Soames Oral Pathology Chapter 7 Flashcards
1
Q
Gingivitis is used to designate?
A
Designate inflammatory lesions that are confined to the marginal gingiva.
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.
3
Q
Chronic inflammatory periodontal disease of varying severity affects practically?
A
All dentate individuals.
4
Q
Gingivitis is common in ____ even by the age of 3 years, and early periodontitis may be detected in ____.
A
Children; teenagers
5
Q
Extent and severity of disease increase with age in general regarding chronic inflammatory periodontal.disease
A
True
6
Q
Prevalence of pocketing/loss of attachment increases with age.
A
True
7
Q
The proportion of teeth affected by periodontitis decreases with age.
A
False, increases with age.
8
Q
Early periodontitis involves some of the teeth in the minority of adults.
A
False, majority of adults.
9
Q
Advanced periodontal disease affects a major percentage of the population.
A
False, only a small percentage
10
Q
Tooth loss as a result of periodontal destruction is common before the age of 50 years.
A
False, it is uncommon.
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
12
Q
What is the essential aetiological agent in chronic periodontal disease?
A
Dental plaque
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
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
15
Q
List classifications of gingivitis
A
- Associated with dental plaque only
- Modified by systemic factors
- Modified by medication
- Modified by malnutrition
16
Q
List classifications of chronic periodontitis
A
- Localised
- Generalised
17
Q
List classifications of aggressive periodontitis
A
- Localised
- Generalised
18
Q
List classifications of periodontitis in systemic diseases
A
- Immunocompromised patients
- Genetic disorders
19
Q
A number of topically applied antimicrobial agents have been shown to inhibit _____ ______ and prevent the onset of ______.
A
Plaque formation; gingivitis
20
Q
Bacteria isolated from human dental plaque are capable of inducing ____ ______ when introduced into the mouths of gnotobiotic animals.
A
Periodontal disease.
21
Q
Gnotobiotic animals
A
Animals raised clear of any bacteria
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.
23
Q
There is increasing evidence that there are differences in bacterial flora associated with ________ and various stages of disease.
A
Healthy gingival crevices
24
Q
Healthy periodontal tissues of humans are associated with a scanty flora located almost entirely ______ on the tooth surface.
A
Supragingivally
25
Microbial accumulations are _____ cells in thickness and comprise mainly gram-positive bacteria.
1-20 cells
26
Predominating gram-positive bacteria?
Streptococcus and Actinomyces
27
In developing gingivitis, the total mass of plaque is ____ and the microbial cell layer often extend to ________ cells in thickness
Increased, 100-300 cells
28
Actinomyces species predominate but the proportion of _____ and ____ organisms increases.
Spirochaetes; capnophilic
29
As gingivitis becomes established, there is a substantial increase in the proportion of _________.
Obligate anaerobic gram-negative bacteria.
30
Examples of obligate anaerobic gram-negative bacteria
- Porphyromonas gingivalis
| - Prevotella intermedia
31
Obligate anaerobic gram-negative bacteria are mostly located?
Subgingivally
32
Microbial examination of subgingival plaque in periodontitis has revealed a complex flora rich in?
- Gram-negative rods
- Motile forms
- Spirochaetes
33
Which other bacteria are prevalent and consistently isolated from subgingival plaque in periodontitis?
- Actinobacillus actinomycetemcomitans
- Porphyromonas gingivalis
- Bacteroides forsythus
- Prevotella intermedia
- Prevotella nigrescens
- Fusobacterium nucleatum
34
List key points of microbiology of periodontal disease
- 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
35
Main species in healthy gingiva?
Streptococcus + actinomyces
36
% Aerobic/anaerobic (facultative anaerobes) in healthy gingiva
75/25
37
% Gram positive/ gram-negative in healthy gingiva
90/10
38
Motile/non-motile in healthy gingiva
Very few motile forms; motile:non-motile = 1:40
39
Main species in chronic gingivitis
- Actinomyces
- Streptococcus
- Porphyromonas
- Prevotella
40
% Aerobic/anaerobic (facultative anaerobes) in chronic gingivitis
60/40
41
% Gram positive/ gram-negative in chronic gingivitis
65/35
42
Motile/non-motile in chronic gingivitis
Number of motile rods and spirochaetes increases with disease
43
Main species in chronic periodontitis
- Actinobacilles
- Porphyromonas
- Bacteroides
- Prevotella
- Fusobacterium
44
% Aerobic/anaerobic (facultative anaerobes) in chronic periodontitis
20/80
45
% Gram-positive/ gram-negative in chronic periodontitis
25/75
46
Motile/non-motile in chronic periodontitis
Abundant motile rods and spirochaetes; motile; non-motile; 1:1
47
Local factors that increase risk of periodontal disease
- 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.
48
List systemic factors that may be associated with increased incidence or severity of periodontal disease
- Diabetes mellitus
- Nutrition
- Blood diseases
49
How can diabetes be a risk factor for periodontal disease?
Vascular changes and defects in cellular defence mechanisms
50
How can pregnancy and sex hormones be a risk factor for periodontal disease?
- 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
51
Localised gingival hyperplasia also occurs during?
Pregnancy, known as pregnancy epulis
52
Increased levels of gingivitis occurring around _____ and in some women taking _______ may also be related to concentration of circulating sex hormones.
Puberty; oral contraceptives
53
Pregnancy and sex hormones are not risk factors for?
Periodontitis
54
How does blood diseases increase risk of periodontal disease?
- Acute leukaemia may be accompanied by a generalized enlargement of the gingiva due mainly to infiltration and packing of the tissues by leukaemic cells
55
Oral signs of generalized enlargement of gingiva can be related to?
- 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
56
Severe gingival inflammation, ulceration and advanced bone destruction may be seen in certain chronic types of neutropenia, such as?
Cyclic neutropenia
57
Functional disorders of neutrophils have also been implicated in ?
Juvenile periodontitis
58
List drugs that affect gingival hyperplasia
Anti-epileptics e.g. phenytoin
59
Which drugs affect equivocal reduction in disease activity?
Immunosuppressants e.g. Azathioprine, corticosteroids
60
Which drugs affect gingival hyperplasia?
Immunosuppressants e.g. cyclosporin
61
Which drugs can affect equivocal reduction in disease activity?
Non-steroidal anti-inflammatory drugs e.g. indomethacin, ibuprofen
62
Which drugs can affect gingival hyperplasia?
Calcium channel blockers e.g. Nifedipine, verapamil
63
Which drugs can affect exacerbation of pre-existing gingivitis?
Sex hormones e.g. oestrogen, progesterone
64
Periodontal status of many HIV-positive patients is similar to the general population.
True
65
Tobacco smoking is an important risk factor for development and progression of periodontal disease.
True
66
Smoking impairs what in periodontal disease?
Impairs phagocytic function of polymorphoneutrophils and impairs healing. Composition of subgingival plaque may also be affected and favour the overgrowth of potential periodontal pathogens
67
List factors that can increase microbial plaque?
- Direct injury
- Toxic products
- Enzymes
- Antigenic challenge
68
List factors that increase host defences?
- Salivary factors
- Crevicular fluid
- Epithelial barrier
- Migrating neutrophils
- Immune response
- Potential for tissue regeneration and repair
69
What is chronic periodontal disease?
A dynamic process reflecting changes in the balance of the host-parasite relationship with time.
70
In healthy, non-inflamed gingiva, there is continuous migration of _______ through the junctional epithelium into the gingival sulcus.
Polymorphonuclear neutrophil leucocytes (PMN)
71
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?
Healthy mouths
72
Initial lesion of gingivitis involves _______ and cannot be detected clinically.
Microscopic area of tissue
73
Gingivitis is essentially an acute inflammatory response characterized by dilatation which manifests as?
An increase in the flow of crevicular fluid.
74
Crevicular fluid contains?
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.
75
List key points in initial gingivitis
- Microscopic area around base of gingival sulcus
- Acute inflammatory changes include: cellular exudate (enhanced migration of PMN); fluid exudate (increased crevicular fluid flow)
76
Describe the full pathogenesis of gingivitis
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.
77
Increasing level of bacterial challenge imapirs function of the junctional epithelium to?
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
78
Gingival pocket permits the development of?
Subgingival plaque and altered environment favours the growth of gram-negative anaerobes.
79
Impairment of the barrier function of the junctional epithelium allows ready ingress of ____ from the subgingival plaque, leading to development of an immune response.
Antigens
80
Early lesion of gingivitis is characterized by?
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.
81
Infiltrate consists of a mixture of?
T and B lymphocytes. T cells predominate in early lesion of gingivitis.
82
In early lesion of gingivitis, cytokines are released, that trigger ?
Connective tissue breakdown, leading to destruction of gingival collagen fibres as the infiltrate expands.
83
Key points of early gingivitis
- Lymphocytic infiltration
- Impairment of barrier function of junctional epithelium
- Gingival pocket formation; growth of subgingival plaque
84
Early gingivitis may remain ____, especially in children.
Stable
85
Area of inflamed gingival tissue continues to expand ?
Apically and laterally, accompanied by continuing destruction of gingival collagen.
86
Characteristic shift in inflammatory cell population from predominantly lymphocytic (early gingivitis) to ?
Plasma cells predominate
87
B lymphocytes are stimulated to differentiate into ______ against plaque bacterial antigens by cytokines from _____ within the infiltrate.
specific antibody-producing plasma cells; T-helper cells
88
Huge amounts of immunoglobulin are present throughout the connective and epithelial tissues in established gingivitis.
True
89
Exacerbation of the inflammation results in further impairment of the barrier function of the junctional epithelium and ________.
Deepening of the gingival pocket.
90
Key points of established gingivitis
- 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
In established gingivitis, pocket epithelium may be?
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
Varying attempts at repair characterized by formation of fibrous tissue isn't as good because?
Newly-formed collagen bundles do not simulate the architecture of the previously existing gingival fibres.
93
Exuberant fibrous tissue formation results in?
Gingival hyperplasia and false pocketing.
94
Destruction of the specifically oriented gingival fibres, fibrosis and hyperplasia contribute to the ?
Loss of normal gingival form seen clinically in chronic gingivitis.
95
____________, resulting from increased vascular permeability associated with inflammation is another factor in chronic gingivitis.
Oedematous enlargement
96
Chronic periodontitis is characterized by destruction of the ____________, _____ and _____.
destruction of the connective tissue attachment of the root of the tooth, loss of alveolar bone and pocket formation.
97
Natural history of the untreated lesion of established gingivitis is not well understood.
True
98
Periodontitis is the result of extension of ?
Extension of inflammation from the gingiva into the deeper tissues.
99
Evidence of the progression of gingivitis to periodontitis is ?
The extension of inflammation beneath the base of the junctional epithelium into the supra-alveolar connective tissue.
100
Inflammatory infiltrate is rich in plasma cells but there are also numerous?
Numerous T lymphocytes and macrophages
101
As the area and density of the infiltrate increase there is destruction of collagen in the supra-alveolar connective tissue and the fibres lose?
Lose their attachment to cementum.
102
Loss of attachment to cementum is accompanied by apical migration of the junctional epithelium to cover?
Cover the denuded root surface; resulting in early true pocket formation.
103
As chronic periodontitis extends into the supporting tissues, there is progressive destruction of the fibres of the _____ accompanied by _________.
periodontal ligament; osteoclastic resorption of the alveolar bone
104
Junctional epithelium continues to migrate apically, leading to ?
Progressive deepening of the pockets.
105
As the junctional epithelium migrates apically the more coronal and inflamed tissue loses its specialized attachment and is converted into?
Pocket epithelium.
106
During chronic periodontitis, the width of the zone of attachment of the junctional epithelium at the base of the pocket remains ?
Fairly constant throughout the course of disease.
107
Pathway of spread of inflammation into the supporting tissues influences the pattern of bone destruction and morphology of the pockets.
True
108
In general, the spread of inflammation follows the course of ?
blood vessels
109
In interdental areas, the infiltrate extends mainly along the?
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
Osteoclastic resorption results in?
Interdental cratering
111
In marginal areas, inflammation follows the course of _______ towards?
Supraperiosteal vessels towards the crest of the marginal alveolar bone.
112
Pathways of spread that follow main vascular supplies tend to result in a horizontal pattern of ?
Bone loss and suprabony pockets.
113
Various factors that modify inflammation to spread towards and directly into the periodontal ligament results in?
Vertical patterns of bone loss and infrabony pockets.
114
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 _______.
not constant; periods of remission.
115
Current hypotheses suggest that loss of attachment occurs as _______?
Brief bursts of destructive activity at random time intervals throughout an individual's life.
116
During periods of remission, there may be attempts at ?
Healing
117
At the base of the pocket, a narrow zone of junctional epithelium mediates ?
the soft-tissue attachment to the root
118
Periodontal pocket contains?
Subgingival calculus, plaque, and inflammatory exudate comprising fluid and cells, mainly PMN.
119
Areas of irregular hyperplasia and rete ridge formation alternate with areas of?
Areas of thinning of the pocket epithelium and even frank ulceration.
120
Vessels in the subadjacent connective tissue are markedly dilated and there is emigration of large numbers of?
Polymorphonuclear cells which transmigrate the pocket epithelium.
121
Underlying connective tissue is densely infiltrated by inflammatory cells, predominated by?
Plasma cells
122
Inflammatory infiltrate may extend into?
Adjacent marrow spaces
123
In actively progressing disease, osteoclasts may be seen along the _____ and within ____ but they are infrequent in relatively stable lesions.
Bone front; adjacent marrow spaces
124
Key points of chronic periodontitis
- 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
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.
Matrix Metalloproteinases (MMPs)
126
MMPs (Matrix metalloproteinases) produced mainly by?
Connective tissue cells, principally fibroblasts, but are also synthesized by other cell types such as macrophages and neutrophils.
127
MMPs are secreted in a _____ form and require _____ before they can degrade matrix proteins.
latent; activation
128
In health, normal remodelling o connective tissue is ?
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
Main group of inhibitors of MMPs present in tissues are known as?
TIMPs (tissue inhibitors of metalloproteinases)
130
TIMPs are produced mainly by?
Fibroblasts and macrophages, probably at the same time as cells release MMPs.
131
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 relative increase in the levels of MMPs.
132
Why is there a relative increase in MMPs in periodontal disease?
- Increase in MMP synthesis or a reduction in the synthesis of TIMPs
133
Production of both MMPs and TIMPs are influenced particularly by?
Cytokines
134
In particular, activity of _____, which induces MMP production by host cells, probably plays a key role.
Interleukin-1
135
Key points of degradation of the extracellular matrix (ECM)
- 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
Identify the three categories of local mediators for stimulating osteoclastic activity.
Cytokines, prostaglandins, growth factors
137
List main cytokines which stimulate bone resorption
- Interleukin-1
- Interleukin-6
- Tumour necrosis factor (TNF)
138
How are the cytokines which stimulate bone resorption mediated ?
Through prostoglandin synthesis especially PGE2 which enhances osteoclastic activity.
139
Which is the most potent stimulator of bone resoprtion known and periodontal inflammation.
Interleukin-1
140
During bone resorption, osteoclasts adhere tightly to the bone matrix and secrete ____ which demineralises the matrix.
Hydrochloric acid.
141
MMPs and other proteases produced by the osteoclast then?
Degrade the organic matrix. This process is comparable to cyst expansion
142
Most common form of chronic periodontal disease?
Chronic periodontitis
143
Onset of disease of chornic periodontitis?
Early adult life or even before, but in majority of patients, does not progress to tooth loss until after 50 years of age.
144
Chronic periodontitis is also referred to as?
Adult-type periodontitis.
145
General pattern of chronic periodontitis?
Predominantly horizontal bone loss is seen with suprabony pocketing.
146
Which part of dentition is involved in chronic periodontitis?
Entire dentition is usually involved, with the loewr incisors and molars tending to show the most advanced bone loss.
147
Key points of pathogenesis of periodontal disease
- 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
Localized form of aggressive periodontitis is referred commonly as?
Juvenile periodontitis
149
Onset of juvenile periodontitis
Usually commences around puberty, rare form.
150
Higher incidence of juvenile periodontitis in which gender?
Females
151
Juvenile periodontitis is characterized by?
Rapid destruction of alveolar bone with vertical bone loss, resulting in deep infrabony pockets.
152
Which teeth are initially affected in juvenile periodontitis?
Permanent first molars, and/or maxillary incisor teeth are affected, usually symmetrically, but the number of teeth involved increases with age.
153
Pattern of involvement of dentition in juvenile periodontitis?
Follows sequence of eruption.
154
Aetiology and pathogenesis of juvenile periodontitis?
Remains obscure.
155
Describe lesions of juvenile periodontitis
Inflammatory
156
Primary aetiological factor of juvenile periodontitis
Bacterial plaque
157
Degree of destruction in juvenile periodontitis is not?
Is not commensurate with the generally small amounts of plaque present.
158
Subgingival flora in juvenile periodontitis differs significantly from?
Adult periodontiti
159
Subgingival flora in juvenile periodontitis is dominated by?
Gram-negative anaerobic rods, particularly actinobacillus actinomycetemcomitans.
160
Generalized form of aggressive periodontitis includes patients previously classified as?
Having rapidly progressive periodontitis.
161
Onset of generalized aggressive periodontitis
Onset in early adult life bvidence of rapid bone destruction.ut lacks well-defined criteria.
162
Describe aggressive periodontitis
Severe periodontal lesions, generalized with evidence of rapid bone destruction
163
Affected dentition of aggressive periodontitis
- Almost entire dentition is usually affected.
164
Progression of aggressive periodontitis
May either progress without remission to tooth loss or subside and become quiescent.
165
Classification of periodontitis in systemic disease
Prepubertal periodontitis, present in childhood
166
Involved dentition of prepubertal periodontitis
Deciduous dentition and subsequently permanent dentition.
167
Prepubertal periodontitis is characterized by?
Extensive destruction of alveolar bone and are associated with a variety of uncommon systemic diseases.
168
Papillion-Lefevre syndrome is characterized by?
Skin lesions of palmar-plantar hyperkeratosis and severe periodontal destruction involving both deciduous and permanent dentition.
169
Papillion-Lefevre syndrome is transmitted how?
Autosomal recessive and is due to mutations in the gene encoding for the lysomal enzyme cathepsin C.
170
It is well established that some degree of gingival enlargement can occur in ____ and other patients taking the anticonvulsant drug ____.
Epipleptics; phenytoin
171
Factors predisposing chronic hyperplastic gingivitis?
Unknown, mostly.
172
Percentage of patients affected by chronic hyperplastic gingivitis?
Ranges from less than 10 percent to over 60 percent in different series.
173
Essential aetiological factor for chronic hyperplastic gingivitis
Dental plaque; any drug that modifies a previously existing chronic gingivitis and good oral hygiene can prevent the gingival hyperplasia.
174
Mechanism by which drug or its metabolites can induce chronic hyperplastic gingivitis?
Unknown, but certain gingival fibroblasts can metabolize phenytoin which may accompany increased production of collagen.
175
List diseases associated with major abnormalities of neutrophils in severe periodontitis in children?
- Agranulocytosis
- Cyclic neutropenia
- Chediak-Higashi syndrome
- Job syndrome
176
List diseases in which there may be associated neutrophil dysfunction with severe periodontitis in children
- Papillon-Lefevre syndrome
- Down syndrome
- Juvenile-onset diabetes mellitus
177
Other systemic diseases associated with severe periodontitis in children
- Hypophosphatasia
- Langerhans cell histiocytosis (histiocytosis-X group)
- Ehlers-Danlos syndrome (Type 8)
178
Clinically, chronic gingival hyperplasia may be more or less generalized but primarily involves?
Interdental tissues, particularly around the labial surfaces of anterior teeth.
179
Enlargement in chronic gingival hyperplasia manifests as ?
firm, pink, often lobulated fibrous masses that may obscure the crowns of the teeth.
180
In patients where marginal gingiva is relatively uninovlved in chronic gingival hyperplasia?
Deep clefts separate adjacent bulbous interdental papillae.
181
Histologically, overgrowth in chronic gingival hyperplasia consists mainly of?
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
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.
cyclosporin; nifedipine; verapamil
183
Gingival fibromatosis is a rare hereditary condition most frequently transmitted as an _______ trait, although autosomal recessive inheritance has been reported.
Autosomal dominant
184
Autosomal dominant type of gingival fibromatosis can be caused by mutations in at least ____ distinct genetic loci.
Two
185
Gingival fibromatosis presents as?
Generalized or occasionally localized, fibrous enlargement of the gingiva which usually begins with the eruption of the permanent or occasionally deciduous teeth.
186
Gingival fibromatosis is rarely present at?
Birth
187
Occasionally, gingival fibromatosis is associated with?
Hypertrichosis, epilepsy and mental retardation.
188
Microscopically, fibrous tissue consists mainly of _______ but mucoid change due to accumulation of _____, is common in gingival fibromatosis.
Coarse bundles of collagen fibres; ground substance.
189
Key points of desquamative gingivitis
- Common clinical manifestation of a variety of different diseases
- Involves full width of attached gingiva.
190
Symmetrical fibrous enlargements in desquamative gingivitis also occur in the __________ region and it is possible some cases are related to gingival fibromatosis.
Maxillary tuberosity
191
Generalized enlargement of the gingiva may be caused by _______ by leukaemic infiltration in acute leukaemia.
Oedema
192
Desquamative gingivitis is not a ______ but a clinical term applied to the gingival manifestation of several different diseases.
Disease entity
193
Clinically, desquamative gingivitis presents as?
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
Commonly affected areas of gingiva in desquamative gingivitis involves?
Buccal and labial gingiva, more commonly affected than lingual or palatal tissues.
195
Desquamative gingivitis are more common in which gender and ages?
Females than males, most cases occur after 30 years of age.
196
Causes of fibrous overgrowths in gingival generalized enlargement
- Gingival fibromatosis
- Chronic hyperplastic gingivitis
- Drug-associated hyperplasias: epanutin, cyclosporin, nifedipine and verapamil
197
Causes of oedematous enlargement in gingival generalized enlargement
- Oedematous gingivitis: puberty, pregnancy, oral contraceptives, scurvy
198
Causes of systemic disease in gingival generalized enlargement
- Acute leukaemias
| - wegener's granulomatosis
199
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.
Suppurative inflammation.
200
Most lateral periodontal abscess arise in patients with _______ and may occur as a direct result of an increase in?
pre-existing advancing periodontitis; increase in virulence and toxic factors released by plaque organisms or secondary to reduction in host resistance.
201
Obstruction to the drainage of exudate from a periodontal pocket predisposes to?
Abscess formation
202
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.
infrabony pockets; fibrosis; oedema
203
Clinically, periodontal abscesses may be ___ or ____.
Acute or chronic
204
Acute abscess develops rapidly and is accompanied by?
throbbing pain, redness, swelling and tenderness of the overlying mucosa.
205
Affected tooth in abscess is usually?
Tender to percussion but most are vital.
206
Deep-seated lesions or where drainage is obstructed, abscess may track and present with?
Sinus opening on the mucosa somewhere along the length of the root.
207
Discharge of pus relieves ______ of periodontal abscesses and the lesion may heal or become chronic with ______.
Acute symptoms; intermittent discharge
208
Chronic periodontal abscess may be?
Asymptomatic or give rise to episodes of dull pain. Acute exacerbations are common.
209
Pericoronitis define?
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
Where is an ideal space for pericoronitis?
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
Pericoronitis' inflammatory oedema leads to?
Swelling of the flap which predisposes to trauma from the opposing teeth and exacerbation of the inflammation.
212
Usual symptoms of pericornitis?
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
In severe cases of pericoronitis, what can develop?
Acute pericoronal abscess may develop which can remain localized or be associated with cellulitis and extension of infection into adjacent surgical spaces.
214
Prevalence and severity of periodontal disease increases with age because?
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
_______ 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.
Gingival recession
216
Is there evidence that the elderly are susceptible to periodontal disease?
No, although this is expected because of the decreased efficiency of both host defence systems and healing associated with ageing.
217
List several histological changes associated with ageing
- Increased apposition of cementum
- Decreased cellularity of periodontal tissues
- Disordered insertions of periodontal ligament fibres into bone and cementum.
