periodontal lesion Flashcards
1
Q
What are the clinical descriptors for health periodontium?
A
Color: Coral Pink
Shape/Size: Knife-edged, thin and scalloped
Consistency: Firm
Surface Texture: Stippling
2
Q
What causes stippling on the gingiva?
A
underlying gingival connective tissue fibers at rete pegs, creating depressions and elevations on the gingival surface.
3
Q
Is stippling a sign of gingival health?
A
Yes, but its absence can also be seen in healthy gingiva or gingivitis.
4
Q
What is the prevalence of gingival stippling?
A
56.4% of individuals
5
Q
Histologic and Radiographic Images of Healthy Periodontium have?
A
No bone loss; no inflammation
6
Q
What is the supra-crestal tissue attachment (biologic width)?
A
histological structure composed of the junctional epithelium(variable parameters) and supracrestal connective tissue.
7
Q
What is the purpose of functional crown lengthening surgery?
A
It reestablishes the supra-crestal attachment (SCA) at a more apical position in cases where future subgingival restorations might impinge on the SCA, ensuring long-term periodontal health.
8
Q
Gingivitis
A
Inflammation of gingiva; no loss of clinical attachment
9
Q
Clinical Description for Gingivitis
A
Color: Red, bluish red/magenta
Shape/Size: Enlarged, rolled, blunted
Consistency: Edematous or fibrotic
Surface texture: No stippling
10
Q
Histologic and Radiographic Images for Gingivitis
A
No bone loss/attachment loss; Inflammation
11
Q
Periodontitis
A
Inflammation of gingiva extending into the adjacent bone and ligament
Loss of clinical attachment
12
Q
Clinical Description of Periodontitis
A
Color: Red, bluish red
Shape/Size: Enlarged, rolled, blunted
Consistency: Edematous or fibrotic
Surface texture: No stippling
13
Q
Histologic and Radiographic Images of periodontitis
A
Bone loss; Inflammation
14
Q
What is the effect of undisturbed dental plaque accumulation over 2-3 weeks (21 days)?
A
It induces gingival inflammation in 100% of cases.
15
Q
Is gingivitis reversible?
A
Yes
16
Q
Establishment of microflora is associated with?
A
difference in health and gingivitis
17
Q
What do differences in the development of gingival inflammation indicate?
A
They suggest varying disease progression and individual susceptibility to gingivitis.
18
Q
PATHOGENESIS OF INFLAMMATORY PERIODONTAL DISEASE AUTHOR
A
Page and Schroeder, 1976
19
Q
Include picture of slide 21
A
20
Q
What are the stages of gingival lesion development and their timelines?
A
Initial lesion: 2–4 days (biopsy).
Early lesion: 4–7 days (biopsy).
Established lesion: 14–21 days (biopsy, reversible).
Advanced lesion: Periodontitis (irreversible).
21
Q
Are Advanced lesion: Periodontitis irreversible?
A
No
22
Q
What occurs during the bacterial colonization in the initial lesion?
A
Bacterial colonization initiates the host response.
23
Q
What vascular changes occur in the initial lesion?
A
Dilation of blood vessels.
Increased blood flow.
24
Q
What is Subclinical Gingivitis?
A
The initial lesion (2-4 days)
25
What happens to the connective tissue in the initial lesion
Increased fibrin deposition and exudation.
Loss of perivascular collagen (5–15%).
26
What immune cells are predominant in the initial lesion?
PMNs (polymorphonuclear neutrophils) are found in connective tissue, junctional epithelium, and sulcus.
27
What is the clinical sign associated with the initial lesion?
Increased gingival crevicular fluid (GCF).
28
What is the function of gingival crevicular fluid (GCF)?
Flushes away bacteria and inflammatory mediators.
Contains serum, tissue breakdown products, inflammatory mediators, and antibodies.
29
What role do PMNs (polymorphonuclear neutrophils) play in the immune response during the initial lesion?
They serve as the first line of defense.
30
What processes do PMNs perform during the immune response?
Bacterial chemotaxis.
Phagocytosis.
Digestion of pathogens.
31
How do PMNs contribute to the progression of the immune response in the initial lesion?
They release destructive enzymes and pro-inflammatory mediators, which exacerbate the immune response.
32
What is Clinically Evident Gingivitis
Early lesion of gingivitis (4-7days)
33
What are the histopathological features of the early lesion?
Accentuation of features from the initial lesion.
Vascular proliferation.
More PMNs (polymorphonuclear neutrophils) and significant loss of collagen (60-70%).
Presence of T cells, macrophages, plasma cells, and mast cells.
Formation of rete pegs or ridges.
Collagen loss beneath the junctional epithelium (JE).
34
What is the clinical presentation of the early lesion?
Bleeding of the gingiva.
Erythema (redness) of the tissue.
35
What is the primary immune cell involved in the early lesion?
T cells
36
What do T cells do during the early lesion phase?
T cells bind to specific antigens and, once activated, secrete cytokines.
37
What are the two types of T cells and their roles in the early lesion?
CD4 helper T cells: Help activate other immune cells.
CD8 cytotoxic T cells: Target and destroy infected cells.
38
Histopathology of healthy periodontium
In CT, few cells other than fibroblasts, blood vessels and dense collagen fibers
39
Histopathology of an early lesion
After 8 days of plaque accumulation
CT is infiltrated with inflammatory cells displacing collagen fibers
Predominant cells are T cells and PMNs
40
What is Clinical Chronic Gingivitis
Established lesion (2-3 weeks)
41
What are the clinical features of an established lesion?
Red/bluish color due to impaired venous return
Changes in color, texture, and size of the gingiva
Bleeding on probing
Elevated flow of gingival crevicular fluid
No separation of gingival fibers from cementum
Creation of a pseudopocket due to gingival inflammation
42
What are the histopathological features of an established lesion?
Epithelial proliferation (apical), referred to as "pocket epithelium"
Discontinuous external basal lamina; possible ulceration
Dense inflammatory infiltrate in the connective tissue (increase in plasma cells)
Extensive loss of collagen
No bone loss
43
Plasma Cells
Originate as B lymphocytes
Secrete antibodies in response to a specific antigen
44
What are the clinical features of an established lesion (Chronic Gingivitis)?
Some lesions remain stable for months or years without progressing.
Other lesions may become more active and progress to advanced periodontal lesions.
45
What happens during the Initial Lesion of gingivitis?
Acute Inflammation Response: PMNs (polymorphonuclear neutrophils) are recruited.
Bacterial Changes: Predominance of Gram-positive and aerobic bacteria.
Tissue Changes: Vascular, connective tissue, and junctional epithelium alterations.
46
What is characteristic of the Early Lesion of gingivitis?
Increased Inflammatory Cells: T cells, PMNs, B cells, macrophages, and plasma cells are present.
Bacterial Changes: More Gram-positive bacteria and less Gram-negative bacteria.
47
What happens during the Established Lesion of gingivitis?
Chronic Inflammation: Involvement of plasma cells and IgGs (immunoglobulins).
Bacterial Changes: Equal number of Gram-positive and Gram-negative bacteria.
48
What did the low response group in the experimental gingivitis model show?
Low concentrations of host mediators despite similar bacterial accumulation.
49
What was down-regulated in all response groups, revealing novel tissue responses during gingival inflammation ?
Neutrophil modulator (IL-6)
50
What can understanding gingival inflammation variations help with?
Identifying individuals susceptible to periodontitis.
51
What happened to monocytes by day 21 of gingivitis?
They showed enhanced adherence to endothelial cells.
52
What was the novel finding of the study?
It was the first to demonstrate the effect of gingival inflammation on circulating IL-6 and monocyte activation, previously seen in periodontitis.
53
T or F: Loss of periodontal attachment is continuous, the progressive destruction of the periodontium leads to tooth loss.
True
54
T or F: 81% of the population falls under moderate progression/grade B
True
55
What defines an advanced lesion (periodontitis)?
Persistence of established lesion changes, loss of gingival collagen, epithelial ulceration, true periodontal pockets, and alveolar bone destruction.
56
What are the predominant cells in the connective tissue in periodontitis?
Plasma cells, with a large number of B cells, T cells, and PMNs.
57
What are the predominant cells in the junctional epithelium and sulcus during periodontitis?
Polymorphonuclear neutrophils (PMNs).
58
What characterizes the course of periodontitis?
Periods of quiescence and exacerbation.
59
What are the clinical features of periodontitis?
Thickened marginal gingiva
Bluish-red vertical zone from gingival margin to mucogingival junction
Bleeding, possible suppuration
Periodontal pocket formation
Possible tooth mobility and migration
60
What leads to the progression from gingivitis to periodontitis?
Bacterial plaque and host immune response initially maintain a balance in gingivitis.
61
What is the characteristic of chronic clinical gingivitis?
there is an equal number of Gram+ and Gram- bacteria.
62
What happens in a susceptible host?
there is dysbiotic microflora and a deregulated immune response, disrupting the balance.
63
What leads to the development of periodontitis?
Disruption of the balance between bacteria and host immune response results in Periodontitis (Advanced Lesion), which has more Gram- anaerobes and fewer Gram+ bacteria.
64
What is a gingival pocket?
occurs due to gingival enlargement without destruction of the supporting tissues.
65
What is a periodontal pocket?
results from the destruction of periodontal supporting tissues. It is composed of the tooth and gingival walls. It can be either suprabony or infrabony.
66
Where is the base of a suprabony pocket located relative to the alveolar bone?
Coronal to the level of the alveolar bone.
67
Where is the base of an infrabony pocket located relative to the alveolar bone?
Apical to the crest of the alveolar bone.
68
What is the pattern of bone destruction in a suprabony pocket?
Horizontal pattern of bone destruction.
69
What is the pattern of bone destruction in an infrabony pocket?
Vertical (angular) pattern of bone destruction.
70
How do periodontal ligament fibers beneath the pocket follow their course in a suprabony pocket?
They follow their normal oblique course.
71
How do periodontal ligament fibers beneath the pocket follow their course in an infrabony pocket?
They follow an angular pattern.
72
How are transseptal fibers arranged in a suprabony pocket?
Horizontally
73
How are transseptal fibers arranged in an infrabony pocket?
Obliquely
74
What is the root surface wall in the periodontal pocket?
Cementum covered by calculus.
75
What is attached plaque in the periodontal pocket?
Attached plaque surrounds calculus and extends apically.
76
What is unattached plaque in the periodontal pocket?
Unattached plaque surrounds attached plaque and extends apically.
77
What is the junctional epithelium in the periodontal pocket?
The junctional epithelium is found at the apical extent of the pocket.
78
What happens to connective tissue fibers in the periodontal pocket?
Connective tissue fibers are semi-destroyed at the apical extent of the pocket.
79
What are the components of the root surface wall in the periodontal pocket?
Bacterial invasion/penetration, endotoxins.
Embedded remnants of Sharpey’s fibers.
Demineralized cementum, potentially leading to root caries.
80
What is the effect of necrotic cementum in the periodontal pocket?
Necrotic cementum is similar to caries, contributing to periodontal damage.
81
Why are areas of remineralization important in the periodontal pocket?
These areas show potential healing, which is why root planing is done to help remove harmful substances and support remineralization.
82
Why is root planing important in periodontal treatment?
Root planing removes bacterial invasion, endotoxins, demineralized cementum, and necrotic tissue from the root surface to support healing.
83
What is found in the gingival wall of the periodontal pocket?
Bacterial accumulation.
Emerging leukocytes.
Leukocyte-bacteria interactions.
Intense epithelial desquamation.
Ulceration.
Hemorrhage.
84
PATHWAYS OF INFLAMMATION: Interproximal
Gingiva to periosteum
Periosteum to bone
Gingiva to PDL
85
PATHWAYS OF INFLAMMATION: Facial and lingual
Gingiva to periosteum
Periosteum to bone
Gingiva to PDL
86
How does inflammation extend to the crestal bone surface?
following blood vessels and collagen bundles to the crestal bone surface.
87
What changes occur in bone structure due to inflammation?
Increased multinuclear osteoclasts and mononuclear phagocytes
Formation of Howship lacunae
Enlargement of marrow spaces
Thinning of bony trabeculae
Replacement of fatty bone marrow with fibrous marrow
88
What factors influence susceptibility to periodontitis?
genetic and environmental factors, along with an imbalance between host protective and destructive mechanisms caused by specific bacteria.
89
How do clinical parameters relate to periodontitis?
indicate the severity of periodontitis but do not measure disease activity. Key parameters include probing depth, attachment level, bleeding on probing, plaque index, and radiographic assessment of alveolar bone loss.
90
Does periodontal tissue destruction occur uniformly throughout the mouth?
No, occurs on a few teeth at a time or even on specific surfaces of a given tooth, rather than uniformly throughout the mouth.
91
What are the two models of periodontal disease activity?
Slow but Continuously Progressive Model
Episodic Burst Model (Random/repeated multiple bursts)
92
What occurs during the periods of exacerbation in the Episodic Burst Model?
High proportions of Gram-negative bacteria
Increased inflammation
Attachment and bone loss
Involvement of plasma cells and PMNs
Release of inflammatory mediators: cytokines (e.g., IL-1, IL-6, IL-8, TNF-ɑ), PGE2, and MMPs
93
What characterizes the periods of quiescence in the Episodic Burst Model?
Reduced inflammation
Little or no loss of bone and connective tissue attachment
