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lecture 3: initiall, early, established and advanced lesions. Flashcards

1
Q

definition of gingivitis

A
  • plaque induced
  • INFLAMMATION (edema, BOP)
  • no destruction of PDL and bone
  • no apical migration of epithelial attachment
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2
Q

if there is epithelial attachment what does that mean

A

the junctional epithelium is at CEJ

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3
Q

definition of periodontitis

A
  • plaque-induced
  • host related
  • INFLAMMATION (edema and BOP)
  • destruction of bone
  • NOT ALL cases of gingivitis progress to periodontitis.
  • this is irreversible only maintain, tx and control
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4
Q

what determines whether gingivitis becomes periodontitis

A

host response

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5
Q

what is the continuous model

A

that it is continuous throughout life at same rate of loss

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6
Q

what is the progressive model

A
  • progressive loss over time of some sites
  • no destruction in others
  • time of onset and extent vary among sites
  • periodontal ds affects mainly post teeth
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7
Q

what is the random burst model

A
  • activity occurs at random at any site
  • some sites show no activity
  • some sites have one or more bursts of activity
  • cumulative extent of destruction varies among sites
  • periodontitis is different among various spots and it is hard to predict attachment loss
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8
Q

this type of bone loss can be due to

A

lack of access

seen in distal areas of bone loss.

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9
Q

which are the least likely teeth to loose due to periodontal ds

A

mand C and PM

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10
Q

what is the most common lost tooth due to periodontal ds

A

mx 2M

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11
Q

what is a secondary etiological factor of periodontal ds

A

an open contact

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12
Q

signs of inflammation

A

rubor

calor

dolor - not really unless they have an abscess

tumor

functio laesa (loss of function) ** misisng of tooth, increase mobility, loss of attachment

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13
Q

inflammation is what type of phenomenon

A

vascular

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14
Q

the process of inflammation

A
  • leukocyte migration
  • vasculitis the biggest change you see
    • ​dilation
    • venous stasis (congestion)
    • increased permeability
      • like transudate and exudate
    • why does it do this? to bring immune mediators
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15
Q

what is the first defense

A

innate immunity

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16
Q

what is the innate immunity

A
  1. the first defense system

non-adaptive and genetic

includes PMNs and monocytes/macrophages (WBC)

kill through phagocytosis

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17
Q

how does the innate system kill by

A
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18
Q

what is the second defense system

A

adaptive immunity

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19
Q

what is adaptive immunity

A
  1. the second defense system

its v specific

uses B and T cells

Plasma cells produce specific ab to individual antigens

done through production of immunoglobulins by antibodies

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20
Q

adaptive immune system produces

A

immunoglobulins by antibodies

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21
Q

B lymphocytes are:

A
  • activated b-cells that become plasma cells
  • plasma cells that produce immunoglobulins
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22
Q

t lymphocytes are:

A
  • developed in the thymus
  • several functions (antigen presentation)
  • help B-cells divide; can destroy virally infected cells; can down-regulate immune response
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23
Q

two major forms of T cells

A

CD4 and CD8

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24
Q

MHC Class II molecules is what

A
  • CD4
  • T helper celss
  • they help B cells to divide
  • Controls leukocyte development
  • activates innate cell lining
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25
Q

what is MHC Class I

A
  • CD8
  • T cytotoxic cells
  • destorys virally infected target cells
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26
Q

**PMNS are

A

phagocytosis; produces lysosomal enzymes

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27
Q

** macrophages are

A
  • phagocytosis; process antigens and cytokine secretion
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28
Q

** b lymphocytes are

A
  • plasma cells; produces antibodies
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29
Q

** t lymphocytes are

A

T helper (CD4)- helps B cells divide

T suppressor (CD8 and CD25) - down-regulates t and b cells

NK cell- kills virally-infected cells

T-cytotoxic cell- destorys infected cells

Killer T cell - kills infected cells

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30
Q

hummoral immunity has two components

A
  • antibodies and complement
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31
Q

antibodies are released by ____ and have ____ major immunoglobulins

A
  1. plasma cells
  2. 5
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32
Q

the 5 immunoglobulins from antibodies

A
  1. IgM
  2. IgG
  3. IgA
  4. IgD
  5. IgE
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33
Q

what is IgM

A

the first responder and the largest in size

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34
Q

what is IgG

A

second responder and most abundant, crosses the placenta

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35
Q

what is IgA

A

salivary IgA; a dimer

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36
Q

what is IgD

A

co-expressed with IgM

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37
Q

what is IgE

A

on mast cells, allergic reactions

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38
Q

what is complement immunity

A

-a part of both innate and adaptive immune systems

  • a biochemical cascade that helps clear pathogens by lysis, opsonization, binding, and clearance of immune complexes
  • acts as a coplayer to recruit more immune cells and clearance
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39
Q

t suppressor cells

A

now t regulatory cells,

they down regulate T and B cells (CD8 and CD25 expression), it prevents autoimmune disease

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40
Q

K (killer) cells

A

a mononuclear cell that kills cells sensitized with antibody (via a Fc receptors)

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41
Q

NK cells

A

natural killer cells that kill virally infected and transformed target cells that have NOT been previously sensitized

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42
Q

other immune cells- monocytes

A

~5%, activation in CT

WILL BECOME MACROPHAGES

43
Q

Other immune cells- Neutrophils

A

more than 70%.

they have a 48 hour lifespan in blood with migration to sites for phagocytosis

44
Q

Other immune cells- esoinophils

A

about 2 to 5% of cells

they cause damage by exocytosis (like histamine release)

45
Q

Other immune cells- mast cells

A

contain mediators of inflammation (histamine, prostaglandins, leukotrienes and cytokines)

they are involved in allergic reactions

46
Q

Other immune cells- basophils

A

less than 0.5% of cells

are in some way functionally similar to mast cells

47
Q

definition of cytokines

A

molecules that send out signals and help orchestrate the process

“soluble, locally active polypeptides; regulate cell growth, differentiation, function; produced by cells of the immune system.

cytokines are depenent on: their concentration, cells that produce them, cells being attracted and acted upon and presence and extent of extracellular matrix

48
Q

** IL-1

A

pro-inflammatory, stimulates osteoclasts, fibroblasts and macrophages

49
Q

what are the 5 important cytokines in this lecture

A

1. IL-1

2. IL-6

3. IL-8

4. TNF

5. PGE2

50
Q

**what is IL-6

A

proinflammatory, stimulates T and B cells

51
Q

** what is IL-8

A

pro-inflammatory; attract and activates PMNs

52
Q

** what is TNF

A

pro-inflammatory; activates osteoclasts

53
Q

** what is PGE2

A

vasodilation

pyrogenic

releases mediatory from mast cells

cell-mediated cytotoxicity

54
Q

what i smore prevelaent in caucasians and which is more prevalent in asians

A

caucasions - IL-1

asians - TNF

55
Q

what is the most potent inflammatory cytokines for periodontitis

A

IL-1

*have tests to see if pt is susceptible by looking at values of IL-1

56
Q

4 growth factors covered in lecture

A

TGF - stims epithelial cells and fibroblasts

PDGF - stimulates fibroblasts

EGF - stimulates epithelial cells

FGF - stimulates fibroblasts

57
Q

can we then accurately predict which patients with gingivitis are going to develop periodontitis

A

no

the answer ius in the host’s immune system and genetics

58
Q

well known risk factors for developing periodontitis

A
  1. smoking (habit)
  2. plaque
  3. diabetes (systemic)
  4. anythihng that affects the immune response

patients with risk factors are more likely to have attachment loss!!!!

59
Q

the order of phases of periodontal ds

A

A. normal - healthy

B. 1. initial - gingivitis

B. 2. early - gingivitis

B. 3. established - gingivitis

C. Advanced - periodontitis

60
Q

clinically healhty ginginva has what:

A
  • some neutrophils and macrophages in CT
  • new neutrophils mirgration through JE
  • no collagen destruciton
  • intact epithelial barrier
  • gingival crevicular fluid is present
  • appears clinically healthy (color, contour, consistency)
61
Q

inflammatory response modifiers

mechanical (plaque retention factors)

A
  • calculus
  • caries
  • restoration chaosm (defective, subg, and overcontoured margins)
  • prosthesis
  • tooth anatomy facots
62
Q

inflammatory response modifiers

systemic

A

-uncontrolled/controlled diabetes**

-hormonal: puberty, pregnancy **

- HIV/AIDS**

- Medications**

- PMN defects

  • hematolgoical
  • immune disturbances
  • nutrition deficiencies
63
Q

inflammatory response modifiers

genetic

A
  • leukocyte adhesion deficiency (LAD)

- hypophosphatasia

- agranulocytosis

  • neutropenias
  • lazy leukocytes
  • down’s syndrome
  • papillon-lefevre
  • chediak-higashi
  • ehlers-danlos syndrome
64
Q

what is the inital lesion

A
  • PLAQUE IS DEPOSITED ON THE TOOTH
  • bacterial biproducts are released into the periodontal tissues (virulence factos)
  • it develops 2 to 4 days after not brushing or flossing
  • cells of acute inflammation are present
  • there is an increase in GCF flow
  • and the start of a pseudopokcet formation (due to the margin going up coronally)
65
Q

what are the two types of virulence factors

A
  • stimulation of the host defense system (attracts inflammatory cells, stimulates cells to release cytokines and chemoattract factors IL-8)
  • degradation of the host tissues (enzymes: collagensae, trypsin-like enzymes, keratinase, phospholipase A)
66
Q

with poor plaque control what do we see

A

stimulation of epithelial cells and fibroblasts to relese IL-* into the CT which attracts and activates PMNS.

PMNS in CT. PMNs are attracted and near the JE and Sulcular epithelium (JE and CT are still intact)

67
Q

what happens with plauqe accumulation *

A

stimulation of inflammatory cells to release cytokines into the CT

PMNs are still attracted and near to the JE and SE.

68
Q

clincial features of initial lesion

A
  • increased GCF flow
  • sulcus increases from 0 to 3mm by forming a pseudopocket
  • alveolar bone is normal on the radiograph but the probing depth has increasd
69
Q

the steps of PMNs

A

~PMNs associated~

  1. diapedesis
  2. chemotaxis
  3. adherence
  4. phagocytosis
  5. killing, digestion and aggregation
70
Q

what is the early lesion

A
  • 4 to 7 days without brushing or flossing
  • acute inflammation persists, there is increased GCF, and pseudopocket formation
  • cells of chronic inflammation appear and then dominate, we see IL-1 and IL-6.

there is a shift from PMNS to t lymph = chronic.

collagen loss continues and MMPs activation begins

71
Q

how is collagen lost?

A
72
Q

what is matrix metalloproteinases

A

MMPs

  • proteases with activity against most, if not all, extracellulat matrix macromolecules

and important sub class of MMP is = interstitial collagenases.

73
Q

histopathology of the early lesion

A
  • loose up to 70% of collagen
  • caused by a combination of bacterial products and host defense system that cause the destruction

PMNs accumulate in gingiva –> in the sulcus –> chronic inflam cells (t cell lesion) accumulate –> chronic predominates –> fibroblsts show cell damage –> rete pegs proleferation of JE into CT.

74
Q

clinical features of an early lesion

A
  1. edema of gingiva
  2. increased GCF flow
  3. loss of gingival stippling
  4. erythema of gingival margin
  5. no migration of JE attachmen t
  6. alveolar bone is normal-no bone loss
  7. reversible
75
Q

what is the establish lesion host defenses

A
  1. inhibit dramatic plaqu growth thus it
  2. prevents infection becoming dramatically worse, but a
  3. stand-off exits since plaque unable to be eliminated and there is a
  4. shift to b-cell/plasma cell lesion
76
Q

what is the established lesion

A
    • acute inflammation persists, after 2-3 weeks it is a stable lesion
      - but chronic inflammation dominates (act b lymph –> plasma cells**)​ b cell lesion which means production of abs
  2. PMN wall tries to contain the infection, micro-ulcerations of pocket epithelium, JE not intact
  3. Bystander damage
  4. Two-edged “sword” of immune system

NO BONE LOSS and JE is still at CEJ

77
Q

established lesion - ds activity

A
  1. 2 processes: damage and repair
  2. a shift to actived b cells to plasma cell lesion
  3. highly vascular
  4. immature CT
78
Q

effect on the ground subtance during established lesion

A
79
Q

when there is a loss of collagen there is

A

decreased rate of synthesis and increased rate of breakdown

(esp during the establish lesion)

80
Q

during the established lesion although there is collagen loss there is also CT repair, how ?

A
  1. attempt to minimze tissue damage
  2. fibroblasts are cytokine regulated
  3. recruitment of new cells like TGF beta, PDGF (cytokine regulated) or chemotatic collagen and elastin fragments
  4. Tissue inhibitors of MMPs = TIMP “the shut down mechanism”
81
Q

histopathology of the established lesion

A
  1. damage of fibroblasts and eptihelium
  2. loss of collagen
  3. microulcerations of pockeet epithelium
  4. acute inflamamtion still there
  5. PMNs in pocket
  6. degreadation of extracellular matric
  7. defense infliltrate so t, b, and plasma cells
  8. JE proliferation and extension into the CT so
  9. Elongation fo rete peg ridges
82
Q

clinical features of established lesion

A

edema

erythema

BOP

gingival cahnges

NO BONE LOSS

83
Q

initial stages of gingivitis

time, cells, collagen loss, sulcular epithelium and clincial findings

A
84
Q

early stages of gingivitis

time, cells, collagen loss, sulcular epithelium and clincial findings

A
85
Q

establish lesion of gingivitis

time, cells, collagen loss, sulcular epithelium and clincial findings

A
86
Q

the established lesion is the final stage of “pure gingivitis” this lesion can maintian stable for how long

A

weeks, months, years

for it to progess to periodontitis is hard to predict but host factors can identify the risk groups

87
Q

what is the advanced lesion

A

PERIODONTITIS

  • have pocket formation results from apical migration of JE
  • loss of fiber attachment (cementum and PDL)
  • LOSS OF BONE and irreversible
88
Q

advanced leison features of periodontal breakdown

A
  1. pocket formation through the destruction of PDL, apical migration of JE, and bone resportion
  2. Asynchronous multiple burst model where there are short bursts of ds activity but long burst of quiescence
  3. Bystander damage
  4. Host balance of damage/repair is upset
89
Q

during the advances lesion there is alveolar bone resportion, what is associated with this

A
  • activation of osteoclasts
  • ruffled border produced = active site
  • hydrolytic enzymes are released
  • cytokinesa are released (IL-1,-11, and TNF)
  • prostaglandins are produced like PGE2
  • leukotrienes are produced (inflammatory mediators and involved in allergic rxn)
90
Q

advanced lesion mechansims of bone loss**

A
  • microbial factors: LPS
  • activates inflammaroty cells to release IL-1 and PGE2
  • activates PMNs to release collagenase
  • COLLAGEN LOSS
  • activates osteoclasts to release collagenase for bone (MMP-13)
91
Q

histopathology of the advanced lesion

A
  1. PMNs
  2. b, plasma cells dominating
  3. inflammatory infiltrate
  4. extension of lesion into PDL and bone
  5. loss of collagen continues
  6. cytopathologically altered plasma cells
  7. progressive pocket formation - attachment loss
  8. quiescence and exacerbation
92
Q

clinical features of advanced lesion

A
  1. periodontal pocket formation
  2. pocket epithelium ulceration
  3. radiographic bone loss (50% of vol/density needs to be lost before detected)
  4. Bleeding on probing
  5. changes in gingival color, contour and consistency
  6. attachment loss
  7. mobility
93
Q

immune cells overview

initial

early

established

advanced

A

initial - PMNs, macrophages

early - ^ + t lymphocytes

established AND established - ^ + b lymphocytes and plasma cells

94
Q

tx of gingivitis

A
  • reversible
  • suppresion of microflora for plaque induced gingivitis (scaling, polishing, pt daily hygiene)
95
Q

tx of periodontitis

A
  • irreversible, no cure just control
  • through suppresion of microflora with SRP maybe ab, surgery, maintenance
  • Modulation of host with low dose doxycycline
96
Q

doxycycline is

A

used at a low dose and it is a collagenase inhibitor

97
Q

is plaque necessary to initial gingivitis and/or periodontitis

A

yes

98
Q

does everybody that has poor plaque control eventually develop gingivitis

A

yes

99
Q

does everyone that has gingivitis because of poor long term plaque control eventually develop periodontitis

A

no

100
Q

plaque is the primary etiology for

A

both gingivitis and periodontits

no plaque (bacteria0 no ds

101
Q
  1. plaque is ___ and ____ to initiate gingivitis
  2. plaque is ___ and ____ to initiate perdiodontitis
A
  1. necessary and sufficient
  2. necessary not sufficient
102
Q

what is plaque dysbiosis

A

the primary etiology of periodontal ds is bacterial plauqe in a susceptible host

103
Q
A

perio (9 decks)

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