Biology Behind Sensitive Skin
July 2002
M any of us who regularly interact with the cosmetic industry have been trying for years to define and understand the group of people who seem to have a sensitivity to a variety of facial products that the majority use without trouble.
Some estimates in the cosmetic industry are that up to as much as 40% of the population will respond with either a neurosensory or an objective irritation-type reaction to concentrations of various molecules that the rest of the population can handle without incident.
Most of us agree that patients with atopic backgrounds, particularly atopic dermatitis (AD) tend to be easily irritated. People with rosacea also tend to be easily irritated, particularly as they age and get more photo damage.
With atopic dermatitis patients, I think their response to inflammatory stimuli and their ability to turn off the response to inflammatory stimuli may be deficient in one way or another. The most sensitive individuals, at least from my analysis, are those who have rosacea and an atopic background — they are the super-sensitive individuals.
Understanding the cellular makeup of the skin and how it works for normal versus sensitive skin is key to helping patients with conditions like rosacea and AD. Here’s a look at what we know and where research is heading.
Topical Retinoids and Sensitive Skin
The molecules that bring out sensitive skin in the most dramatic and obvious fashion are topical retinoids.
Some years ago, we learned that rosacea-prone people are particularly likely to get vasodilation-type reactions from sorbic acid — a preservative in topical tretinoin products that was very common in products used on the face. This agent is no longer a viable option for preservatives used in cosmetics and toiletries.
But for drugs in dermatology, it’s a different story. You can’t just replace one preservative for another. You need FDA approval and need to prove that the new preservative won’t cause a problem. So, for example, many hydrocortisone products have sorbic acid as a preservative and you can see this kind of vasodilation, which really isn’t frank irritation. This isn’t erythema due to injury to the epidermis and then secondary vasodilation from cytokine release and seepage into the dermis. This is a direct pharmacological effect that can occur if sorbic acid or other agents find their way into the dermis.
But why do rosacea-type patients tend to get this more than others? How does something turn on that intense stinging? How do we get vasodilation and non-immunologic urticarias? Is the permeability of their skin fundamentally different? Or, is the cutaneous nerve pattern of their skin and/or their vascular pattern in the papillary dermis anatomically different. These are questions that haven’t been asked, let alone studied. For the last few years, we’ve been studying various retinoids, and if you look over time, after application in a laboratory-kind of setting at peeling or dryness, which is the consequence of frank irritation, and look at erythema, you can easily separate rosacea-type patients from non-rosacea patients. We can conclude there’s something fundamentally interesting or different about their skin.
Looking Deeper
Let’s take a look at the stratum corneum. Everyday, mostly invisibly, we shed cells into the environment. As long as a program of proliferation and differentiation occurs normally, there’s a very nicely orchestrated process of old cells shedding and new ones developing. The cells differentiate and form the protective layer of our skin that interfaces with our environment and keeps us from leaking.
At a higher power, you can see tightly compacted corneocytes where tonafilaments have been flattened and condensed by filaggrin, the filament aggregating substance. Human stratum corneum forms a membrane. Light penetrates it fairly easily, and it has certain flexibility, physical/chemical-type characteristics. If you add water to it, it becomes more flexible. If you remove water, it becomes stiffer and tends to crack.
A very important aspect of our skin is that as cells migrate from the basal layer, highly membrane-like structures, called Odland bodies, develop, migrate to the cell membrane, fuse and then form the intracellular space in the stratum corneum.
There’s been a lot of work in this area during the last 15 to 20 years that has mostly gone unnoticed by people involved in clinical medicine. But to make a long, complicated series of studies and experiments over the years very simple, these highly structured lamellar-like structures that are seen in the intracellular space are composed of certain constituents, particularly fatty acids, and cholesterol, along with ceramides which are essential for this normal intracellular environment.
In the last few years, much research has focused on this area, which has implications for us in practice.
The Unilever Research
Ceramides, which are an essential part of the intra-cellular corneum space, play an important role in dry skin. For the last 7 or 8 years, there’s been a lot of work looking at stratum corneum ceramides. A wide range of people whose focus of interest is very disparate and not obviously connected, have all come up with the same answer. The phenotype that we call rough, scaly, dry skin, be it in a rosacea patient, an atopic, certain inborn errors of metabolism — they all have decreased amounts of ceramide, particularly ceramide 1.
Much of what we know comes from work done by Unilever research led by Tony Rawlings, who was primarily interested in detergent chapped skin (dishpan hands). This research group was the first to show the model that in both people with chapped skin from their occupation or activities in the home or from experimentally induced situations with a variety of detergents, there was a change in the ceramide levels in the stratum corneum lipid profile. And with increasing levels of “dryness” there were decreasing ceramides, associated with changes in fatty acids. And through a series of experiments, they concluded that by decreasing ceramides, particularly ceramide 1, which contains linoleic acid, the environment of the intracellular space was changed in a way that the normal breakdown of desmosomal attachments was interfered with and desquamation process was altered. As the stratum corneum thickened, microfissures would develop and skin would look and feel rough or “dry.”
One very interesting fact is that one of the functions of the stratum corneum membrane is to limit the amount of water that leaks across it. This can now be measured quantitatively. If you remove sebaceous lipids, you really don’t interfere or influence or change that membrane’s capacity to limit water. However, as much of the work of Peter Elias, M.D., has demonstrated, if you use other lipid solvents, like acetone, and remove the intracellular lipids, you get a profound change in that ability to limit water evaporation.
The kinetics of the recovery have been well worked out, and it’s fascinating that there’s an orderly, sequential replacement of these intracellular lipids. And if you use various inhibitors of enzymes involved in the biosynthesis pathways of these lipids, you can specifically interfere with the replenishment of these lipids, and the membrane doesn’t function in its capacity to limit water.
What I find most interesting is that you can fool the skin. If you put an occlusive membrane over the skin, such as Saran wrap, the lipids aren’t replenished. It’s as if the skin is tricked into thinking, “Well, the roof is okay, we don’t have to repair it.” But if you just extract these lipids, then without influencing epidermal proliferation, without turning on DNA synthesis, you do turn on metabolic activity that will selectively and sequentially replace these lipids and restore that membrane to its normal function and capacity.
So you can take people with perfectly normal looking/feeling skin, and if you chronically extract lipids with acetone, you can eventually produce rough, scaly, cracked, dry skin.
How the Skin Becomes Irritated
What does that mean for skin in terms of irritation? We’ve known for some time that really dry, cracked skin doesn’t desquamate in the normal fashion. It has a very thick stratum corneum. And as the outer layers become slightly less hydrated, they become a little stiffer and crack. When we treat dry skin, we’re using a variety of ingredients to influence this desquamation process. If all goes well, we end up with a compact stratum corneum, the outer layers of which are histologically undetectable because they’re in the process of falling off. “Dry skin” is a disorder of desquamation that causes the stratum corneum to become progressively thicker, which could cause it to crack as the outer most layer loses water.
And this is where there’s potential for irritation.
As the skin drys, microscopic fissures develop in the epidermis. When something is applied to the surface, it has rapid access to the epidermis, providing a potential for adverse interaction with the epithelium.
These “holes” in the skin are potential sources of entry or exposure to the underlying epithelium, which is obviously much more vulnerable.
Toll Receptors: Potential Protectors
First found in fruit flies, toll receptors are clearly an important part of what’s known as innate immunity, as opposed to acquired humoral or cell immunity. These receptors, at least 10 of them, can interact with microbial cell wall constituents, including lipoproteins, lipopolysaccharides, peptidoglycans, and induce host protective inflammatory responses. This system of receptor-initiated responses provides an inherent, innate way of protecting ourselves from invasion by microbial organisms.
There’s a group at the National Institutes for Health Institute for Occupational Health that has been studying toll receptors as potential sites for activation by chemical irritants. Researchers suspect detergents can interact with these receptors and cause a variety of responses, including the release of keratinicyte cytokines. These receptors have been identified on keratinicytes and human epithelium and are likely generated when the epithelium has been exposed to chemicals. They probably play an important role in contact irritation.
Take-Home Message
Now I’ve told you everything I know about sensitive skin and briefly given you an overview of where the field of irritation has been going. Now the question is: What does that mean for our patients who have sensitive skin?
For me, it means we need to simplify these patients’ skincare regimens, particularly for our adult patients who often are using numerous products as part of their skin-care regimen. We need to find out what they’re doing and encourage them to use gentle detergent systems and minimize use of astringent “clarifying lotions,” facial scrubs, and similar products.
Advances in detergent systems have been tremendous with many products available that are less toxic to the skin. It takes more to irritate skin with some of the newer detergent systems, such as the liquid detergent and foam-like systems that have been introduced. I think these are good choices for our patients who have sensitive skin whether their sensitivity is linked to atopy, rosacea or acne.
Using these more friendly detergent systems in a less aggressive way, minimizing the use of things such as astringents for skin care, and encouraging the use of moisturizers makes sense. These recommendations go a long way in helping patients tolerate the drugs we want them to use on the surface of their skin.
Editor’s Note: This article was adapted from Dr. Leyden’s presentation in April at the Valley of the Sun Conference on Clinical Dermatology, sponsored by an unrestricted educational grant from Medicis and the Phoenix Dermatologic Society.
M any of us who regularly interact with the cosmetic industry have been trying for years to define and understand the group of people who seem to have a sensitivity to a variety of facial products that the majority use without trouble.
Some estimates in the cosmetic industry are that up to as much as 40% of the population will respond with either a neurosensory or an objective irritation-type reaction to concentrations of various molecules that the rest of the population can handle without incident.
Most of us agree that patients with atopic backgrounds, particularly atopic dermatitis (AD) tend to be easily irritated. People with rosacea also tend to be easily irritated, particularly as they age and get more photo damage.
With atopic dermatitis patients, I think their response to inflammatory stimuli and their ability to turn off the response to inflammatory stimuli may be deficient in one way or another. The most sensitive individuals, at least from my analysis, are those who have rosacea and an atopic background — they are the super-sensitive individuals.
Understanding the cellular makeup of the skin and how it works for normal versus sensitive skin is key to helping patients with conditions like rosacea and AD. Here’s a look at what we know and where research is heading.
Topical Retinoids and Sensitive Skin
The molecules that bring out sensitive skin in the most dramatic and obvious fashion are topical retinoids.
Some years ago, we learned that rosacea-prone people are particularly likely to get vasodilation-type reactions from sorbic acid — a preservative in topical tretinoin products that was very common in products used on the face. This agent is no longer a viable option for preservatives used in cosmetics and toiletries.
But for drugs in dermatology, it’s a different story. You can’t just replace one preservative for another. You need FDA approval and need to prove that the new preservative won’t cause a problem. So, for example, many hydrocortisone products have sorbic acid as a preservative and you can see this kind of vasodilation, which really isn’t frank irritation. This isn’t erythema due to injury to the epidermis and then secondary vasodilation from cytokine release and seepage into the dermis. This is a direct pharmacological effect that can occur if sorbic acid or other agents find their way into the dermis.
But why do rosacea-type patients tend to get this more than others? How does something turn on that intense stinging? How do we get vasodilation and non-immunologic urticarias? Is the permeability of their skin fundamentally different? Or, is the cutaneous nerve pattern of their skin and/or their vascular pattern in the papillary dermis anatomically different. These are questions that haven’t been asked, let alone studied. For the last few years, we’ve been studying various retinoids, and if you look over time, after application in a laboratory-kind of setting at peeling or dryness, which is the consequence of frank irritation, and look at erythema, you can easily separate rosacea-type patients from non-rosacea patients. We can conclude there’s something fundamentally interesting or different about their skin.
Looking Deeper
Let’s take a look at the stratum corneum. Everyday, mostly invisibly, we shed cells into the environment. As long as a program of proliferation and differentiation occurs normally, there’s a very nicely orchestrated process of old cells shedding and new ones developing. The cells differentiate and form the protective layer of our skin that interfaces with our environment and keeps us from leaking.
At a higher power, you can see tightly compacted corneocytes where tonafilaments have been flattened and condensed by filaggrin, the filament aggregating substance. Human stratum corneum forms a membrane. Light penetrates it fairly easily, and it has certain flexibility, physical/chemical-type characteristics. If you add water to it, it becomes more flexible. If you remove water, it becomes stiffer and tends to crack.
A very important aspect of our skin is that as cells migrate from the basal layer, highly membrane-like structures, called Odland bodies, develop, migrate to the cell membrane, fuse and then form the intracellular space in the stratum corneum.
There’s been a lot of work in this area during the last 15 to 20 years that has mostly gone unnoticed by people involved in clinical medicine. But to make a long, complicated series of studies and experiments over the years very simple, these highly structured lamellar-like structures that are seen in the intracellular space are composed of certain constituents, particularly fatty acids, and cholesterol, along with ceramides which are essential for this normal intracellular environment.
In the last few years, much research has focused on this area, which has implications for us in practice.
The Unilever Research
Ceramides, which are an essential part of the intra-cellular corneum space, play an important role in dry skin. For the last 7 or 8 years, there’s been a lot of work looking at stratum corneum ceramides. A wide range of people whose focus of interest is very disparate and not obviously connected, have all come up with the same answer. The phenotype that we call rough, scaly, dry skin, be it in a rosacea patient, an atopic, certain inborn errors of metabolism — they all have decreased amounts of ceramide, particularly ceramide 1.
Much of what we know comes from work done by Unilever research led by Tony Rawlings, who was primarily interested in detergent chapped skin (dishpan hands). This research group was the first to show the model that in both people with chapped skin from their occupation or activities in the home or from experimentally induced situations with a variety of detergents, there was a change in the ceramide levels in the stratum corneum lipid profile. And with increasing levels of “dryness” there were decreasing ceramides, associated with changes in fatty acids. And through a series of experiments, they concluded that by decreasing ceramides, particularly ceramide 1, which contains linoleic acid, the environment of the intracellular space was changed in a way that the normal breakdown of desmosomal attachments was interfered with and desquamation process was altered. As the stratum corneum thickened, microfissures would develop and skin would look and feel rough or “dry.”
One very interesting fact is that one of the functions of the stratum corneum membrane is to limit the amount of water that leaks across it. This can now be measured quantitatively. If you remove sebaceous lipids, you really don’t interfere or influence or change that membrane’s capacity to limit water. However, as much of the work of Peter Elias, M.D., has demonstrated, if you use other lipid solvents, like acetone, and remove the intracellular lipids, you get a profound change in that ability to limit water evaporation.
The kinetics of the recovery have been well worked out, and it’s fascinating that there’s an orderly, sequential replacement of these intracellular lipids. And if you use various inhibitors of enzymes involved in the biosynthesis pathways of these lipids, you can specifically interfere with the replenishment of these lipids, and the membrane doesn’t function in its capacity to limit water.
What I find most interesting is that you can fool the skin. If you put an occlusive membrane over the skin, such as Saran wrap, the lipids aren’t replenished. It’s as if the skin is tricked into thinking, “Well, the roof is okay, we don’t have to repair it.” But if you just extract these lipids, then without influencing epidermal proliferation, without turning on DNA synthesis, you do turn on metabolic activity that will selectively and sequentially replace these lipids and restore that membrane to its normal function and capacity.
So you can take people with perfectly normal looking/feeling skin, and if you chronically extract lipids with acetone, you can eventually produce rough, scaly, cracked, dry skin.
How the Skin Becomes Irritated
What does that mean for skin in terms of irritation? We’ve known for some time that really dry, cracked skin doesn’t desquamate in the normal fashion. It has a very thick stratum corneum. And as the outer layers become slightly less hydrated, they become a little stiffer and crack. When we treat dry skin, we’re using a variety of ingredients to influence this desquamation process. If all goes well, we end up with a compact stratum corneum, the outer layers of which are histologically undetectable because they’re in the process of falling off. “Dry skin” is a disorder of desquamation that causes the stratum corneum to become progressively thicker, which could cause it to crack as the outer most layer loses water.
And this is where there’s potential for irritation.
As the skin drys, microscopic fissures develop in the epidermis. When something is applied to the surface, it has rapid access to the epidermis, providing a potential for adverse interaction with the epithelium.
These “holes” in the skin are potential sources of entry or exposure to the underlying epithelium, which is obviously much more vulnerable.
Toll Receptors: Potential Protectors
First found in fruit flies, toll receptors are clearly an important part of what’s known as innate immunity, as opposed to acquired humoral or cell immunity. These receptors, at least 10 of them, can interact with microbial cell wall constituents, including lipoproteins, lipopolysaccharides, peptidoglycans, and induce host protective inflammatory responses. This system of receptor-initiated responses provides an inherent, innate way of protecting ourselves from invasion by microbial organisms.
There’s a group at the National Institutes for Health Institute for Occupational Health that has been studying toll receptors as potential sites for activation by chemical irritants. Researchers suspect detergents can interact with these receptors and cause a variety of responses, including the release of keratinicyte cytokines. These receptors have been identified on keratinicytes and human epithelium and are likely generated when the epithelium has been exposed to chemicals. They probably play an important role in contact irritation.
Take-Home Message
Now I’ve told you everything I know about sensitive skin and briefly given you an overview of where the field of irritation has been going. Now the question is: What does that mean for our patients who have sensitive skin?
For me, it means we need to simplify these patients’ skincare regimens, particularly for our adult patients who often are using numerous products as part of their skin-care regimen. We need to find out what they’re doing and encourage them to use gentle detergent systems and minimize use of astringent “clarifying lotions,” facial scrubs, and similar products.
Advances in detergent systems have been tremendous with many products available that are less toxic to the skin. It takes more to irritate skin with some of the newer detergent systems, such as the liquid detergent and foam-like systems that have been introduced. I think these are good choices for our patients who have sensitive skin whether their sensitivity is linked to atopy, rosacea or acne.
Using these more friendly detergent systems in a less aggressive way, minimizing the use of things such as astringents for skin care, and encouraging the use of moisturizers makes sense. These recommendations go a long way in helping patients tolerate the drugs we want them to use on the surface of their skin.
Editor’s Note: This article was adapted from Dr. Leyden’s presentation in April at the Valley of the Sun Conference on Clinical Dermatology, sponsored by an unrestricted educational grant from Medicis and the Phoenix Dermatologic Society.
M any of us who regularly interact with the cosmetic industry have been trying for years to define and understand the group of people who seem to have a sensitivity to a variety of facial products that the majority use without trouble.
Some estimates in the cosmetic industry are that up to as much as 40% of the population will respond with either a neurosensory or an objective irritation-type reaction to concentrations of various molecules that the rest of the population can handle without incident.
Most of us agree that patients with atopic backgrounds, particularly atopic dermatitis (AD) tend to be easily irritated. People with rosacea also tend to be easily irritated, particularly as they age and get more photo damage.
With atopic dermatitis patients, I think their response to inflammatory stimuli and their ability to turn off the response to inflammatory stimuli may be deficient in one way or another. The most sensitive individuals, at least from my analysis, are those who have rosacea and an atopic background — they are the super-sensitive individuals.
Understanding the cellular makeup of the skin and how it works for normal versus sensitive skin is key to helping patients with conditions like rosacea and AD. Here’s a look at what we know and where research is heading.
Topical Retinoids and Sensitive Skin
The molecules that bring out sensitive skin in the most dramatic and obvious fashion are topical retinoids.
Some years ago, we learned that rosacea-prone people are particularly likely to get vasodilation-type reactions from sorbic acid — a preservative in topical tretinoin products that was very common in products used on the face. This agent is no longer a viable option for preservatives used in cosmetics and toiletries.
But for drugs in dermatology, it’s a different story. You can’t just replace one preservative for another. You need FDA approval and need to prove that the new preservative won’t cause a problem. So, for example, many hydrocortisone products have sorbic acid as a preservative and you can see this kind of vasodilation, which really isn’t frank irritation. This isn’t erythema due to injury to the epidermis and then secondary vasodilation from cytokine release and seepage into the dermis. This is a direct pharmacological effect that can occur if sorbic acid or other agents find their way into the dermis.
But why do rosacea-type patients tend to get this more than others? How does something turn on that intense stinging? How do we get vasodilation and non-immunologic urticarias? Is the permeability of their skin fundamentally different? Or, is the cutaneous nerve pattern of their skin and/or their vascular pattern in the papillary dermis anatomically different. These are questions that haven’t been asked, let alone studied. For the last few years, we’ve been studying various retinoids, and if you look over time, after application in a laboratory-kind of setting at peeling or dryness, which is the consequence of frank irritation, and look at erythema, you can easily separate rosacea-type patients from non-rosacea patients. We can conclude there’s something fundamentally interesting or different about their skin.
Looking Deeper
Let’s take a look at the stratum corneum. Everyday, mostly invisibly, we shed cells into the environment. As long as a program of proliferation and differentiation occurs normally, there’s a very nicely orchestrated process of old cells shedding and new ones developing. The cells differentiate and form the protective layer of our skin that interfaces with our environment and keeps us from leaking.
At a higher power, you can see tightly compacted corneocytes where tonafilaments have been flattened and condensed by filaggrin, the filament aggregating substance. Human stratum corneum forms a membrane. Light penetrates it fairly easily, and it has certain flexibility, physical/chemical-type characteristics. If you add water to it, it becomes more flexible. If you remove water, it becomes stiffer and tends to crack.
A very important aspect of our skin is that as cells migrate from the basal layer, highly membrane-like structures, called Odland bodies, develop, migrate to the cell membrane, fuse and then form the intracellular space in the stratum corneum.
There’s been a lot of work in this area during the last 15 to 20 years that has mostly gone unnoticed by people involved in clinical medicine. But to make a long, complicated series of studies and experiments over the years very simple, these highly structured lamellar-like structures that are seen in the intracellular space are composed of certain constituents, particularly fatty acids, and cholesterol, along with ceramides which are essential for this normal intracellular environment.
In the last few years, much research has focused on this area, which has implications for us in practice.
The Unilever Research
Ceramides, which are an essential part of the intra-cellular corneum space, play an important role in dry skin. For the last 7 or 8 years, there’s been a lot of work looking at stratum corneum ceramides. A wide range of people whose focus of interest is very disparate and not obviously connected, have all come up with the same answer. The phenotype that we call rough, scaly, dry skin, be it in a rosacea patient, an atopic, certain inborn errors of metabolism — they all have decreased amounts of ceramide, particularly ceramide 1.
Much of what we know comes from work done by Unilever research led by Tony Rawlings, who was primarily interested in detergent chapped skin (dishpan hands). This research group was the first to show the model that in both people with chapped skin from their occupation or activities in the home or from experimentally induced situations with a variety of detergents, there was a change in the ceramide levels in the stratum corneum lipid profile. And with increasing levels of “dryness” there were decreasing ceramides, associated with changes in fatty acids. And through a series of experiments, they concluded that by decreasing ceramides, particularly ceramide 1, which contains linoleic acid, the environment of the intracellular space was changed in a way that the normal breakdown of desmosomal attachments was interfered with and desquamation process was altered. As the stratum corneum thickened, microfissures would develop and skin would look and feel rough or “dry.”
One very interesting fact is that one of the functions of the stratum corneum membrane is to limit the amount of water that leaks across it. This can now be measured quantitatively. If you remove sebaceous lipids, you really don’t interfere or influence or change that membrane’s capacity to limit water. However, as much of the work of Peter Elias, M.D., has demonstrated, if you use other lipid solvents, like acetone, and remove the intracellular lipids, you get a profound change in that ability to limit water evaporation.
The kinetics of the recovery have been well worked out, and it’s fascinating that there’s an orderly, sequential replacement of these intracellular lipids. And if you use various inhibitors of enzymes involved in the biosynthesis pathways of these lipids, you can specifically interfere with the replenishment of these lipids, and the membrane doesn’t function in its capacity to limit water.
What I find most interesting is that you can fool the skin. If you put an occlusive membrane over the skin, such as Saran wrap, the lipids aren’t replenished. It’s as if the skin is tricked into thinking, “Well, the roof is okay, we don’t have to repair it.” But if you just extract these lipids, then without influencing epidermal proliferation, without turning on DNA synthesis, you do turn on metabolic activity that will selectively and sequentially replace these lipids and restore that membrane to its normal function and capacity.
So you can take people with perfectly normal looking/feeling skin, and if you chronically extract lipids with acetone, you can eventually produce rough, scaly, cracked, dry skin.
How the Skin Becomes Irritated
What does that mean for skin in terms of irritation? We’ve known for some time that really dry, cracked skin doesn’t desquamate in the normal fashion. It has a very thick stratum corneum. And as the outer layers become slightly less hydrated, they become a little stiffer and crack. When we treat dry skin, we’re using a variety of ingredients to influence this desquamation process. If all goes well, we end up with a compact stratum corneum, the outer layers of which are histologically undetectable because they’re in the process of falling off. “Dry skin” is a disorder of desquamation that causes the stratum corneum to become progressively thicker, which could cause it to crack as the outer most layer loses water.
And this is where there’s potential for irritation.
As the skin drys, microscopic fissures develop in the epidermis. When something is applied to the surface, it has rapid access to the epidermis, providing a potential for adverse interaction with the epithelium.
These “holes” in the skin are potential sources of entry or exposure to the underlying epithelium, which is obviously much more vulnerable.
Toll Receptors: Potential Protectors
First found in fruit flies, toll receptors are clearly an important part of what’s known as innate immunity, as opposed to acquired humoral or cell immunity. These receptors, at least 10 of them, can interact with microbial cell wall constituents, including lipoproteins, lipopolysaccharides, peptidoglycans, and induce host protective inflammatory responses. This system of receptor-initiated responses provides an inherent, innate way of protecting ourselves from invasion by microbial organisms.
There’s a group at the National Institutes for Health Institute for Occupational Health that has been studying toll receptors as potential sites for activation by chemical irritants. Researchers suspect detergents can interact with these receptors and cause a variety of responses, including the release of keratinicyte cytokines. These receptors have been identified on keratinicytes and human epithelium and are likely generated when the epithelium has been exposed to chemicals. They probably play an important role in contact irritation.
Take-Home Message
Now I’ve told you everything I know about sensitive skin and briefly given you an overview of where the field of irritation has been going. Now the question is: What does that mean for our patients who have sensitive skin?
For me, it means we need to simplify these patients’ skincare regimens, particularly for our adult patients who often are using numerous products as part of their skin-care regimen. We need to find out what they’re doing and encourage them to use gentle detergent systems and minimize use of astringent “clarifying lotions,” facial scrubs, and similar products.
Advances in detergent systems have been tremendous with many products available that are less toxic to the skin. It takes more to irritate skin with some of the newer detergent systems, such as the liquid detergent and foam-like systems that have been introduced. I think these are good choices for our patients who have sensitive skin whether their sensitivity is linked to atopy, rosacea or acne.
Using these more friendly detergent systems in a less aggressive way, minimizing the use of things such as astringents for skin care, and encouraging the use of moisturizers makes sense. These recommendations go a long way in helping patients tolerate the drugs we want them to use on the surface of their skin.
Editor’s Note: This article was adapted from Dr. Leyden’s presentation in April at the Valley of the Sun Conference on Clinical Dermatology, sponsored by an unrestricted educational grant from Medicis and the Phoenix Dermatologic Society.
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