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Benign Chronic White Mucosal Lesions — Transcript

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0:02Okay. In the name of God, the Most
0:03Gracious, the Most Merciful. I wish you
0:05all the best. Today we begin a new
0:08chapter. Chapter 18 from Cawson's book.
0:10Regarding chronic white mucosal lesions
0:13. To start, let's recall the concept of
0:16keratinization. Keratinization is a
0:19process where keratin production occurs
0:22. By epithelial cells. They actually
0:25transform. Stratum. Granulosum cells in
0:30the stratum granulosum into keratin. By
0:34a process called keratinization.
0:37Sometimes keratinization is more than
0:40the normal limit. It causes
0:42hyperkeratinization for us. Sometimes
0:44we have keratinization in tissue that
0:46is non-keratinized tissue. This is also
0:49abnormal. Whether hyperkeratinization
0:52or keratosis. This is abnormal. If it
0:55exceeds its limit. Or if it is in a
0:57place that usually doesn't have
0:59keratinization. The keratin produced by
1:02the keratinization process is a protein
1:05. One of the characteristics of this
1:08protein is that it is a protein.
1:10Hydrophilic. It likes water. It absorbs
1:13moisture. Saliva. It appears to us as.
1:19We have. A protein or. Material. Okay,
1:31Linda. Okay. We also know that in the
1:40oral cavity, we have keratinized and
1:42non-keratinized mucosa. Normally,
1:44keratinized mucosa is mostly in the
1:46masticatory mucosa. The gingiva. The
1:49tongue. And the hard palate. Some
1:52dorsum papillae might also be
1:54keratinized. The rest is
1:56non-keratinized. The buccal and labial
1:59vestibules. The soft palate is entirely
2:01considered. The floor of the. Mouth,
2:03ventral part of the tongue. All are
2:05considered lining, non-keratinized
2:07mucosa. Any change in the lining mucosa
2:10and its transformation from
2:12non-keratinized to keratinized is
2:14considered abnormal. We study it as.
2:40Also. As we know, it is caused by
2:49candidal infection. But lichen planus,
2:51we don't know its cause. However, we
2:54know the pathophysiology is an
2:55inflammatory condition. We have
2:58activation of CD8-positive cytotoxic T
3:03cells. Resulting in one of the
3:06phenotypes, which is reticulated lichen
3:08planus. A white lesion appears to us.
3:12Also, among the common causes of
3:15lesions are chemical trauma. It can
3:18cause white trauma for us. Or a white
3:22lesion due to chemicals. Exposure to
3:30chemicals. Hairy leukoplakia. This is
3:33caused by Epstein-Barr virus. At. White
3:37sponge nevus. It is. Due to a mutation
3:41in keratin. Those who have it also
3:50develop the condition. It creates a
3:56white lesion for us. Also, among the
4:02lesions that resemble warts. Its cause
4:07is unknown. But it also creates a white
4:10lesion in one of the presentations. And
4:13skin grafts. Finally, psoriasis. It
4:16also creates white lesions for us. Oral
4:19white lesions. They all share the fact
4:21that they are white and benign. They do
4:23not carry the risk of dysplasia. They
4:25do not carry the risk of malignant
4:27transformation. Let's redefine
4:30leukoplakia. We have defined it before
4:33as a term. Let's go into a bit of its
4:36detail. Leukoplakia is a term composed
4:39of two parts. Or plaque. I don't call a
4:52white lesion leukoplakia. Unless its
4:56cause is unknown. Whether clinically or
5:00histologically. What does that mean? If
5:05I see lichen planus with white striae.
5:10In lichen planus, I don't call it
5:12leukoplakia. I say it. Okay. So,
5:18effectively, I don't call any white
5:21lesion leukoplakia until I ensure it
5:24isn't candidiasis. It isn't lichen
5:29planus. It isn't leukoedema. It isn't
5:32candida. Okay. Then I call it
5:35leukoplakia. Why is leukoplakia defined
5:38as something unknown? Or rather, it
5:43occurred without a specific cause. Huh?
5:48So when I call it leukoplakia...You are
5:57labeling a white lesion with a risk of
6:00transformation or cancer. Just like
6:05these cases we will study today. Okay,
6:10the key is that leukoplakia is not
6:11called leukoplakia unless it is
6:13idiopathic in cause. The cause is
6:16unknown. Okay. So when I want to call a
6:19white lesion leukoplakia, I have to
6:21rule out. I must rule out all the
6:24causes. All the diseases that cause
6:26leukoplakia. Then I call it leukoplakia
6:29. The exclusion is done...Through
6:33clinical and histological
6:35investigations. Okay. Meaning, I
6:39exclude, for example, by taking
6:40histology. I exclude that this patient
6:42has an autoimmune disease. Has an
6:43inflammatory disease, or has
6:45hypersensitivity. I exclude
6:47histologically, okay. I exclude via
6:49blood work, I exclude clinically. That
6:52he has, for example, psoriasis, skin
6:54psoriasis that appeared in the oral
6:56cavity. So I exclude leukoplakia. This
6:59patient has psoriasis, oral psoriasis,
7:01not leukoplakia, even if I see it as a
7:03white lesion inside the cavity. So,
7:06leukoplakia is a diagnosis of exclusion
7:08. Okay. Unfortunately, the term
7:26leukoplakia is used, or misused, in
7:29diagnosing squamous carcinomas, okay.
7:33It was called leukoplakia, but it
7:35turned out to be squamous carcinoma.
7:40Candidiasis diagnosed as leukoplakia,
7:42when it is hyperplastic candidiasis.
7:47For example, hairy leukoplakia,
7:49diagnosed as leukoplakia, but it is
7:51hairy leukoplakia. It is an EBV-caused,
7:55or Epstein-Barr virus-caused lesion, a
7:58white lesion, not leukoplakia, okay. So
8:03we use the term leukoplakia incorrectly
8:07, okay. I call all white lesions
8:10leukoplakia, but this is wrong.
8:13Leukoplakia is called leukoplakia when
8:16I do not know the cause of these white
8:19patches. If the cause is known, it must
8:22be named after the disease causing it.
8:29Among the benign ones...Are Fordyce
8:36spots. Fordyce spots are small spots.
8:41Their diameter ranges from 0.5 to 2
8:44millimeters. They are small points,
8:48soft, creamy, yellowish spots.
8:52Distributed on the buccal mucosa, and
8:55possibly on the labial mucosa. They are
8:57bilateral, right like the left. Buccal
9:00mucosa, labial mucosa, right and left;
9:02they are not unilateral, they are
9:05bilateral. And they are symmetrical,
9:07similar in distribution. What is the
9:10cause of Fordyce spots? Fordyce spots
9:12...We know they are sebaceous glands
9:20that are in the skin. We know that we
9:23find sebaceous glands in the oral
9:24mucosa, but their percentage is much
9:26lower than in the skin, okay. I find
9:29them in the labial mucosa, I find them
9:31in the buccal mucosa. Sometimes they
9:34are prominent on the surface, appearing
9:37as creamy, yellowish spots. These
9:41yellowish spots are...In the oral
9:49cavity. 80%of adults have them. Do they
9:58need treatment? They do not. Treatment?
10:01Fordyce spots are glands. Sebaceous,
10:04found in the oral mucosa. Okay. How can
10:08I differentiate if this person has
10:10chronic hyperplastic candidiasis or...
10:15It is smooth. Okay. Smooth. If I want
10:22to take a biopsy...What do we see? I
10:31actually see Fordyce sebaceous glands.
10:34As you can see here, between the
10:36epithelium and the connective tissue.
10:38Okay. And without a hair follicle. In
10:42the skin; in the mucosa, we don't have
10:44hair like the skin. Usually, the
10:46sebaceous gland is around a hair
10:48follicle. Here, we have a sebaceous
10:50gland without a hair follicle.
10:57Leukoedema is a white lesion. It
11:03appears on the...buccal mucosa. It
11:13might spread to the labial mucosa. Its
11:16borders are...or blending with the
11:23surrounding normal mucosa. Normal
11:29transition. It affects those of African
11:34descent most. 80%to 90%of people who
11:37have leukoedema. Or 90%of Africans have
11:42leukoedema. Okay. Actually, leukoedema
11:48is a thickening of the epithelium. We
11:54get hyperkeratinization. With
11:56hyperplasia in the epithelium. It
12:00appears as a grayish translucent white
12:03...patch, lesion, or plaque on the
12:06buccal mucosa bilaterally. What
12:10distinguishes leukoedema? How do I
12:12diagnose leukoedema besides the
12:14patient's dark complexion? In most
12:16cases, leukoedema is distinct. If I
12:19stretch the buccal or labial mucosa, it
12:22disappears. We no longer have this
12:26gray-white membrane. It goes away and
12:29returns to looking like normal mucosa.
12:31Once you relax the buccal mucosa, the
12:34leukoedema returns. Okay, so what is
12:37leukoedema? It is...in those who have
12:54leukoedema? They show hyperplasia with
12:57hyperkeratinization. There is
13:01parakeratinization in the buccal and
13:03labial mucosa. However, there is a very
13:07unique feature of leukoedema: inside
13:11the epithelial cells of the mucosa, we
13:14get vacuolations or vacuoles. The
13:18cytoplasm appears as if it is empty.
13:21The cause of the vacuolations in the
13:23epithelial cells is unknown. But
13:26because of these multiple vacuolations,
13:29the epithelium appears like what? Like
13:31a basket-weave appearance. Like a
13:35wicker basket. Do you see the wicker
13:37basket? Even though the threads or
13:39strands are intertwined. There are
13:42still spaces. These vacuolations inside
13:45the cytoplasm of the epithelial cells.
13:47Give us the effect of the basket-weave
13:50appearance as...you see in this area.
13:53As you see in this area. Okay. As a
13:56characteristic feature of leukoedema. I
14:01have here also a basket-weave
14:02appearance in the epithelium. I have
14:11this leukoedema. Look at it in the
14:15video. Okay, this lesion, if you
14:23stretch it, the leukoedema disappears.
14:28Okay. Does anyone have a question
14:32regarding leukoedema? Clear. Okay.
14:38Frictional keratosis; as the name
14:40implies, we get keratosis or
14:42hyperkeratinization due to friction,
14:45which is called frictional keratosis.
14:48So the keratinization that occurs due
14:51to friction, it is called frictional
14:53keratosis. This means clinically, I can
14:56guess what the image will look like,
14:58the clinical image or clinical
15:00presentation of frictional keratosis.
15:03First, we have...the lesion is...mild
15:12keratinization, meaning it's in simple
15:15stages of keratinization. But as the
15:19friction increases or continues, the
15:23keratinization becomes a white, dense
15:26keratinization. And around it, we have
15:31translucent grayish keratinization.
15:34What causes it? What causes the
15:36friction? There might be, for example,
15:38a rough surface on a tooth. It keeps
15:41causing friction. Or, for example, the
15:45plastic of a denture might be rough. So
15:48it keeps causing friction. Calculus, if
15:52it is very hardened, rough, or has
15:55sharp edges, also causes friction. If I
16:00have an edentulous ridge against teeth,
16:03every time the patient closes, it keeps
16:06causing friction. It can cause
16:09frictional keratosis on the surface of
16:11the ridge. All these things can cause
16:15frictional keratosis, as you can see in
16:17this picture. The good thing about
16:21frictional keratosis is that once we
16:24remove the cause, management leads to
16:26regression of the keratosis, and it can
16:29return to its normal state. Frictional
16:33keratosis does not have specific
16:35margins; it is ill-defined. The borders
16:38and margins are poorly defined. It is
16:41interspersed with the normal mucosa
16:44around the frictional area. However, it
16:49is not bilateral. It is only confined
16:51to the source of the friction. If it is
16:54on the buccal mucosa of the upper right
16:58area, or if it is, for example, on the
17:01lower left ridge. Wherever there is
17:04friction, I get frictional keratosis,
17:07it is not. It is not symptomatic.
17:10Confined to the area where the friction
17:12occurs, okay. And we agreed that
17:15management is by elimination. How do I
17:18see it? If we are concerned and want to
17:21take a biopsy, what do I see? I see an
17:23area of hyperkeratinization. It could
17:28be para-or orthohyperkeratinization,
17:31okay. The epithelium is hyperplastic.
17:34Regarding inflammation, the epithelium
17:36has a mild inflammatory reaction.
17:39Unlike leukoedema, it is not
17:41accompanied by inflammation. It is not
17:44accompanied by edema. Even though it is
17:47called leukoedema, we do not have edema
17:50.
17:51>> Okay, another condition that can cause
17:56white mucosal lesions is cheek biting
17:59or tongue biting. Here, we are not
18:01talking about biting force that causes
18:03an ulcer or erosion. Here, we are
18:06talking about soft biting. Like those
18:10who keep putting their cheek between
18:11their teeth and biting on it while at
18:13rest. Not when we are eating and
18:15chewing with all our force, and we
18:17accidentally bite our cheek or tongue.
18:19No, here, while I am thinking, I keep
18:22my cheek between my teeth and bite on
18:24it. Okay, this habit, if it continues
18:29for a long time, causes
18:30hyperkeratinization. This
18:33hyperkeratinization is also accompanied
18:36by erythematous areas, okay? And it is
18:38also accompanied by small indentations
18:41of the cusps. Where are the cusps along
18:44the occlusal line? And we have shredded
18:47epithelial tags. Meaning shreds of
18:50epithelium are visible to us. Like in
18:54this picture, and we have this area of
18:56cheek biting. Okay, so I do not need to
19:04perform a biopsy. No treatment is
19:07needed other than giving the patient
19:09instructions to stop this habit. Okay,
19:14how can I diagnose this condition? If I
19:18am unsure because its location is
19:19exactly along the occlusal line. I let
19:21the patient bite; I tell them to bite.
19:23I just open the corner of the mouth.
19:26Usually, the biting areas that have
19:28caused the indentation look like an
19:31impression of the cusps of the upper
19:33and lower teeth. Okay, so I can easily
19:38diagnose that I have cheek or tongue
19:40biting. Another condition that can
19:46cause white mucosal lesions is
19:48stomatitis nicotina. From its name, I
19:50have stomatitis, or inflammation of the
19:53oral cells, with "nicotina," which is
19:56caused by nicotine. Well, it has other
20:00names such as smoker's palate, or pipe
20:03smoker's keratosis. Actually,
20:07stomatitis nicotina occurs exclusively
20:10in people who smoke pipes. Not the
20:14hookah or regular cigarettes, but only
20:17those who smoke pipes. Why? Actually,
20:22the heat of smoking from a pipe is much
20:25, much higher than the heat from
20:27cigarettes and hookah. So what does
20:31this heat do? The first place it
20:34touches, it irritates—the first place
20:37this heat touches is the posterior hard
20:40palate and part of the soft palate,
20:43stimulating the oral mucosa. It makes
20:46it feel the injury. It feels threatened
20:48. So what is the result of this threat?
20:50What? We get. We get
20:52hyperkeratinization in the posterior
20:55area. Or a lesion. So, where does "
21:06stomatitis" come from? We mentioned
21:08there is inflammation. Here, the minor
21:11salivary glands, which are already
21:13located in the posterior part of the
21:15hard palate, become inflamed.
21:17Inflammation. So the inflammation here
21:20is of the minor salivary glands. The
21:22inflammation of the minor salivary
21:24glands appears to me. What? Distributed
21:31on the white plaque. Once again,
21:36patients who have stomatitis nicotina,
21:39due to the heat from pipe smokers who
21:41first. Something comes into contact
21:44with the posterior palate. We get
21:45injury to the posterior palatal area.
21:48As a result of this injury and
21:50stimulation, we get hyperkeratinization
21:52. It appears diffuse. It's not very
21:59clear, okay. However. We have.
22:07Hyperkeratinization. Inflammation. It
22:15appears to us as red spots. Like. As
22:21you see here. If we want to take a
22:24biopsy from a patient suffering from
22:26stomatitis nicotina. I see that I have
22:29hyperkeratinization on the palate. If
22:32you see it here. I have
22:34hyperkeratinization of that. Okay. We
22:39have hypertrophy of the epithelium. We
22:41have inflammation. But where is this
22:43inflammation? Around the minor salivary
22:46gland orifices. I have a minor salivary
22:48gland here. Around the orifice, there
22:50is a connective tissue infiltrate.
23:04Distributed among the whiteness. Okay.
23:11Of course, this is a benign formation.
23:16Look at it here. This illustration
23:19clarifies stomatitis. Nicotina patient.
23:25We get hyperkeratinization. On the
23:29palate. Inside this hyperkeratinization
23:34. We have inflammation in the minor.
23:44Due to the heat. If the patient puts.
23:52Or. The covered area will be protected
24:00from stomatitis nicotina. But the
24:04exposed area will be affected by
24:06stomatitis nicotina. Okay. Another
24:12cause or condition that can cause white
24:15mucosa. So far, we have talked about
24:19stomatitis nicotina. We also talked
24:21about. Remember cheek biting. We talked
24:27about frictional keratosis. Leukoedema,
24:31okay. And Fordyce spots. We want to
24:36continue with oral hairy leukoplakia.
24:40Oral hairy leukoplakia involves a white
24:42lesion on the lateral borders of the
24:44tongue. The shape of this white lesion
24:48can be on the labial mucosa. The shape
24:52of the white lesion is vertically
24:55corrugated. You see, it is vertically
25:00wavy. You see it is vertically wavy, or
25:05it is shaggy. Like, you know a shaggy
25:11dog, how its hair is messy and sticks
25:15out randomly, okay. So it is corrugated
25:19, vertically corrugated, longitudinally
25:22wavy. And the surface is shaggy, a soft
25:26, shaggy surface. So what causes it?
25:28Hyperkeratinization.
25:30Hyperkeratinization causes our vertical
25:33corrugated appearance. What is the
25:36cause of this hyperkeratinization?
25:38There must be a cause. The cause is an
25:42infection. In HIV patients, common in
25:47patients who have an HIV infection,
25:49okay. Positive for HIV, and they are
25:53infected with the Epstein-Barr virus.
25:56What happens to them? They may develop
25:58oral hairy leukoplakia. So, oral hairy
26:01leukoplakia is induced. The cause is
26:04the Epstein-Barr virus in HIV-positive
26:08patients. It causes us EBV virus
26:12infection. It causes hyper-It has a
26:19distinct characteristic that is...We
26:26have several characteristics. We have
26:29hyper-[para] keratosis or
26:32orthohyperkeratosis. The appearance of
26:36the keratin is crinkled or ridged. As
26:41for the epithelium, especially the
26:43prickle layer, what happens to it? We
26:46have a symptom/sign of EBV infection.
26:51So what is the sign of EBV infection?
26:53What happens to the cells infected with
26:55EBV? They become koilocytes. The cell
26:59becomes known as a koilocyte, the
27:01infected cell. It becomes, it is called
27:07a koilocyte or koilocytosis. What is
27:10koilocytosis? We have shrunken nuclei.
27:15The nucleus becomes shrunken in this
27:18way. We have ballooning degeneration.
27:21And we have margination of the
27:23chromatin. So the epithelial cells
27:27appear as if they have hollow or empty
27:29cytoplasm. So, the cells infected by
27:34the EBV become koilocytes. Koilocytosis
27:38is a group of...symptoms happening
27:41inside the cell due to EBV infection.
27:44Among them are shrunken nuclei. The
27:47nucleus, the nuclei are shrunken and
27:50small. Or they have a primitive look,
27:54ballooning degeneration of the
27:56cytoplasm. Okay. It is one of the most
27:59important characteristics of hairy
28:03leukoplakia, which is koilocytosis.
28:07Well, I have koilocytosis as a feature
28:10for EBV. We might see koilocytosis with
28:15HSV. All viral or some viral infections
28:18can cause koilocytosis. Like HSV or
28:21like EBV. But how do I verify that I
28:24actually have EBV? I use
28:27immunohistochemistry against EBV
28:31antigens. Or I use an in situ
28:35hybridization probe. Which is a DNA
28:38probe that aligns with the analogous
28:42DNA of the Epstein-Barr virus. In both
28:47cases, whether I use an antibody or an
28:51in situ hybridization probe, if I have
28:55suspected EBV, it shows up as positive
28:59cells. As you can see here with us. All
29:04the cells we have in this image here.
29:07Where the nucleus is stained dark
29:10purple. It is a positive EBV infection.
29:15Okay. So I know that this patient
29:18actually. The white lesion is oral
29:21hairy leukoplakia. Due to the presence
29:23of EBV. So. Okay. Because it is an HIV
29:30infection. This hyperkeratosis that I
29:33see in oral hairy leukoplakia. It might
29:36also have superimposition by candidal
29:38infection. Okay. So I often might. See
29:43a patient, take a sample from a patient
29:46who has oral hairy leukoplakia, see
29:48that they have EBV, the epithelial
29:50cells are positive for EBV. Also
29:53positive for Candida. It may be, okay.
29:59Someone wants me to correct "hairy
30:01leukoplakia" or "hairy." Leukoplakia.
30:07Understood. Okay. The management of the
30:15oral, it’s normal, it’s not normal,
30:18okay. Of course, it is an infection. It
30:24does not have transformation. However,
30:27the treatment. It is dependent on the
30:30immune condition. Of the patient who
30:34has HIV, so if I control. The AIDS with
30:37antiretroviral therapy, I can put the
30:39patient in remission. And the oral
30:42hairy leukoplakia might subside. Okay,
30:47if there are symptoms of
30:48immunosuppression or immunocompromise.
30:51Due to AIDS or due to an HIV infection.
30:54It experiences more growth, it grows
30:57more. Okay, it's not a transformation
31:02of oral hairy leukoplakia that I
31:04control. And the management is that I
31:07control the HIV condition or the
31:09immunosuppression. White is white
31:20sponge nevus, meaning a mole. Okay,
31:24these patients have moles or a nevus
31:26that looks like a sponge and is white
31:29in color. So it is called white sponge
31:32nevus. White sponge nevus is a
31:34developmental anomaly. Caused by a
31:41condition in a gene specifically on a
31:43chromosome number. This condition
31:47appears after the patient is born.
31:52Which is hyperkeratinization in the
31:54buccal mucosa and labial mucosa. It
31:58appears to us as white sponge nevus, as
32:00you can see it in these photos. These
32:03patients will have white. It may reach
32:12its would be meaning it disappears,
32:22okay, or shown In addition to...of
32:27course, it only affects the buccal and
32:29labial mucosa because. Because of this
32:33mutation, we get hyperkeratinization in
32:36the mucosa. Okay. It may also affect
32:40several other areas, such as the vagina
32:44. And like the mucosa, several other
32:47mucous membranes like the vagina and
32:50the nasal mucosa. Especially in a
32:55syndrome called Cannon's syndrome.
32:57Cannon's syndrome, okay. Cannon's
33:01syndrome is a syndrome caused by the
33:09mother or the father. They pass it on
33:11to the boys or the girls. Okay. As a
33:14result of this, we have these, part of
33:19which is the white. Sponge, look at the
33:21facial features. They have macrocephaly
33:24. They have maxillary bossing,
33:27hypertelorism. They have frontal
33:31bossing, macrognathia. They have
33:37problems. Histologically If we take a
33:42sample of white sponge nevus, what do I
33:44see? I see hyperplastic epithelium. I
33:48see hyperkeratinization in the stratum
33:51superficialis. This keratinization is
33:56shaggy or corrugated. Meaning it has
33:59something like hairs. Okay, which we
34:01see on the surface. Look how the
34:06surface here is not flat, it has.
34:08Protrusions. Well, what else
34:10characterizes it here? Like leukoedema,
34:14we get vacuolation in what? In the
34:17cytoplasm. The entire cytoplasm becomes
34:20full of vacuoles. These vacuoles also
34:23give us the basket-weave appearance,
34:25like the one we see in what? In
34:28leukoedema, we don't have no
34:34inflammation. No inflammation. Does it
34:40need treatment? No, it does not need
34:43any kind of treatment. A condition
34:48where there is white mucosa, which is
34:51uremic renal failure. Renal retention.
34:59For this reason, they get
35:01hyperkeratinization on the ventrum and
35:06the floor, just as you see it here.
35:10What is the cause of it? Renal failure
35:12condition because it does not undergo
35:15malignant transformation, okay. It is
35:18related to the chronic disease the
35:20patient is suffering from. It has
35:23typical hyperplasia and
35:24hyperkeratinization in the area, with a
35:36jagged white lesion that is.
35:44Verruciform xanthoma, verruciform
35:47xanthoma. Verruciform xanthoma, from
35:51its name verruciform, which is a wart
35:54or a pimple-like. A pimple, so the
35:56shape of the lesion is a pimple.
35:58Xanthoma, xanth which is lipids, okay.
36:03So actually, xanthoma is macrophages
36:06filled with lipids, okay. So
36:09verruciform xanthoma, verruciform
36:11describes the shape of the lesion.
36:13Xanthoma describes the characteristic
36:16histological feature which is
36:18lipid-filled macrophages. Okay,
36:21clinically, what is the verruciform
36:23xanthoma like? It is a wart-like lesion
36:27. As we mentioned, its color can be
36:39white, or it could be pinkish, okay.
36:45Where is the most common place patients
36:48get verruciform xanthoma? In the
36:51keratinized mucosa, masticatory mucosa,
36:55tongue, and gingiva. These are the most
36:58common sites for verruciform xanthoma.
37:01What is the cause of verruciform
37:03xanthoma? Unknown, it is not known. It
37:08is said that inflammation, trauma, or
37:11an immune reaction triggers lipid
37:13secretion. Thus, a verruciform xanthoma
37:17develops. The people most affected by
37:20xanthoma are older adults between 50
37:23and 60 years old. Look here, the most
37:27common site for verruciform xanthoma is
37:30the gingiva. Pay attention, this is how
37:33it looks, okay. Like the palate. Like
37:37this, followed by the tongue as shown
37:40in this image. Okay, we might find it
37:44in other places, but at much lower
37:46rates. What are the characteristic
37:50histologic features? A characteristic
37:54feature of verruciform xanthoma is that
37:58I see foamy macrophages. What are foamy
38:01macrophages? These foamy macrophages
38:04are macrophages that, instead of
38:06looking like normal macrophages, are
38:09filled with lipid rafts or lipid-laden
38:11vacuoles, okay. Which are vacuoles with
38:17these macrophages filled with lipids.
38:20Under the microscope, they look like
38:22foamy macrophages. It's as if the
38:25macrophage has foam or froth in it,
38:28okay. And it is called xanthoma. So,
38:32effectively, xanthoma cells are foamy
38:34macrophages filled with lipid rafts or
38:37lipid-laden, as you can see in this
38:39picture. Okay, what else do I see? I
38:42see, of course, hyperkeratinization. I
38:45see epithelial hyperplasia in various
38:47forms, exactly. Also causing a white
38:54lesion. Skin graft. For example, those
39:00who suffered from squamous cell
39:02carcinoma. In squamous cell carcinoma,
39:05we have severe loss due to resection or
39:11removal of tissues, okay. So, what does
39:15this result in? It results in a defect.
39:18How do we compensate for this defect? I
39:20take a skin graft, or a patch of skin.
39:23Sometimes it is from the hand, the arm,
39:26or sometimes from the thigh, okay. We
39:29take it according to the area we need
39:31to cover and graft it to the oral
39:34mucosa. However, because skin is highly
39:38orthokeratinized, when it enters the
39:42oral cavity, it absorbs saliva. So it
39:47appears as a white lesion as you can
39:49see here. But because I have a good
39:52history and know the patient had a skin
39:54graft, I don't worry. With a skin graft
39:56, I tell the patient this isn't a white
39:58lesion. It is from the graft, because
40:00it is skin. Of course, I might find
40:03hair because the skin contains hair
40:05appendages. The last disease is
40:10psoriasis. Psoriasis is an autoimmune
40:14condition. In which the body attacks
40:17healthy skin. As a result of attacking
40:20healthy skin, several symptoms may
40:22appear in the patient. Including
40:25scaling or desquamation of the
40:27epithelium, accompanied by significant
40:29itching. In addition to this, they
40:32might develop erythema and pustules,
40:34which are pus-filled bumps. They might
40:37also have ulcerations or erosions.
40:39Several symptoms depending on the
40:41severity of the autoimmune disease.
40:45Pustular or erythrodermic psoriasis is
40:47often accompanied by oral psoriasis.
40:52Just as we have it on the skin, we can
40:54have it orally as well. We might see
40:59whitish or reddish lesions, or even
41:01papules. We might also see scaly lips
41:07and scaly cheeks. We could also have
41:11desquamative gingivitis. Okay, in
41:15addition to soreness, they get a
41:17burning sensation in the lips and
41:20tongue, and food sensitivity. These
41:26patients may be affected, as we said,
41:28with oral psoriasis at the
41:29mucocutaneous junction. Between the
41:32vermilion border and the skin, it
41:35causes scaling and these types of
41:38lesions. Okay, and of course, it's
41:42accompanied by limited lip movement and
41:46pain. And it can also affect areas like
41:49the tongue. The mucosa can become scaly
41:54. This scale might be accompanied by
41:57desquamation and also erythema. Okay,
42:00let me tell you about a patient who
42:03came to our clinic. This patient had a
42:07face that looked like she was in her
42:10late forties or fifties. However, her
42:15hands looked like those of a very old
42:19woman. Someone who has been exposed to
42:23the sun and working in the fields, very
42:25scaly, swollen, and fissured. She came
42:29for her first visit to get a scaling
42:31and to see if she had any oral cavity
42:32problems. We examined her intraorally
42:35and extraorally. Intraorally, we saw
42:37white lesions. I was afraid it might be
42:41leukoplakia. I took a step back and
42:43started asking her, "What's wrong?""Are
42:45you taking any medications?" Of course,
42:47she had filled out the patient record,
42:50not listing any diseases or medications
42:52. "Do you take medications?""No, I only
42:54take vitamins, Vitamin D, some other
42:56vitamins.""Well, did you use to take
42:59medications?""Yes, I actually did take
43:00a medication." She told me the name, a
43:02new medication I didn't know; I didn't
43:04recognize it. I asked, "What were you
43:05taking it for?""No, it was just my
43:07condition, and I recovered from it." I
43:10said, "Okay, let me look at your hands,
43:12" but she didn't agree. I mean, I
43:14wanted to hold off on treatment to ask
43:17her properly; I wanted to know if she
43:19was hiding something. So I said to her,
43:21"Listen, I want to tell you something."
43:24"Your face looks young, younger than
43:25your age, but your hands look like they
43:26belong to a 90-year-old; why the
43:27difference?""Why is there a difference
43:29regarding your hands?""Do you have
43:30eczema, for example?" I thought maybe
43:33she had eczema or some specific skin
43:36disease. She said, "No, I had psoriasis
43:41, but I treated it.""I got psoriasis in
43:44my late 20s and it stayed with me until
43:47five years ago." Five years ago, she
43:50went to a dermatologist who prescribed
43:53this drug, a new immunotherapy,
43:56something new for psoriasis. According
44:00to her, the medication didn't help.
44:02However, she used herbal mixtures,
44:04which were what helped her and cleared
44:07all the psoriasis, leaving it only on
44:09her hands. Now I was reassured that the
44:13oral psoriasis she had, or the white
44:16lesions she had, were indeed oral
44:18psoriasis. A patient with psoriasis.
44:22And when she described it to me, she
44:24described it as arthritic psoriasis.
44:26Meaning she has bleeding, itching, and
44:28her skin turns red; it’s not scaly
44:30like psoriasis. I was reassured that
44:34the lesions she has inside her mouth, I
44:37think on the floor of the mouth, they
44:39aren't leukoplakia; they are oral
44:41psoriasis. And everything I told her is
44:44an indication that she should continue
44:48every six months. Okay, well, that's it
44:52for this chapter. Thank you all, second
44:56. K.

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