of a gingival pocket

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78
Q

Gingival pocket permits the development of?

A

Subgingival plaque and altered environment favours the growth of gram-negative anaerobes.

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79
Q

Impairment of the barrier function of the junctional epithelium allows ready ingress of ____ from the subgingival plaque, leading to development of an immune response.

A

Antigens

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80
Q

Early lesion of gingivitis is characterized by?

A

lymphocytic infiltrate which develops around the site of the initial lesion, but as it evolves it expands laterally and apically beneath the junctional epithelium, extending towards the amelocemental junction.

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81
Q

Infiltrate consists of a mixture of?

A

T and B lymphocytes. T cells predominate in early lesion of gingivitis.

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82
Q

In early lesion of gingivitis, cytokines are released, that trigger ?

A

Connective tissue breakdown, leading to destruction of gingival collagen fibres as the infiltrate expands.

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83
Q

Key points of early gingivitis

A
  • Lymphocytic infiltration
  • Impairment of barrier function of junctional epithelium
  • Gingival pocket formation; growth of subgingival plaque
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84
Q

Early gingivitis may remain ____, especially in children.

A

Stable

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85
Q

Area of inflamed gingival tissue continues to expand ?

A

Apically and laterally, accompanied by continuing destruction of gingival collagen.

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86
Q

Characteristic shift in inflammatory cell population from predominantly lymphocytic (early gingivitis) to ?

A

Plasma cells predominate

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87
Q

B lymphocytes are stimulated to differentiate into ______ against plaque bacterial antigens by cytokines from _____ within the infiltrate.

A

specific antibody-producing plasma cells; T-helper cells

88
Q

Huge amounts of immunoglobulin are present throughout the connective and epithelial tissues in established gingivitis.

A

True

89
Q

Exacerbation of the inflammation results in further impairment of the barrier function of the junctional epithelium and ________.

A

Deepening of the gingival pocket.

90
Q

Key points of established gingivitis

A
  • Expansion of area of inflammation and destruction of gingival connective tissue
  • Predominance of plasma cells in inflammatory infiltrate
  • Deepening of gingival pocket; thinning/ulceration of pocket epithelium
91
Q

In established gingivitis, pocket epithelium may be?

A

Hyperplastic, with long anastomosing rete processes extending into the gingival connective tissue.

May be thinned with only one or two layers of cells separating the underlying engorged vascular bed from the external environment; or it may show frank ulceration.

Engorged vascular bed and thinning or ulceration of the pocket epithelium are related to the clinical signs of redness and bleeding.

92
Q

Varying attempts at repair characterized by formation of fibrous tissue isn’t as good because?

A

Newly-formed collagen bundles do not simulate the architecture of the previously existing gingival fibres.

93
Q

Exuberant fibrous tissue formation results in?

A

Gingival hyperplasia and false pocketing.

94
Q

Destruction of the specifically oriented gingival fibres, fibrosis and hyperplasia contribute to the ?

A

Loss of normal gingival form seen clinically in chronic gingivitis.

95
Q

____________, resulting from increased vascular permeability associated with inflammation is another factor in chronic gingivitis.

A

Oedematous enlargement

96
Q

Chronic periodontitis is characterized by destruction of the ____________, _____ and _____.

A

destruction of the connective tissue attachment of the root of the tooth, loss of alveolar bone and pocket formation.

97
Q

Natural history of the untreated lesion of established gingivitis is not well understood.

A

True

98
Q

Periodontitis is the result of extension of ?

A

Extension of inflammation from the gingiva into the deeper tissues.

99
Q

Evidence of the progression of gingivitis to periodontitis is ?

A

The extension of inflammation beneath the base of the junctional epithelium into the supra-alveolar connective tissue.

100
Q

Inflammatory infiltrate is rich in plasma cells but there are also numerous?

A

Numerous T lymphocytes and macrophages

101
Q

As the area and density of the infiltrate increase there is destruction of collagen in the supra-alveolar connective tissue and the fibres lose?

A

Lose their attachment to cementum.

102
Q

Loss of attachment to cementum is accompanied by apical migration of the junctional epithelium to cover?

A

Cover the denuded root surface; resulting in early true pocket formation.

103
Q

As chronic periodontitis extends into the supporting tissues, there is progressive destruction of the fibres of the _____ accompanied by _________.

A

periodontal ligament; osteoclastic resorption of the alveolar bone

104
Q

Junctional epithelium continues to migrate apically, leading to ?

A

Progressive deepening of the pockets.

105
Q

As the junctional epithelium migrates apically the more coronal and inflamed tissue loses its specialized attachment and is converted into?

A

Pocket epithelium.

106
Q

During chronic periodontitis, the width of the zone of attachment of the junctional epithelium at the base of the pocket remains ?

A

Fairly constant throughout the course of disease.

107
Q

Pathway of spread of inflammation into the supporting tissues influences the pattern of bone destruction and morphology of the pockets.

A

True

108
Q

In general, the spread of inflammation follows the course of ?

A

blood vessels

109
Q

In interdental areas, the infiltrate extends mainly along the?

A

Rich anastomotic supply running from beneath the interdental col towards the midpoint of the crest of the interdental septa and into underlying marrow spaces.

110
Q

Osteoclastic resorption results in?

A

Interdental cratering

111
Q

In marginal areas, inflammation follows the course of _______ towards?

A

Supraperiosteal vessels towards the crest of the marginal alveolar bone.

112
Q

Pathways of spread that follow main vascular supplies tend to result in a horizontal pattern of ?

A

Bone loss and suprabony pockets.

113
Q

Various factors that modify inflammation to spread towards and directly into the periodontal ligament results in?

A

Vertical patterns of bone loss and infrabony pockets.

114
Q

Chronic periodontal disease is characterized by destruction of the connective tissue attachment of the teeth, rate of progression of the lesions is _______ and phases of tissue destruction and bone resorption may alternate with _______.

A

not constant; periods of remission.

115
Q

Current hypotheses suggest that loss of attachment occurs as _______?

A

Brief bursts of destructive activity at random time intervals throughout an individual’s life.

116
Q

During periods of remission, there may be attempts at ?

A

Healing

117
Q

At the base of the pocket, a narrow zone of junctional epithelium mediates ?

A

the soft-tissue attachment to the root

118
Q

Periodontal pocket contains?

A

Subgingival calculus, plaque, and inflammatory exudate comprising fluid and cells, mainly PMN.

119
Q

Areas of irregular hyperplasia and rete ridge formation alternate with areas of?

A

Areas of thinning of the pocket epithelium and even frank ulceration.

120
Q

Vessels in the subadjacent connective tissue are markedly dilated and there is emigration of large numbers of?

A

Polymorphonuclear cells which transmigrate the pocket epithelium.

121
Q

Underlying connective tissue is densely infiltrated by inflammatory cells, predominated by?

A

Plasma cells

122
Q

Inflammatory infiltrate may extend into?

A

Adjacent marrow spaces

123
Q

In actively progressing disease, osteoclasts may be seen along the _____ and within ____ but they are infrequent in relatively stable lesions.

A

Bone front; adjacent marrow spaces

124
Q

Key points of chronic periodontitis

A
  • Apical extension of destructive inflammation: into the supra-alveolar connective tissues; into alveolar bone; into periodontal ligament
  • Loss of connective tissue attachment and destruction of alveolar bone
  • Apical migration of junctional epithelium and pocket formation
  • Periods of quiescence/stability; random bursts of destructive activity
125
Q

Destruction of the extracellular matrix in periodontal disease involves the activity of a family of proteolytic enzymes, the _______, of which the collagenases are the best known.

A

Matrix Metalloproteinases (MMPs)

126
Q

MMPs (Matrix metalloproteinases) produced mainly by?

A

Connective tissue cells, principally fibroblasts, but are also synthesized by other cell types such as macrophages and neutrophils.

127
Q

MMPs are secreted in a _____ form and require _____ before they can degrade matrix proteins.

A

latent; activation

128
Q

In health, normal remodelling o connective tissue is ?

A

tightly controlled, resulting in a balance between rates of synthesis and degradation which reflects the balance between the activity of the MMPs and their inhibitors

129
Q

Main group of inhibitors of MMPs present in tissues are known as?

A

TIMPs (tissue inhibitors of metalloproteinases)

130
Q

TIMPs are produced mainly by?

A

Fibroblasts and macrophages, probably at the same time as cells release MMPs.

131
Q

In periodontal disease with destruction of connective tissue, there is an imbalance between the levels of MMPs and TIMPs in the tissues, resulting in?

A

A relative increase in the levels of MMPs.

132
Q

Why is there a relative increase in MMPs in periodontal disease?

A
  • Increase in MMP synthesis or a reduction in the synthesis of TIMPs
133
Q

Production of both MMPs and TIMPs are influenced particularly by?

A

Cytokines

134
Q

In particular, activity of _____, which induces MMP production by host cells, probably plays a key role.

A

Interleukin-1

135
Q

Key points of degradation of the extracellular matrix (ECM)

A
  • MMPs degrade ECM, TIMPs inhibit MMPs
  • Activity of MMPs and TIMPs is in balance in health
  • Imbalance in disease leads to increased MMP activity
  • Imbalance reflects fluctuations in cytokine activity in inflammation
  • Activity of interleukin-1 probably plays a key role
136
Q

Identify the three categories of local mediators for stimulating osteoclastic activity.

A

Cytokines, prostaglandins, growth factors

137
Q

List main cytokines which stimulate bone resorption

A
  • Interleukin-1
  • Interleukin-6
  • Tumour necrosis factor (TNF)
138
Q

How are the cytokines which stimulate bone resorption mediated ?

A

Through prostoglandin synthesis especially PGE2 which enhances osteoclastic activity.

139
Q

Which is the most potent stimulator of bone resoprtion known and periodontal inflammation.

A

Interleukin-1

140
Q

During bone resorption, osteoclasts adhere tightly to the bone matrix and secrete ____ which demineralises the matrix.

A

Hydrochloric acid.

141
Q

MMPs and other proteases produced by the osteoclast then?

A

Degrade the organic matrix. This process is comparable to cyst expansion

142
Q

Most common form of chronic periodontal disease?

A

Chronic periodontitis

143
Q

Onset of disease of chornic periodontitis?

A

Early adult life or even before, but in majority of patients, does not progress to tooth loss until after 50 years of age.

144
Q

Chronic periodontitis is also referred to as?

A

Adult-type periodontitis.

145
Q

General pattern of chronic periodontitis?

A

Predominantly horizontal bone loss is seen with suprabony pocketing.

146
Q

Which part of dentition is involved in chronic periodontitis?

A

Entire dentition is usually involved, with the loewr incisors and molars tending to show the most advanced bone loss.

147
Q

Key points of pathogenesis of periodontal disease

A
  • Disturbance in host-parasite relationship leading to:
  • activation of host inflammatory and immune response, leading to:
  • enhanced synthesis of inflammatory mediators/cytokines, leading to:
  • burst of breakdown of connective tissue/bone respiration leading to:
  • new equilibrium in host-parasite relationship as host response contains the challenge from plaque bacteria.
148
Q

Localized form of aggressive periodontitis is referred commonly as?

A

Juvenile periodontitis

149
Q

Onset of juvenile periodontitis

A

Usually commences around puberty, rare form.

150
Q

Higher incidence of juvenile periodontitis in which gender?

A

Females

151
Q

Juvenile periodontitis is characterized by?

A

Rapid destruction of alveolar bone with vertical bone loss, resulting in deep infrabony pockets.

152
Q

Which teeth are initially affected in juvenile periodontitis?

A

Permanent first molars, and/or maxillary incisor teeth are affected, usually symmetrically, but the number of teeth involved increases with age.

153
Q

Pattern of involvement of dentition in juvenile periodontitis?

A

Follows sequence of eruption.

154
Q

Aetiology and pathogenesis of juvenile periodontitis?

A

Remains obscure.

155
Q

Describe lesions of juvenile periodontitis

A

Inflammatory

156
Q

Primary aetiological factor of juvenile periodontitis

A

Bacterial plaque

157
Q

Degree of destruction in juvenile periodontitis is not?

A

Is not commensurate with the generally small amounts of plaque present.

158
Q

Subgingival flora in juvenile periodontitis differs significantly from?

A

Adult periodontiti

159
Q

Subgingival flora in juvenile periodontitis is dominated by?

A

Gram-negative anaerobic rods, particularly actinobacillus actinomycetemcomitans.

160
Q

Generalized form of aggressive periodontitis includes patients previously classified as?

A

Having rapidly progressive periodontitis.

161
Q

Onset of generalized aggressive periodontitis

A

Onset in early adult life bvidence of rapid bone destruction.ut lacks well-defined criteria.

162
Q

Describe aggressive periodontitis

A

Severe periodontal lesions, generalized with evidence of rapid bone destruction

163
Q

Affected dentition of aggressive periodontitis

A
  • Almost entire dentition is usually affected.
164
Q

Progression of aggressive periodontitis

A

May either progress without remission to tooth loss or subside and become quiescent.

165
Q

Classification of periodontitis in systemic disease

A

Prepubertal periodontitis, present in childhood

166
Q

Involved dentition of prepubertal periodontitis

A

Deciduous dentition and subsequently permanent dentition.

167
Q

Prepubertal periodontitis is characterized by?

A

Extensive destruction of alveolar bone and are associated with a variety of uncommon systemic diseases.

168
Q

Papillion-Lefevre syndrome is characterized by?

A

Skin lesions of palmar-plantar hyperkeratosis and severe periodontal destruction involving both deciduous and permanent dentition.

169
Q

Papillion-Lefevre syndrome is transmitted how?

A

Autosomal recessive and is due to mutations in the gene encoding for the lysomal enzyme cathepsin C.

170
Q

It is well established that some degree of gingival enlargement can occur in ____ and other patients taking the anticonvulsant drug ____.

A

Epipleptics; phenytoin

171
Q

Factors predisposing chronic hyperplastic gingivitis?

A

Unknown, mostly.

172
Q

Percentage of patients affected by chronic hyperplastic gingivitis?

A

Ranges from less than 10 percent to over 60 percent in different series.

173
Q

Essential aetiological factor for chronic hyperplastic gingivitis

A

Dental plaque; any drug that modifies a previously existing chronic gingivitis and good oral hygiene can prevent the gingival hyperplasia.

174
Q

Mechanism by which drug or its metabolites can induce chronic hyperplastic gingivitis?

A

Unknown, but certain gingival fibroblasts can metabolize phenytoin which may accompany increased production of collagen.

175
Q

List diseases associated with major abnormalities of neutrophils in severe periodontitis in children?

A
  • Agranulocytosis
  • Cyclic neutropenia
  • Chediak-Higashi syndrome
  • Job syndrome
176
Q

List diseases in which there may be associated neutrophil dysfunction with severe periodontitis in children

A
  • Papillon-Lefevre syndrome
  • Down syndrome
  • Juvenile-onset diabetes mellitus
177
Q

Other systemic diseases associated with severe periodontitis in children

A
  • Hypophosphatasia
  • Langerhans cell histiocytosis (histiocytosis-X group)
  • Ehlers-Danlos syndrome (Type 8)
178
Q

Clinically, chronic gingival hyperplasia may be more or less generalized but primarily involves?

A

Interdental tissues, particularly around the labial surfaces of anterior teeth.

179
Q

Enlargement in chronic gingival hyperplasia manifests as ?

A

firm, pink, often lobulated fibrous masses that may obscure the crowns of the teeth.

180
Q

In patients where marginal gingiva is relatively uninovlved in chronic gingival hyperplasia?

A

Deep clefts separate adjacent bulbous interdental papillae.

181
Q

Histologically, overgrowth in chronic gingival hyperplasia consists mainly of?

A

Bundles of collagen fibres but fibroblasts are common and there is scattered chronic inflammatory cell infiltration.

Surface epithelium is also often markedly hyperplastic and shows long slender rete processes extending into the underlying connective tissue

182
Q

Hyperplastic gingivitis similar to chronic gingival hyperplasia may also occur in patients taking the immunosuppressive drug _____ following transplant procedures, and in those taking calcium channel blocking agents or calcium antagonists, such as ______ and _____ for cardiovascular disorders.

A

cyclosporin; nifedipine; verapamil

183
Q

Gingival fibromatosis is a rare hereditary condition most frequently transmitted as an _______ trait, although autosomal recessive inheritance has been reported.

A

Autosomal dominant

184
Q

Autosomal dominant type of gingival fibromatosis can be caused by mutations in at least ____ distinct genetic loci.

A

Two

185
Q

Gingival fibromatosis presents as?

A

Generalized or occasionally localized, fibrous enlargement of the gingiva which usually begins with the eruption of the permanent or occasionally deciduous teeth.

186
Q

Gingival fibromatosis is rarely present at?

A

Birth

187
Q

Occasionally, gingival fibromatosis is associated with?

A

Hypertrichosis, epilepsy and mental retardation.

188
Q

Microscopically, fibrous tissue consists mainly of _______ but mucoid change due to accumulation of _____, is common in gingival fibromatosis.

A

Coarse bundles of collagen fibres; ground substance.

189
Q

Key points of desquamative gingivitis

A
  • Common clinical manifestation of a variety of different diseases
  • Involves full width of attached gingiva.
190
Q

Symmetrical fibrous enlargements in desquamative gingivitis also occur in the __________ region and it is possible some cases are related to gingival fibromatosis.

A

Maxillary tuberosity

191
Q

Generalized enlargement of the gingiva may be caused by _______ by leukaemic infiltration in acute leukaemia.

A

Oedema

192
Q

Desquamative gingivitis is not a ______ but a clinical term applied to the gingival manifestation of several different diseases.

A

Disease entity

193
Q

Clinically, desquamative gingivitis presents as?

A

Red gingiva, oedematous, and glazed.

Areas of superficial ulceration or desquamation of varying extent.

Vesicles, bullae, white flecks, or striae may also be seen depending on the underlying aetiology.

194
Q

Commonly affected areas of gingiva in desquamative gingivitis involves?

A

Buccal and labial gingiva, more commonly affected than lingual or palatal tissues.

195
Q

Desquamative gingivitis are more common in which gender and ages?

A

Females than males, most cases occur after 30 years of age.

196
Q

Causes of fibrous overgrowths in gingival generalized enlargement

A
  • Gingival fibromatosis
  • Chronic hyperplastic gingivitis
  • Drug-associated hyperplasias: epanutin, cyclosporin, nifedipine and verapamil
197
Q

Causes of oedematous enlargement in gingival generalized enlargement

A
  • Oedematous gingivitis: puberty, pregnancy, oral contraceptives, scurvy
198
Q

Causes of systemic disease in gingival generalized enlargement

A
  • Acute leukaemias

- wegener’s granulomatosis

199
Q

Lateral periodontal abscess is a localized area of ________ arising within the periodontal tissues alongside a tooth and is distinct from the more common periapical abscess.

A

Suppurative inflammation.

200
Q

Most lateral periodontal abscess arise in patients with _______ and may occur as a direct result of an increase in?

A

pre-existing advancing periodontitis; increase in virulence and toxic factors released by plaque organisms or secondary to reduction in host resistance.

201
Q

Obstruction to the drainage of exudate from a periodontal pocket predisposes to?

A

Abscess formation

202
Q

Abscess formation may occur particularly in _____ pursuing a tortuous course around the root, or where ____ or ____ in the superficial parts of the pocket cause tight approximation of the soft-tissue wall to the neck of the tooth.

A

infrabony pockets; fibrosis; oedema

203
Q

Clinically, periodontal abscesses may be ___ or ____.

A

Acute or chronic

204
Q

Acute abscess develops rapidly and is accompanied by?

A

throbbing pain, redness, swelling and tenderness of the overlying mucosa.

205
Q

Affected tooth in abscess is usually?

A

Tender to percussion but most are vital.

206
Q

Deep-seated lesions or where drainage is obstructed, abscess may track and present with?

A

Sinus opening on the mucosa somewhere along the length of the root.

207
Q

Discharge of pus relieves ______ of periodontal abscesses and the lesion may heal or become chronic with ______.

A

Acute symptoms; intermittent discharge

208
Q

Chronic periodontal abscess may be?

A

Asymptomatic or give rise to episodes of dull pain. Acute exacerbations are common.

209
Q

Pericoronitis define?

A

This is inflammation of the soft tissues around the crown of a partially erupted tooth and is seen commonly in association with mandibular third molars

210
Q

Where is an ideal space for pericoronitis?

A

Space between the crown of the tooth and the overlying gum flap is an ideal area for the accumulation of bacterial plaque and food debris, leading to inflammation.

211
Q

Pericoronitis’ inflammatory oedema leads to?

A

Swelling of the flap which predisposes to trauma from the opposing teeth and exacerbation of the inflammation.

212
Q

Usual symptoms of pericornitis?

A

Pain, tenderness in the gum flap, and a bad taste which is associated with persistent oozing of pus from beneath the flap.

Limitation of opening and discomfort on swallowing may also be present.

213
Q

In severe cases of pericoronitis, what can develop?

A

Acute pericoronal abscess may develop which can remain localized or be associated with cellulitis and extension of infection into adjacent surgical spaces.

214
Q

Prevalence and severity of periodontal disease increases with age because?

A

Most likely the result of repeated attacks of active destruction occurring with time rather than an intrinsic change associated with the ageing process itself.

215
Q

_______ has been considered as an age change, but is now thought to be part of the clinical spectrum of periodontitis in which plaque and mechanical trauma are aetiological factors.

A

Gingival recession

216
Q

Is there evidence that the elderly are susceptible to periodontal disease?

A

No, although this is expected because of the decreased efficiency of both host defence systems and healing associated with ageing.

217
Q

List several histological changes associated with ageing

A
  • Increased apposition of cementum
  • Decreased cellularity of periodontal tissues
  • Disordered insertions of periodontal ligament fibres into bone and cementum.

CPEBLS Stage 1 (7 decks)

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