Aetiology and Pathogenesis Flashcards
1
Q
Describe the appearance of gingival health?
A
Knife edge, scalloped gingival margin, stippling, pink
2
Q
What are the physiological bone levels for gingival health?
A
1-3mm apical to the cemento-enamel junction
3
Q
What is gingival health defined as?
A
10% bleeding sites with probing depths <3mm
4
Q
What is clinical gingival health characterized by?
A
Absence of bleeding on probing, erythema and oedema, patient symptoms, attachment and bone loss
5
Q
What are the local plaque retention factors for the pathogenesis of gingivitis?
A
Calculus, restoration margins, crowding, mouth breathing
6
Q
What are the systemic modifying factors of the pathogenesis of gingivitis?
A
Sex hormones and medication
7
Q
What is the primary thing needed for clinical gingivitis to occur?
A
Microbial challenge (plaque)
8
Q
Is gingivitis reversible?
A
Yes
9
Q
If gingivitis progresses what can it turn into?
A
Periodontitis
10
Q
What can be seen in periodontitis?
A
Inflammation and loss of periodontal attachment
11
Q
What is a false pocket?
A
Proliferation of sulcular epithelium and enlargement on gingivae when placing the probe into the pocket it will disappear but there is no loss of attachment so is deemed a false pocket
12
Q
What is a true pocket?
A
Plaque accumulation on the root surface causing apical migration of epithelium which causes bone loss
13
Q
How do you check bone level?
A
Using radiographs and looking for consistency in bone level
14
Q
What are the two types of bone loss?
A
Horizontal and vertical
15
Q
What is horizontal bone loss?
A
Bone level more than a couple mm from ACJ and is continuous throughout
16
Q
What is vertical bone loss?
A
Where bone loss varies on each side of the tooth (one side is deeper than other)
17
Q
how do the different types of bone loss arise?
A
Due to the thickness of the alveolar bone that rests between the teeth
18
Q
If there is thick alveolar bone between teeth which type of bone loss will occur?
A
Vertical
19
Q
If there is thin alveolar bone between teeth which type of bone loss will occur?
A
Horizontal
20
Q
How is furcation bone loss classified?
A
By how extensive it is
21
Q
What is class 1 furcation bone loss?
A
Bone loss is 3mm into the furcation (about half way)
22
Q
What is class 2 furcation bone loss?
A
More than 3mm into the furcation (over halfway)
23
Q
What is class 3 furcation bone loss?
A
Probe can go all the way through the furcation
24
Q
Once in periodontitis what can the progression of attachment loss be?
A
Episodic or continuous
25
What is the usual progression of attachment loss per year
0.05-1mm
26
What would be considered rapid progression of periodontitis?
>2mm of attachment loss over 5 years
27
Where does the plaque biofilm migrate with periodontitis?
Apically
28
What is the keystone pathogen for periodontitis?
P. gingivalis
29
What does a collection of bacteria do for the oral environment?
Perpetuates the inflammation which creates good conditions for inflammatory thriving bacteria
30
What does periodontitis need to occur?
The presence of bacteria
31
What is the host immune response to periodontitis and bacteria?
Saliva, epithelium barrier shreds cells and produces inflammatory mediators, gingival crevicular fluid produce, inflammatory and immune responses
32
What contributes to the connective tissue matrix degradation?
Matrix metalloproteinases and osteoclasts
33
What produces MMPs in periodontitis?
Host inflammatory cells
34
What are MMPs
Family of zinc and calcium dependent proteolytic enzymes including collagenases
35
What do local risk factors for periodontitis include?
Anatomical risk factors (enamel projections, grooves, gingival recession), tooth position (malalignment, crowding, migration), iatrogenic risk factors (restoration overhangs, defective crown margins)
36
What is the effect of smoking on periodontitis?
Vasoconstriction of gingival vessels and increased gingival keratinization, impaired antibody production, depressed numbers of Th lymphocytes, impaired PMN function, increased production of pro-inflammatory cytokines
37
What is the genetic risk for periodontitis?
Polymorphisms in the gene for IL-1 (greater production of IL-1)
38
What are the environmental risk factors for periodontitis?
The local risk factor, local microbiome, stress
39
What is the casual theory for the aetiology of periodontitis?
You must have teeth and microbial challenge to get periodontitis but these 2 alone are not sufficient enough to get eh disease so other factors are included
40
Roughly how many people suffer from periodontal disease in the population?
50%
41
What is the primary aetiological agent in inflammatory periodontal diseases?
Microbial plaque
42
What is the extent and severity of periodontal disease dependent on?
Interaction between microbe and host
43
What type of risk factors convey susceptibility for periodontitis?
Ones which interfere with host defences
44
what is gingivitis
inflammation localised to gingival tissues, acute inflammation, normal physiological response to infection or injury
45
what is periodontitis
inflammation of the gingival tissues and supporting periodontal structures, chronic inflammation, pathological inflammatory response associated with tissue destruction
46
what type of plaque has saliva as a major immune defence strategy?
supragingival
47
what contents of saliva target and inhibit microbial growth?
antimicrobials, peptides and antibodies
48
what is the most successful intervention for preventing caries and periodontal disease?
mechanical intervention (brushing)
49
what types of barriers do the oral mucosa provide?
physical and functional
50
how does the oral mucosa provide a physical barrier?
prevents microbes accessing underlying tissues
51
how does the oral mucosa provide a functional barrier
by detecting and responding to microbial challenge through activation of TLR which activates inflammatory pathways
52
where does gingival crevicular fluid have a predominant effect?
subgingival portion of tooth
53
what is the primary aetiological factor for periodontal diseases?
poor oral hygiene
54
what is the unique biofilm profile determined by?
interactions by microbiomes and host factors and interactions amongst bacteria
55
what are the first species to colonise the tooth surface?
gram+ streptococcal
56
what do gram+ streptococcal species do on the tooth surfaces?
modify the environment and create new attachment sites for different species and bind directly or provide metabolites to support other species
57
what are the early colonisers of the oral biofilm?
aerobic gram+ species
58
what are the late colonisers of the oral biofilm?
gram- anaerobic species
59
what is the red complex?
triad of periodontal pathogens
60
what species are in the red complex?
porphyromonas gingivalis, tannerlla forsythia, treponema denticola
61
do all periodontal patients have the red complex?
no
62
what does periodontitis need to occur?
bacteria
63
comment on the presence of periodontal pathogens?
present at low numbers in healthy sites, increased numbers in diseased sites or can be absent from diseased sites
64
what is polymicrobial dysbiosis?
periodontitis associated with community of microorganisms which work together to disrupt the homeostasis of health
65
how does gingivitis occur?
the homeostatic relationship is disrupted through the accumulation of plaque or transition of periodontal pathogens leading to modest inflammation
66
what is the effect of persisting inflammatory reactions in the oral biofilm?
it exerts an ecological pressure on species present in biofilm and gives some species a competitive advantage allowing them to exist while others succumb to inflammation
67
what type of species succumb to inflammation and are eliminated
commensal species
68
what type of species can persist and adapt in inflammatory environments
accessory pathogens and periodontal pathogens
69
what is periodontitis associated with?
a shift to dysbiotic biofilm which actively disrupts homeostasis for its own benefit which damages host tissues
70
what are the virulence factors of P gingivalis?
asaccharolytic, gingipains, atypical LPS, inflammophilic, drives dysbiosis
71
what does asaccharolytic mean?
it takes nutrients from the breakdown or proteins and peptides
72
what are gingipains
proteases with broad specificity
73
what does the atypical LPS of p. gingivalis do?
it is a TLR4 antagonist so it blocks inflammatory signalling
74
what does inflammophilic mean?
inflammatory environment favours expression of virulence
75
what do virulence factors do?
give immune system something to attack and alerts the immune system to the presence of microbes
76
how are virulence factors regulated
in response to environmental conditions
77
how does p. gingivalis persist in the oral environment
atypical LPS is used to hide from the immune system and persist in oral health, plaque accumulation stimulates inflammation and then P. gingivalis can express full virulence factors
78
name some factors which cause dysbiosis in the oral environment
smoking, salivary flow rates, diet, oral hygiene, innate/adaptive immune factors
79
what is the aetiology of periodontitis associated with?
accumulated plaque bacteria, presence of periodontal pathogens, polymicrobial dysbiosis, in susceptible hosts, host-pathogen interactions
80
what is the false pocket in gingivitis due to?
inflammation and swelling, no attachment loss
81
how does periodontitis have attachment loss?
PDL has came away from tooth surface so larger pocket, exposes more tooth surface available for biofilm accumulation deeper into the pocket and degradation of alveolar bone
82
what are the 2 hallmark signs of periodontitis
attachment loss and alveolar bone loss
83
what is the pathogenesis of gingivitis?
1 - increased TLR stimulation
2 - increased pro-inflammatory mediators (cytokines, peptides, chemokines)
3 - acute inflammatory response
4 - neutrophils remain predominant cell type
5 - monocytes recruited and differentiate to macrophages
6 - lymphocytes recruited to fine-tune the immune response (T cells coordinate and B cells release antibodies)
84
what do neutrophils do in the pathogenesis of gingivitis?
phagocytose, degranulate and release enzymes into GCF which bathes the attachment surface
85
how does increased vasodilation help immune cell defence?
it allows immune cells to migrate and control infection
86
what can you see histologically with periodontitis in the PDL?
large aggregates of granular cells which overwhelm and destruct the integrity of the tissue
87
what is the role of neutrophils in periodontal destruction?
they are crucial for maintaining healthy periodontium so when gingivitis occurs there is excessive infiltration which is associated with chronic inflammation (microbial subversion, degradative enzymes, inflammatory cytokines and oxygen radicals make a hypoxic environment, connective tissue destruction)
88
what does a loss of neutrophil function present like at a young age?
aggressive periodontitis as neutrophils are not available to control bacterial growth in a healthy gingivae
89
what is excessive infiltration of neutrophils associated with?
inflammation but is ineffective at controlling periodontal pathogens so it starts to contribute to periodontal tissue destruction
90
what is the role of adaptive immunity in periodontal destruction?
T and B lymphocytes present , aggregates rich in CD4 T cells and B cells evident as lesion progresses, unable to regulate dysbiotic biofilm, B cells predominant in advanced lesions, IgG fails to regulate dysbiotic biofilm, inflammation induced alveolar bone loss
91
what is the protective role of the adaptive immunity in periodontal destruction?
it prevents systemic infection by creating a barrier between pathogens and blood vessels
92
what do osteoblasts do?
synthesis and secrete bone tissue and contribute to bone formation
93
what do osteoclasts do?
resorbs bone, derived from monocyte/macrophage lineage
94
what is bone formation and resorption regulated by?
RANK/RANKL/OPG triad
95
how does inflammation lead to bone loss?
1. T and B cells in gingival tissues are activated
2. Lymphocytes release cytokines with RANKL and secrete into periodontal lesion
3. RANKL binds to RANK on pre-osteoclast e.g., monocyte
4. monocyte turns into osteoclasts
5. OPG binds to RANKL to prevent RANKL binding to RANK and further osteoclast production - HEATH
6. high levels of RANKL due to lots of T and B cells, low levels of OPG so it cannot inhibit RANKL binding
7. large numbers of monocytes recruited
8. osteoclast differentiating
9. resorbed bone, alveolar bone resorption, tooth loss
96
on a cellular level how does bacterial induced inflammation and pathologic tissue destruction occur?
1 - bacterial products bind TLR on epithelium which stimulates cytokines, chemokines and AMPs
2 - vasodilation and recruitment of leukocytes (neutrophils)
3 - bacterial products activate neutrophils and further release of pro-inflammatory mediators
4 - activated lymphocytes express RANKL so RANKL/OPG balance disrupted
5 - RANKL binds RANK on osteoclast precursors (monocytes) so osteoclastogenesis activated and alveolar bone resorption occurs
6 - pro-inflammatory cytokines contribute to bone resorption by inhibiting bone formation
7 - elevated and dysregulated MMP activation contributes to connective tissue destruction
97
what is the outcome of the initial infection determined by?
host/biofilm interactions
98
what is the nature of interactions between host and biofilm modified by?
environmental and genetic risk factors
