Periodontal Disease Flashcards
(98 cards)
1
Q
Name 1-6
A
Review This
1. Gingival Margin
2. Free gingiva
3. Ginigival groove
4. Attached gingiva
5. Mucogingival junction
6. Alveolar mucosa
7. Intern dental gingiva
2
Q
The root of the tooth is covered by?
A
Cementum
3
Q
Union of the cementum and enamel
A
CEJ
4
Q
What percent of indv do cementum and enamel not meet?
What does it result in?
A
5-10%
* More sensitivity
5
Q
Why do older people experience less sensitivity than younger?
A
tertiary dentin which is more compact and closed channels which means they have less sensitivity compared to an 18 year old.
6
Q
below the free gingiva is where you probe 1-3mm is healthy, 3-10mm is disease
A
GIngival Sulcus
7
Q
What is the parameter for pocket depth?
A
Gingival Margin
8
Q
Non-keratinized tissue
A
Sulcular Epithelium
9
Q
at the base of the sulcus and connective tissues attachment
A
Junctional Epithelium
9
Q
Keratinized
A
Outer Epithelium
10
Q
Characteristic of Healthy Periodontum
A
- 10% or less bleeding
- No bone loss
- Attached gingiva
- Normal Subclinical inflmmation
- 1-3mm probing
11
Q
WHat does this shwo?
A
Healthy periodontum, no bone loss noted
12
Q
Inflammation and infection of gums, reversible! 1st.
A
GIngivitis
13
Q
Bones loss, decrease in clincal attachment, gingival recession. Irreversible
A
Periodontitis
14
Q
What are the 2 elements of periodontal diseases?
A
- GIngivitis
- Periodontitis
15
Q
What is the most common
Periodontal disease?
A
Gingivitis associated with or without Biofilm
Intial, moderate, severe
16
Q
What is the best peramete for periodontal disease?
A
BOP= bleeding or probing
17
Q
What are the parameters of localized gingivitis?
A
10-30% sies with BOP
18
Q
What are the parameters of generalized gingivitis?
A
Greater than 30%
19
Q
Why is the 30% rule important?
A
Helps classify gingivitis to general vs localized
20
Q
What is the etiology of Periodontal disease?
Cause
A
Dental Biofilm Bacteria
21
Q
What was the objective of the 1965 study of gingivitis?
A
Produce gingivitis in pt. with healthy gingiva and to study the sequence of changes in the microbiota and in the gingiva
22
Q
GI
A
Gingival Index
23
Q
PI
A
Plaque Index
24
WHat were the clincal results of the 1965 gingivitis study?
**when oral hygine stopped**
* Increased PI
* Increased GI (lots of bleeding)
* All subjects developed gingivitis
* GIngivitis start at 5th day, developed within 15-21 days
**when oral hygine re-started**
* GIngivits revered in 1 week
25
Explain bacteriological results of the 1965 study when **gingivitis at the start when OH stopped?**
G+ cocci & short rods (90-100%) little inflmmation, imediate increase of:
* cocci
* Desquamated epithelial cells
* Small increase in PMNL (neutrophils)
26
Increase in Polumorphnuclear Leukocytes results in what?
Inflmmation!
27
Explain bacteriological results of the 1965 study at **2-4 days post stopping OH**
* Increase in filamaents
* Increase in slender roods
* Cocci stil there
* Increase in PMNL
28
Explain bacteriological results of the 1965 study at **6-10 days post stopping OH**
Gradual transtion to:
* Vibrios
* Spirochetes
* Cocci, rod, filaments still there
* HEAVY PMNL accumilation
| Shift from good to harmful bacteria
29
Explain bacteriological results of the 1965 study **when health restablished?**
**Return to predominance of cocci and short rods.** Two patients still had filaments present.
No more: **spirochetes or vibrios.**
30
What wasthe **conclusion** of the 1965 gingivitis study?
**Mass of plaque buildup = gingival inflmation**
* Removal of plaque can revert gingivitis symptoms
31
Explain Non-specific theory
Mass of plaque results in gingival inflamation
32
What 2 complexes inn the socransky are considered early colonzers?
Green and Orange
33
How to the early colonizing bacteria necessary for other bacteria assc. with periodontal disease?
They **adhere to the pellicle** and are necessary for the colonization of other bacteria associated with periodontal disease.
**act as a base**
34
The bacteria in the orange complex act as what?
A bridging species between bacteria int he green and red.
35
What are orange complex bacteria assocated with?
**increased pocket depth** and and **progressive attachment loss**
36
P. intermidia is what complex?
Orange
37
The Red complex and Aa complex are what?
**final bacteria** that colonize and lead to the **destruction of the periodontium. **
38
What occurs if the green and orange complex bacteria are not present int he mouth?
the red complex bacteria are rarely able to colonize.
39
What di the socransky complex disprove from teh 1965 gingivitis study?
A **mass of plaque is not required **for the establishment of gingivitis and periodontisits.
**Sepcific bactera are what cause destruction**
40
What is the specific theory?
Specific bacteria causes the destruction (red complex)
41
What is the current etiology of periodontitis?
Periodontitis is a **multifactorial inflammatory disease caused by a dysbiotic (Unbalanced) microbiota**
42
Does calculus cause disease?
**NO!**
* mineralized plaque, no active bacteria
BUT it perpetuates the disease by **allowing plaque biofilm to adhere to it. **
43
What is the dysbiosis of periodontisits characterized by?
**the microbial shift that occurs in the biofilm**
* decrease in beneficial symbionts
* and/or an increase of pathobionts, as microorganisms become pathogenic when host-microbe homeostasis breaks down.
44
Interaction between host immune system and microbiome resulting in damage to self tissue
Host microbiome homeostasis breakdown
45
What is associated with an oral mucrobiota dysbiosis and disease progression?
Host & enviromental factors
46
* smoking tobacco
* poor oral hygiene
* diabetes mellitus
* pregnancy
modifiable risk factors
| Can be altered
47
* age a
* heredity, including genetic diseases
non-modifiable risk factors,
| You cant change
48
What does polymicrobial synergy and Dybiosis model?
Questioned the Red complex, some pathogens are incapable of pathogenicity alone. They require a commmunity to become pathogenic.
49
What are the 3 fundamental pre-reqs for periodontal pathogens to emerge as pathogenic?
1. Formationof a diverse community with **appropriate receptor**
2. Each rep in a community is **co-operative and harmonious**
3. The community will **withstand host immunity** and add to inflammation of periodontal tissue
50
What is a virulence factor of periodontal pathogens?
Adhesion & receptors
51
What are the 2 new emerging periodontal pathogens?
**2 gram (+) anerobic bacteria**
* Filifactor alocis
* P. Stomatis
52
What is the virulence factor of the 2 new periodontal pathogens
**Manipulate neutrophil effector functions**
* even if engulfed by neutrophil they are NOT destroyed through phagocytosis
* F. alocis, P. Stomatis
53
After dysbiosis of the host and pathogen occurs, and PAMPS are recognized what 2 paths can be taken?
1. Pattern recogntion & cytokiene release
OR
2. Complement protiens
**both lead to reqruitment & activation of neutrophil and macrophages and inflmmatory response and then tissue damage**
54
What is a PAMP on gram - bacteria?
Lipopolysachrides (LPS)
55
What are the histopathologic events and types of cells involved in the **initiation and progression of inflammatory periodontal** disease?
1. Inital Lesion (2-4 days rev)
2. Early lesion (4-10 days rev)
3. Established lesion (14-21 days rev)
4. Advanced Lesion (Time depends on pt. Irreversible)
56
Explain the intial lesion.
* Develops 2-4 days post accumulation of plaque
* Low grade inflamamtion
* **neutrophil & monocytes** migrate through connective tissue into the sulcues
* GFC (transudate) flow increases to try and flush bactera out of crevice.
57
# What Lesion?
Classic accute exudative ____ with **loss of perivascular collage** in gingival tissue, acute injury
Vasculitis, Initial Lesion 2-4 days
| Dialation of blood vessels, shift from symbiotic to pathobiotic bacteria
58
Most individuals will develop gingivitis in response to an
accumulation of plaque
59
____ is fundamental for determining which individuals may progress (some stay with initial, some progress depending on strength of immune system)
Host immune system
60
Explain the early lesion
* Develops between day **4 - 10** after continued plaque accumulation
* Corresponds with **early stages of gingivitis**
* The gingiva becomes **erythematous (red, lots of RBC)** in appearance due to a **proliferation in capillaries,** the opening of microvascular beds and **continued vasodilation**
61
What cells are associtated with early lesions?
* Lymphocyes
* Neutrophils
62
# What lesion?
Dense inflitrate of **lymphocytes and other mononuclear** cells, fibroblast morphology alteration, **initiation of connective tissue loss**.
Early lesion (4-10 days)
63
What 3 things occur during early lesion?(4-10 days)
* Fibroblast degenerate
* Collagen destruction
* Basal cell proliferate
64
# Early Lesion
What does fibroblast degeneration result in?
increases the ability for leukocytes to increase infiltration
65
# Early Lesion
Where does collagen destruction occur?
In the areas **apical and lateral** to the junctional epithelium and sulcular epithelium
| Note destruction, more whiteness apical and lteral to the dark purple JE
66
# Early Lesion
What is the purpose of basal cell layer proliferation?
to maintain an intact barrier against the bacteria
67
Explain an established lesion
* Occurs approximately **14 to 21 days**
* **Progression depends** on:
. Plaque challenge
. Host susceptibility factors
. Risk factors
* **Inflammatory cell infiltrate** occupies a considerable volume of the connective tissues
* **Plasma cells** predominate in older subjects
* **Lymphocytes** predominate in younger subjects
| Revesible
68
What does establish lesion progression depend on?
* Plaque challange
* Host suseptibility factos
* Risk factros
69
In an established lesionw what cells can be see? How does this differ with age?
* Lymphocytes in younger pt.
* Plasma cells in older pt.
70
Is there bone loss during established lesions?
No, plasma cells predominate but bone remains stable until it converts to an edvanced lesion.
| Gingivitis.
71
what occurs in collagen levels with established lesions?
**Collagen depeletion continues** with further proliferation of epithelium into the connective tissue space
72
WHat accumulates during the **established lesion phase**? What does this result in?
**neutrophils accumulate**
in tissues and **release lysosomal** contents extracellularly which kills bacteria but also **increases further tissue destruction**
73
What occurs in the **Sulcus epithelium** during the **established lesion phase**?
* Lining becomes **saturated with neutrophils**
* **Highly permeable** to substances inot or out of underlying connecitve tussves
* SE begins to **ulcertate**, increases bleeding.
| **inflammation & damage is STILL reversible**
74
Explain Advanced lesion
* Transition from **gingivitis to periodontitis**
* **Collagen destruction** that now extends into the *periodontal ligament and into the alveolar bone*
* **Neutrophils** predominate in the epithelium
* **Plasma cells** predominate in the connective tissue
| Irreversible!
75
What cells predominate in an advanced lesion? Where?
1. **Neutrophils** predominate in the *epithelium*
2. **Plasma cells** predominate in the *connective tissue*
| Connective tissue is no longer dense!
76
what occurs in collagen in advanced lesion?
Collage destrcution extends into the PDL and Alveolar bone.
**bone loss and PDL loss, pockets!**
| IRREVERSIBLE
77
Define a periodontal pocket
The pathological apical migration of the junction epithelum.
| Advanced lesion, to evade attacks
78
What do osteoclast do during an advanced lesion?
begin to**resorb bone as a defense mechanism** to prevent the spread of bacteria into the bone
79
The **seperation of the gingiva** and deepining of the JE forms a?
Periodontal Pocket
80
Where does periodontisis (adavanced lesion) usually being?
Interproxmally!
81
Explain this photo
Look!
82
In an advanced lesion what occurs as the pocket deepens?
**creates a protected, warm, moist anaerobic environment**
* Encourages more bacterial growth (anerobic)
* Cycle continues until bacteria is removed or tooth is lost
83
What occurs once teeth are cleaned post an advanced lesion?
**Interproximal bone loss & cleanincal attachment loss** remains, but inflmmation & bleeding goes away/
84
Summary
Summary
85
85
What new development has come up about neutrophils?
They are in both acute and chronic phases of inflammation
86
Explain how periodontisis can predispose people to **cardiovascular disease**?
people with periordontal pockets
have oral pathogens that can migrate to the heart
87
Explain Nosocomial Pneumonia and how people can be predisposed to this through periodontitis
Pneumonia that you get in the hospital. People with periodontitis that are intubated can allow bacteria to travel to the lungs and cause this.
| Respiratory Tract Infection
and Pneumonia
88
Explain how periodontisis can predispose people to **adverse pregnancy outcomes**?
Inflmmator yreaction of pregnant women in the mouth can travel travel to the plaenta and cause early fetal birth
89
Explain how periodontisis can predispose people to **Type 2 diabetes & insulin resistance**?
Its a cycle, diabetes promotes more periodontisits, vise versa.
Periodontisis common in diabetic pt. Also more prone to periodontal abscesss
90
What are other things that periodontis can predispose you too?
* Gastrointestinal disease
* Oral & colorectal cancer
* Lupus
* Rheumatoid arthrisis
91
Explain relationship of alzhimers & periodontitis
In 2017, **P. gingivalis** found in necropsies of 1 pt. with Alzheimer disease.
92
The gingiva is always in a state of ____ due to the presence of bacteria.
mild inflammation
93
Bacteria are required, but ____ to initiate the onset of periodontal disease.
not enough alone
94
A few novel pathogens that play a role in the ____ have recently been discovered.
onset and disease progression
95
____ is a part of the bigger picture.
Host susceptibility
96
The ____ microbiome can overwhelm the host defenses. This may lead to **further inflammation and eventual bone loss (periodontitis).**
dysbiotic microbiome
