lecture 16: gingivitis

8/12/2019 Lecture 16: Gingivitis

http://slidepdf.com/reader/full/lecture-16-gingivitis 1/13

Transcribed by Leslie Afable January 30, 2014

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Basic Tissues Lecture 16 – Gingivitis by Dr. Robert Davidson

Slide 1 – Clinical Case Presentation: Chronic Gingivitis

Dr. Harvey Wishe – This is Dr. Robert Davidson, he’s a member of the perio

department and we are going to talk about gingivitis.

Dr. Robert Davidson–

Good morning, today I am going to talk to you about gingivitis.

Slide 2 – Today

Dr. Robert Davidson –Gingivitis is by definition, an inflammation, an inflammatory

process in the GINGIVAL tissues. Ok, you’ve had some dental anatomy already I’m

sure. Soft tissue, hard tissue, ok. Uh.. And what I will do is review the clinical

features of gingivitis if it’s something you are not familiar with. And then look at a

link/the connection between a couple of aspects of cell physiology and what

manifests clinically when we see a patient with gingivitis. A very typical clinical

manifestation. If you have any questions, don’t hesitate, raise your hand. I think I

have material that will fill up 45-46 minutes so there’s little time in the lecture to

answer questions.

Slide 3 – What is Gingivitis?..

Dr. Robert Davidson –Uh, do you all have the printout or not? Because it’s been

posted. Ok so what is gingivitis? Tell me what gingivitis is, a definition. Gingivitis is

an inflammatory process in the gingival tissues. What causes gingivitis? Any idea?

What causes infection? Bacteria.

Slide 4 – What is Gingivitis?

Dr. Robert Davidson –Clinically, what does gingivitis look like? Probably all of us

have had some manifestation of gingivitis during our lifetimes and it ranges from

very mild to almost imperceptibly detectable clinically, to much more severe. I willshow you some pictures of typical gingivitis. But again, the definition is

inflammation of the soft tissue surrounding the teeth and specifically that aspect of

the soft tissue referred to as GINGIVAL TISSUE -- it’s typically KERATINIZED and it

is characteristic of what we see clinically.

Slide 5 – Mild Gingivitis

Dr. Robert Davidson –So this is what mild gingivitis looks like. Does anything look a

little abnormal? Anything a little abnormal or very abnormal? Can you see anything

here? Any changes in what you would expect to see in a healthy individual? Anyone?

Can you point me to something that looks abnormal? Does this look normal to you?

This is probably fairly normal. This is what is abnormal in this picture. There is alittle bit of puffiness/swelling and there’s also what is referred to as ERYTHEMA -- a

change in the color of what ’s typically seen in normal healthy tissue. There’s a

change towards REDNESS. OK.

Slide 6 – Severe Gingivitis

Dr. Robert Davidson –This is much more severe gingivitis. It is the same

phenomenon. In this case, it is actually associated with a reaction to a drug, and I




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will talk about that in a little bit more detail in a moment. But that drug induces

enlargement of normal gingival tissue and predisposes patients to a form of

gingivitis, more severe inflammatory gingivitis. This can also occur in patients that

are NOT taking medication.

Slide 7 – Risk Assessment, Diagnosis and PrognosisDr. Robert Davidson –But before I start talking about gingivitis, I want to talk about

risk assessment, diagnosis, and prognosis because it turns out that..

Slide 8 – Patients Are Not Equally Susceptible to Periodontitis..

Dr. Robert Davidson –.. the same bacteria which gingivitis in one patient has no effect

on another patient. What ’s the difference between these 2 patients? If the bugs are

the same, and there’s disease in one case, inflammatory periodontal disease in the

form of gingivitis, and another case we can’t detect any changes clinically, what’s

different here? So when you think about the immune response, we have to ID the

host as the variable. So in one case, the host is susceptible and in the other case the

host is not susceptible.

Slide 9 – Not Everyone Appears Equally Susceptible to Periodontal Diseases…

Dr. Robert Davidson –Because everyone’s susceptibility is NOT the same. Ok.

Slide 10 – For Many Chronic Inflammatory Diseases There Exist Risk Factors..

Dr. Robert Davidson –And here you see, for many chronic inflammatory diseases,

there is something that is called RISK FACTORS. Is this something you are familiar

with? Has anyone talked to you about that before? OK. So it’s intuitive, they don’t

directly cause disease. A risk factor is NOT something that is etiological/causative

but it changes the manifestation of the disease. So a patient who is more susceptible

to a disease may end up with a more severe condition than a patient who is not assusceptible. Can anyone tell me what a risk factor for gingivitis might be? Anything,

just pick a number. (someone says: “diabetes”) diabetes? Not exactly, but a little bit.

Umm uhh it.. What causes gingivitis? Bacteria/plaque. So PLAQUE IS A RISK

FACTOR FOR GINGIVITIS. And we will talk about that in a minute in more detail.

Slide 11 – For Periodontal Disease, While Bacteria are Still Required to..

Dr. Robert Davidson –So for periodontal diseases, including gingival diseases, again

while bacteria still are required to initiate the patient’s response, certain risk factors

again modulate or amplify that response which manifests in clinical disease.

Slide 12 –Because Risk Factors Put Certain Patients at Higher Risk..Dr. Robert Davidson –And here you see because they put patients at a higher risk for

increased severity, they should be an integral part of our diagnostic workup. When

you think about it, patients present with a profile, a specific profile. The best doctors

are the ones that can predict the future. When you go to a doctor you’re really not as

much interested in what ’s wrong with you on that day but what ’s going to happen to

you a week from now, a year from now, 10 years from now. In other words, the risk

for future disease. And the best doctors are the doctors that can predict the future.




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The best way to predict the future is to understand the risk factors that are inherent

in the patient that you are treating and then that way you can in a way, anticipate

the risk for future disease and, ideally, prevent it from happening.. Take measures to

prevent those risk factors from manifesting. Does that make sense to everyone? It’s

as much an issue for gingival disease as it is for caries, for cardiac disease, for lung

disease or anything we see clinically.

Slide 13 – Untitled Slide

Dr. Robert Davidson –This is a diagram that shows the relationships between the

risk factors . There are genetic modifiers that are inherent. Can we change these?

Typically NOT. There are also environmental modifiers. What is one really

important environmental/acquired risk factor that can cause disease or modulate

the manifestation of disease? So people who smoke typically are sicker than people

who don’t smoke. People with uncontrolled or poorly controlled diabetes are at

higher risk for infection than people who have well controlled diabetes. So those are

inherent/acquired risk factors. There are genetic risk factors for certain diseases

that we really can’t alter. But basically we ID a causative agent, we understand the

risk factors that are acting on those or modulating the relationship between the

causative agent and the host and we end up with a degree of severity of disease and

also a type and that really represents a diagnosis. We really can’t diagnose properly

without understanding the risks involved.

Slide 15 – Untitled Slide

Dr. Robert Davidson –It turns out that not only does risk affect the diagnosis but it

also affects the outcome of therapy. So if we’re treating a patient who is a heavy

smoker, do you think that that patient will respond as well as a patient who doesn’t




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smoke, to the same therapy? Of course NOT. What’s the major target of smoking?

What system do you think is affected most profoundly by smoking? Is it a local effect

or systemic effect first? SYSTEMIC. So when you smoke there’s local effects like

VASOCONSTRICTION, of course, but there’s also a profound effect on the IMMUNE

SYSTEM and that ’s basically what puts people at risk who smoke. It’s in the same

way that poorly controlled diabetes puts people at risk. The affect is basically on theimmune system and the immune system is what really represents the major

response to infection in the host. Anything that compromises that puts the host at a

more susceptible state.

Slide 16 – Risk Factors for Gingivitis

Dr. Robert Davidson –Ok so here are the risk factors for gingivitis. Bacterial plaque

are the microbes/bacteria/bugs that we have identified that cause BOTH gingivitis

& periodontitis, but I’m not going to talk about that specifically today. Local factors,

what do you think is a local factor is? What is a local factor? What am I talking

about? You have.. Well I will show you in a minute, I don’t want to spend too much

time. Certain drugs put patients at higher risk for gingival disease. Each of thesedrugs, the Ca channel blocking agents which are treating hypertension among the

most widely prescribed drugs on earth, anticonvulsants that treat epilepsy and also

immunosuppressant drugs that permit solid organ transplants by suppressing the

immune response and preventing rejection. In each case these drugs induce in some

patients, gingival enlargement, the overgrowth of gingiva which predisposes

patients to bacteria, no sorry, to INFLAMMATION. Finally, there are certain

endocrine related conditions like pregnancy or changes in hormonal cycle that

predispose patients again to gingivitis.

Slide 17 – Endocrine-related Risk for Gingivitis


You can see here these are endocrine related risks forgingivitis during pregnancy, mild, and severe. There are changes that take place. The

more bacteria, the worse the condition. These patients, in the sense that the

hormonal changes are NOT causative but they are RISK FACTORS that predispose

patients for these conditions. And puberty, you can see in this graph that the

incidence of gingivitis spikes at around AGE 13 and then as adults, everyone is more

or less susceptible.

Slide 18 – Risk Factor: Bacterial Plaque

Dr. Robert Davidson –So here’s a case. The risk factor in this case is simply bacterial

plaque. A patient who fails to maintain proper adequate plaque control ends up with

gingivitis. It’s a causative agent AND a risk factor.

Slide 19 – Risk Factors: Bacterial Plaque, Local Factors

Dr. Robert Davidson –Here is a case where there is bacterial plaque associated with a

local factor. This is a periodontal probe. Is that something you are familiar with?

What’s the local factor here? What is a local factor? It could be one of a number of

factors, it could be a poorly contoured restoration that traps bacteria. It could be an

OPEN MARGIN between a crown and a tooth. It could be RECURRENT CARIES,




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which in effect, is a risk factor for inflammatory gingival disease. But local factors

are not really biological but they are factors which place patients at higher risks for

a condition.

Slide 20 – Risk Factors: Bacterial Plaque, Antihypertensive


Here you have an anti-hypertensive, this is that patient that Ishowed you before, along with bacterial plaque.

Slide 21 – Patient: 25 Year-Old Female

Dr. Robert Davidson –So here is a patient, 25 year old who comes in with a chief

complaint of bleeding gums. You are going to meet these patients every day of the

week.

Slide 22 – History of Present Illness

Dr. Robert Davidson –It’s gone on for a long time, 5 years. It’s all over, a generalized

condition. It happens every day after brushing or eating and there really aren’t anysymptoms and she has had no treatment so far.

Slide 23 – Medical History

Dr. Robert Davidson –She is in good health, she’s had an uncomplicated pregnancy

and she really is not taking any medication other than multivitamins and oral

contraceptives.

Slide 24 – Dental History

Dr. Robert Davidson –She had an exam a few years ago, well now it’s 10 years ago.

Third molars were extracted, some routine fillings and occasional cleanings

periodontally. So some RED FLAGS should go up right away. What is one red flag forthis person? When she says “I’ve had OCCASIONAL cleanings.” Is that as good as

“routine/periodic?” This is the kind of patient that probably comes to the dentist

when she perceives a problem. someone who is NOT proactive, sort of speak. If you

think about it, it’s a behavioral issue. It’s a risk factor for disease, people who really

don’t take care of themselves it represents a risk factor. Can that be changed? Sure.

Slide 25 – Clinical Status

Dr. Robert Davidson –It’s something to think about. So clinical status, what is wrong

with this picture? I think there are some things, surface texture, shape, color, size of

the gingiva. All of these things we can ID as something OTHER than what we would

consider to be normal clinical gingival tissue.

Slide 26 – Are There Clinical Signs of Periodontal Disease…?

Dr. Robert Davidson –First step is are there signs of clinical periodontal disease?

We’re really talking about GINGIVITIS here and not periodontitis. I will explain that

in a minute.

Slide 27 – Clinical Signs of Periodontal Diseases




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Dr. Robert Davidson –These are the FOUR CLINICAL SIGNS OF GINGIVITIS!!! Edema

is swelling. Erythema is redness. Bleeding, typically in response to a mechanical

insult like a probe, or air, or a gauze pad rubbing against the gingiva you induce

bleeding and ulceration. We’re NOT talking about peritonitis here when I talk about

attachment loss. Is that something that you understand yet? Do you know what

attachment loss is? Anyone? Do you all know what attachment loss is? I will explainit in a minute. I don’t want to review things.

Slide 28 – Edema, Erythema

Dr. Robert Davidson –So here edema is a change in shape, swelling. Erythema is a

change in color.

Slide 29 – Bleeding

Dr. Robert Davidson –Here is bleeding on probing or in response to any other

mechanical challenge like air, syringe, pressure, gauze pad. Anything that disturbs

the gingival surface that induces bleeding is a CARDINAL SIGN OF INFLAMMATION.

It’s a direct reflection of the patient’s clinical status with respect to inflammatorygingival disease. The absence of bleeding on probing in patients who have no other

risk factors, is a sign of gingival stability/health and the presence of gingival

bleeding on probing, is a sign of inflammation. What’s one risk factor that might

alter that response? A minute ago I talked about what smoking does locally. What

does it do? It constricts the vessels peripherally so if you have a heavy smoker you

will have a blood supply that is not nearly as animated or vigorous as a person who

doesn’t smoke. So you probe a smoker, and very often there is NO bleeding even

though there is inflammation. It’s just that the inflammation doesn’t manifest in a

normal way.

Slide 30 – Ulceration… Dr. Robert Davidson –Anyone have a question about that? I will talk about that or

someone will talk about that when you meet pathogenesis next year. So here is

ulceration and ulceration really specifically to the GINGIVAL CREVICE, I should

identify. This is cross section of the periodontium. This is the enamel, the CEJ,

cementum, dentin, this is the keratinized gingiva. The little blue dots represent the

INFLAMMATORY RESPONSE and it’s an INFILTRATE. This is the epithelial

attachment. There’s a little bit of a defect up here as a result of ulceration of the

interior of the sulcus here. This is bone, this part and these are collagen fibers,

fibroblasts, and a blood vessels. So who are the players? There’s bacteria, infiltrate,

and what ’s called a gingival pocket. So when you put a perio probe in here it will go

a little bit deeper than in a site that is healthy. Ok so that ’s it.

Slide 31 –Clinical Signs of Periodontal Diseases

Dr. Robert Davidson –So clinical signs of periodontal diseases. We talked about

gingivitis, I will spend a moment talking about periodontitis and the distinction

between the 2 which is simply ATTACHMENT LOSS!!

Slide 32 – Loss of Epithelial Attachment




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Dr. Robert Davidson –Here is a patient who’s gingiva looks healthy. This is a

periodontal probe that is 10 mm into the sulcus, that ’s a periodontal pocket. That

represents ATTACHMENT LOSS.

Slide 33 – Healthy Gingiva


You can see here , I’m just going to go over the anatomy veryquickly. There’s the tooth. There’s the gingival sulcus and the free gingival margin.

This is the keratinized tissue and this is the mucosa in healthy gingiva.

Slide 34 – Loss of Attachment

Dr. Robert Davidson –Here is what loss of attachment looks like. So here’s the probe

in a healthy site. Ok now here’s the probe in a site with perio disease on right. The

difference is the level of the attachment of the epithelium. Here is the epithelial

attachment, and here is the epithelial detachment right here. And it’s actually

damaged by this infiltrate and undergoing sort an inflammatory response. But loss

of attachment distinguishes gingivitis from periodontitis. This is in fact, and just as

an aside, this is REVERSIBLE, inflammatory gingival disease. This is largelyirreversible, you lose attachment and it’s GONE. What’s the structure between the

connective tissue here, the bone, and the tooth? What ’s this called? PERIODONTAL

LIGAMENT. That ’s the attachment, the periodontal ligament, and that ’s what gets

damaged and that ’s when we talk about loss of attachment we’re talking about the

loss of the attachment between the tooth and the periodontal ligament. If that’s lost,

it’s gone forever. If there’s anything at all that periodontal research would like to do,

it’s to figure out a way to reattach the PDL, periodontal ligament to the tooth. So far,

it has not been successful.

Slide 35 – What Structural Components are Affected?


So what structural components are affected? There’s collagen,vascular cells, immune system cells and resident fibroblasts. That ’s basically what

we see in health.

Slide 36 – What’s the Sequence…?

Dr. Robert Davidson –What ’s the sequence? There’s a collection of plaque. So

someone doesn’t clean their teeth, plaque accumulates. You can see it

visibly/clinically and you can DISCLOSE it. Have you done disclosing? You will get to

that. There’s a chemical like a wash we use that is bright purple and att aches to

plaque and shows you where the visible plaque is; if you can’t see it clinically, you

disclose it using disclosing solution. So then there’s is MIGRATION of immune

system cells, the first wave is typically NEUTROPHILS. As a result of this infiltratethere’s damage done to collagen. Then fibroblast damage and finally changes in the

vascular system. That ’s what we’ll concentrate on for the next 35 minutes or so. If

you can think ahead, if the vascular system, the microvascular begins to change,

what changes do you think will take place? Are the vessels going to constrict during

inflammation or enlarge? ENLARGE. That means there will be more blood flow so

you can start to think of the 2 clinical signs that I talked about before, EDEMA and

ERYTHEMA. That ’s where it comes from. The idea today to give you a little sense of




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the physiology that underlies the clinical manifestation of probably the most

common oral disease on earth. More common than caries, I think is the gingivitis

Slide 37 – Clinical Signs of Periodontal Diseases

Dr. Robert Davidson –So here we get edema, erythema, bleeding and ulceration. I will

just go over that.

Slide 39 – Edema & Erythema…

Dr. Robert Davidson –We will talk about again, where edema and erythema come

from. Ok you’ve had some anatomy, right? The trigeminal nerve? Am I correct? Ok,

so in inflammation, there’s release of CGRP, calcitonin gene-related peptide, and that

induces smooth muscles to activate adenylate cyclase. Ok.

Slide 40 -- .. and CGRP-induced Activation…

Dr. Robert Davidson –And CGRP-induced activation of adenylate cyclase leads to an

increase in cAMP. At the expense of what? ATP.

Slide 41 – How Does This Happen?

Dr. Robert Davidson –Ok so why does this happen? Why is it important?

Slide 42 – Untitled

Dr. Robert Davidson –Here’s the sequence. The CGRP binds to the Gs receptor

complex, here, and that liberates the Gs moiety right here and that induces GTP to

go to GDP and then that activates ADENYLATE CYCLASE which changes ATP to

cAMP and basically the end result is a reduction intracellularly of ATP. This is fairly

typical of basically ALL CELLS.

Slide 43 – Smooth Muscle Cell at Rest


So in general, smooth muscle cells at rest, and this is nowphysiology. There is a lot of K in the cell and Na outside the cell. Very little Na inside

and very little K outside. At resting levels, there’s a very relatively high conc. of ATP

which induces a change potential gradient between the inside and the outside of the

cell. Is this familiar at all to anyone? Ok ok, so this is basic cell physiology.

Slide 44 – CGRP-Induced Potassium Current…




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Dr. Robert Davidson –When CGRP, which during inflammation there is CGRP in the

system, with HIGH intracellular ATP. So in HIGH intracellular ATP, there is a LOW

AMPLITUDE K+ current that is essentially AMBIENT. Here you can see the scale is

20 pico amps. This is 20. This represents a K-current. This is where the CGRP is

introduced into the system. This is under HOMEOSTATIC conditions. I will show you

that now.

Slide 45 – Smooth Muscle Cell At Rest

Dr. Robert Davidson –Under homeostatic conditions, there is still a lot of K+ inside,

very little K+ outside, a lot of Na outside and a lot of ATP and a very low amplitude K

current that is leaving the cell. There’s an ongoing K+ leaving the cell and it’s

compensated by Na coming in -- there’s an exchange and there’s a lot of different

mechanisms involved. It basically keeps the inside of the cell with respect to the

outside, at about essentially a 0 mV gradient ,there is EQUILIBRIUM. This is a resting

cell!. Ok so then what happens?

Slide 46 – CGRP-Induced Potassium Current… Dr. Robert Davidson –At LOW ATP, and remember there is LESS ATP INSIDE THE

CELL because CGRP is induced, there is a reduction in ATP because cAMP has gone

up. The same CGRP induces a very large K+ current. So here is very low ATP, a big K

current. Here it’s 40 pico amps instead of 20 and there is a very large K+ current.

Slide 47 – Smooth Muscle Cell

Dr. Robert Davidson –And there’s a very large K current which is that big arrow in

green. So there’s little ATP, big K current going out, so what happens to the inside of

the cell? It gets more positive or negative? Negative. I don’t know if you remember

or if you know that the more negative the inside of a cell is, the less excitable it is. In

effect, it relaxes. If a cell is a muscle cell around a blood vessel, if the muscle cellrelaxes the blood vessel gets BIGGER. That’s one of the reasons why there is EDEMA.


Dr. Robert Davidson –Here is very simply, this is an experiment, in-vitro experiment

measuring the POTENTIAL electrophysiologically inside a cell. Here it is the

difference between inside and outside is near 0, they then introduce CGRP into the

bath and almost immediately there is a 10mV shift towards the NEGATIVE of the

inside of the cell. So this is a cell that is less excitable and it’s not contracting as

vigorously as a cell at rest. So it dilates and gets a little bigger.




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Slide 49 – CGRP-Gated K Channels

Dr. Robert Davidson –This is another way that CGRP induces negative potential

inside a cell. It’s simply a CGRP activated K channel, the CGRP comes along and

opens this ion channel. Anyone not know what an ion channel is? Ok, opens an ion

channel and because there’s a lot of K inside the cell and very little outside the cell,the K rushes OUT and makes the inside of the cell more NEGATIVE. So this is a direct

effect of CGRP. It doesn’t have to do it all with ATP, it doesn’t have to do it all wit h

the stimulatory moiety but basically it’s a direct effect that induces a decrease in the

potential making it more negative which is associated with closing K channels, so K

goes down and the physiology of muscle cells is such that there is going to be a

VASODILATION. This in a sense, amplifies the effect related to ATP reduction. It’s

kind of a double whammy of CGRP. CGRP again is a NEUROTRANSMITTER that is

very typically associated with INFLAMMATION. It’s released by nerve endings and

has a very sort of widespread effect on many different structures. But specifically on

smooth muscle, it relaxes smooth muscle. By the same token, in the absence of

CGRP, channels are NOT open and there is more and more positive charge INSIDEthe cell as these charges build up and the cell becomes more excitable. In other

words it begins to CONSTRICT if it’s a muscle cell or it’s more predisposed to

constriction if it’s a muscle cell which reduces the lumen which reduces the blood

flow and there won’t be edema or erythema.

Slide 50 –Untitled

Dr. Robert Davidson –So here are the 2 ways this works. CGRP increases cAMP, ATP

goes down and K current increases. Here is CGRP opening K channels and the K

current increases. Membrane hyper-polarization meaning it is more negative with

respect to the outside, it’s HYPERPOLARIZED. When a cell, when a muscle cell

contracts, it’s the result of DEPOLARIZATION of the cell. Positive charges RUSHINTO the cell and it’s depolarized and becomes LESS polarized. Our country is

polarized, there are RED states and BLUE states so when you get depolarization it’s

like PURPLE , you know it depolarizes. Actually it goes towards blue if you want to

think about it in those terms. Umm, decrease of smooth muscle excitability and

vasodilation. Anyone have any questions about this? I’m not sure if this is something

you are familiar with physiologically but I hope I explained it in a logical way.




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Slide 51 – Within 24 Hours:

Dr. Robert Davidson –Within 1-2 days you will see the beginnings of in some

patients, the clinical manifestation of gingivitis. These are tissues that are inflamed

among many cytokines and molecules that are released during inflammation is

CGRP which has a myriad of effects. I just explained 2 specific effects of CGRP that

could explain, in part, the manifestation of erythema and edema.

Slide 52 – Are There Additional Effects of ATP Depletion?

Dr. Robert Davidson –Are there any other effects of ATP depletion?

Slides 53 -- Untitled

Dr. Robert Davidson –So here’s healthy gingiva again and here is diseased gingiva.

There is an incipient gingival pocket, the beginning of… and this is terminology

associated with periodontal disease. The formation, and I will go backwards one

slide (Note -- the 2 slides he is referring to are superimposed on each other forming 1

single slide in our version of the lecture). We’re looking here at a SULCUS, there is

always a little bit of plaque and always 1-2 immune cells floating around. But this is

healthy gingiva, the epithelial attachment basically allows the probe to go about 1-2

mm below the free gingival margin. That is fundamentally health. In inflammatory

disease, you get the beginning of the breakdown of the epithelial attachment, itdoesn’t go away but it’s damaged. So the probe instead of 1 mm, it can sink in 2-3

mm depending on the patient. That ’s called a GINGIVAL POCKET. an incipient

pocket. The PMNs neutrophils go into junctional epithelium. The lymphocytes into

sub-epithelial tissue. There are big changes in FIBROBLASTS and as the fibroblasts

change, there is a loss of collagen. This explains what happens during gingivitis.

What is one reason you might see collagen depletion during inflammation as the

result of release of certain cytokines? What are some of the cytokines that may

relate to collagen breakdown? (Student answers, cannot hear). Exactly,

COLLAGINASE . So collagenase is one of the key factors that are released during

inflammation and directly effects the stability and integrity of the resident collagen.

But I’m going to talk about something that is sort of opposite to that.

Slide 54 – Cytopathic Changes in Fibroblasts

Dr. Robert Davidson –Um you can see cytoplasmic changes in fibroblasts leads to loss

of collagen. The fibroblasts themselves, can actually produce, during inflammation,

can produce collagenases along with many other cells. Most immune system cells

that are stimulated release some sort of enzyme that can affect collagen.




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Slide 55 – Collagen Production Decreases…

Dr. Robert Davidson –Here you get collagen production decrease. In fact, the

fibroblast number goes DOWN because they’re damaged so there’s less synthesis of

collagen by cells that are just no longer there. The collagen synthesis of the cells that

are still alive DIMINISHES. And what I just mentioned a moment ago, collagenase

activity increases. That’s during inflammation and these are BAD EFFECTS, they arenot good effects, they disrupt the tissue. When you think of the 3rd cardinal sign, of

gingivitis, do you remember what it is? There is erythema, edema and one other

sign. BLEEDING. So what maintains the integrity of tissue, blood, collagen? As

collagen begins to break down, tissue begins to get FRIABLE, it weakens and you

stick a probe in it and you can induce bleeding. So here you have, in a way, an

explanation in part of some of the clinical signs that we see during inflammation.


Dr. Robert Davidson –On the other hand, If ATP increases, you get more collagen so

you can see how a reduction in ATP very indirectly can ultimately increase or

amplify the effect of inflammation in general. Along with the direct and indirect

effects on collagen of fibroblast activity, there is also a sort of subtle effect on

lowering ATP and ultimately effecting collagen synthesis. Does that make sense? Ihope I make sense.

Slide 57 – What Other Factors In This Patient’s History Might..

Dr. Robert Davidson –This is I think the last slide, so I’m almost right on the money

here. What are the other factors in the patient’s history that might explain the

gingivitis? I mentioned it in passing when we started.

Slide 58 – Risk Factors for Gingival Diseases…

Dr. Robert Davidson –So the patient risk factors, remember these are the risk factors

for gingival disease. There’s plaque and certain endocrine related conditions.

Slide 59 – Medical History

Dr. Robert Davidson –This patient to begin with was probably not the greatest

patient on earth in terms of what we call compliance. Anyone, what do I mean by

compliance? Someone who comes when it’s a good idea for them to come to get

checked. If they come every 3 months or 6 months, depending on the... what would

be determinant on how often you should see a patient? This is the beginning of

understanding the importance of risk assessments. So you have office full of patient




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and you have a staff that is overburden, does every patient have to come every 6

months? Maybe not. Maybe some should come 1x a year and what determines that

cycle? How susceptible they are or how at risk are they for disease. Then there are

other patients you probably see every 2 months because you perceive a high risk for

ongoing disease and you want to make sure you’re there to eit her prevent or

mitigate this. This has a clear economic and psychological and psychosocialimportance and significance . Understanding risk, how it translates into how you

basically live life whether you are against it or in control. One of the ways, again, is

understanding your patient so that your treatment is consistent with their

susceptibility or resistance to disease. It also saves them money.

Slide 60 – Is There Also An Effect of Oral Contraceptives…?

Dr. Robert Davidson –So here we are, the patient is on oral contraceptives. Now this

could have an effect on hormones and it certainly does have an effect on hormones,

but then again it could also have an effect on as a risk factor disease. It turns out that

oral contraceptives are more 20-30 yrs. ago than now, but it has an effect on the

permeability of the microvasculature which speaks to what? It speaks to edema. Notso much erythema but edema. It’s going to be a lot of fluid or more fluid in the

connective tissue and you might see some edema. When I talked about it before as a

risk factor for gingivitis, it turns out that hormones change not the substrate, but the

cell’s predilection for certain substrates. It turns out that there’s a predilection for

pathogenic bacteria as a result of oral contraceptives in some patients. That is a

REAL risk factor for inflammatory disease. I think I’m done. Does anyone have any

questions? So I’m going back to clinic now, I work in Dr. Shackman’s clinic on

Wednesday mornings so if you’re in Dr. Shackman’s group I’ll see you. I work in Dr.

Resnick’s clinic.. Oh no today is Thursday, I work in Dr. Resnick’s clinic this morning

and on Wednesday afternoon I work in Dr. Berkowtiz’s clinic. I will certainly see you

next year in D2 in lecture. If you have any questions that you think of when you gohome, feel free to email me. I’m really good at responding. Thank you, thank you,

thank you.

lecture 16: gingivitis

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