Actinic keratosis (AK) is so common — we tend to see it, treat it and move on. We don’t think about the name or why it’s named what it is. (Nor do we tend to think a lot about the biology behind AK.) The name wasn’t chosen because of its biology or pathology but because of its crusty texture. In truth, it’s a misnomer. It’s not a keratosis like a seborrheic keratosis but instead an evolving malignancy. In my opinion, as well as that of many others, it’s time to change the name of this lesion to reflect what it is rather than the way it feels.
AK Beginnings
The history of AK lesions dates back to 1926 when Walter Freudenthal diagnosed these lesions and named them keratoma senilis. Before this, they were often lumped with seborrheic keratoses and were considered hypertrophies of the skin. Other lesions classified as “keratoses” included keratosis palmaris et plantaris, and keratosis pilaris. All of these processes were called keratoses because of their thick, keratotic crusty textures, not because of their biological make-up. Originally, AKs were not thought to be related to skin cancer at all.
The History Behind the Name
In 1958, dermatopathologist, Herman Pinkus was the first person to scientifically describe AKs in the context of their histopathology. He first coined the term actinic keratosis. In the 1960s, Walter Lever referred to AK as squamous cell carcinoma (SCC) in situ, grade 1/2. A quote from his textbook reads, “Actinic keratoses, or squamous cell carcinoma in situ…” In 1979, the term solar keratosis was used, as opposed to AK, to indicate the lesions were caused by UV sunlight versus other types of light or types of rays. In the 1990s, the Health Care Financing Administration (now known as the Centers for Medicare & Medicaid Services) redefined AKs as cosmetic lesions rather than evolving neoplasms. As a consequence, this government body concluded these lesions didn’t require treatment.
As most dermatologists know, in 1999, dermatology achieved a victory when a national coverage policy for solar keratoses with no restrictions on treatment became effective. Many dermatologists spent a significant amount of time in Washington lobbying and trying to educate decision-makers about AKs and the need to treat them. Today, insurance carriers and many patients understand that AKs lie on a neoplastic spectrum and that they require management and some type of treatment.
Clinical Background
Regarding the science of the neoplastic transformation, UVB is the main culprit. It causes the formation of thymidine cyclobutane dimers in DNA, which result in genetic mutations that lead to altered protein synthesis. The primary site of these mutations is at the p53 gene, which is a tumor suppressor gene. If that gene is mutated, the growth and proliferation of neoplastic cells occurs. This gene mutation is seen in 53% of AKs and in 69% of SCCs. These numbers are quite similar, which is strong evidence the two represent the same process at different stages of evolution. Virtually all cutaneous SCCs that involve the dermis develop from AKs. If you examine cutaneous SCC under the microscope, more than 90% will have features of actinic keratosis overlying or to the side of the cancer in the dermis. Also, virtually all cutaneous SCCs develop secondary to longstanding sun damage. This is analogous to melanoma in situ, which if left untreated, may evolve into invasive melanoma involving the dermis. In the majority of invasive melanomas, there is evidence of melanoma in situ in the epidermis. Like AK in some cases, melanoma in situ progresses and in some cases it doesn’t.
Even though AK and SCC represent the same disease in different stages, we give it a different name when it’s in an early stage. This used to be the situation in melanoma, but now we refer to early intraepidermal melanoma as melanoma in situ. This leads to definitive treatment and has been a boon to patients and physicians alike. What is the incidence of solar keratosis progressing to involve the dermis as squamous cell carcinoma? We don’t know the exact number, and it would be impossible to determine. There are too many of these lesions to study all of them. The likelihood of an individual solar keratosis giving rise to SCC has been estimated at 0.75% to 0.96% per person per year. It may not seem like a lot, but if you take this number and extrapolate it over the total number of lesions out there, they range anywhere from 13% to 20% over a 10-year period. That’s a significant number. So, if we don’t treat these lesions or manage them in some fashion, we run the risk of patients developing serious complications. It’s not a cosmetic disease at any stage of the game.
Finally, the progression of AK to SCC is analogous to epithelial neoplasms that develop in other organs such as intra-epithelial neoplasia of the uterine cervix progressing to cervical carcinoma. It’s well recognized by our colleagues in gynecology that early intraepithelial neoplasia is just that — evolving cancer. This is even recognized by Medicare and other carriers. Although we don’t have a test to detect SCC early, such as a Pap smear helps to detect early malignancies of the cervix, we do need to diagnose AKs early and appropriately treat them to prevent their evolution to invasive SCC. What’s In A Name? To better reflect its insidious nature maybe it’s time to re-name this lesion. Others have suggested a name change to solar keratotic type of squamous cell carcinoma in situ.
We previously suggested “keratinocytic intraepithelial neoplasia” and a system to grade the lesions. While this may not be popular from a clinical point of view, it’s valuable for research studies because you can quantitate the extent of involved epidermis as well as cytologic atypia. Nevertheless, both of these names emphasize the point that this is a neoplasm and not simply a benign cosmetic process. While some have objected to renaming AKs to indicate they’re evolving cancers because it may “alarm” patients, in my opinion, it’s important to point out that these lesions are neoplasms. I want my patients who have solar keratoses to understand they’ve been exposed excessively to the sun to the point that neoplastic transformation has taken place on their body. I want them to get the message loud and clear that they’re now at risk and that the next neoplasm to develop might be more serious. To me renaming AK to reflect its more serious nature is an opportunity to talk with patients about the fact that they have a condition that’s going to eventually worsen if they don’t start taking better care of themselves. It might be a wake-up call to some of our baby-boomer patients.
Final Thoughts
I’m not sure what the new name for AKs should be. In some settings, people are actually using the term solar keratotic squamous cell carcinoma in situ. I’m not against that terminology but I don’t think all the clinicians given those diagnoses know what to do with it yet and if this is the term we choose, we will need to couple it with an educational program. I’ve seen cases of wide excisions performed on lesions that would be routinely called AK both clinically and histologically. On the other hand, I’ve had some dermatologists say that if the name is changed to squamous cell carcinoma in situ regardless of the subtype, it creates a situation of medico-legal liability for the physician if the lesion is not excised or treated more aggressively. It’s an important consideration, and guidelines to specifically point out the rational approaches to treating these lesions will need to be developed as well. Finally, we don’t want a situation where governmental agencies or insurers claim that dermatologists are calling these lesions squamous cell carcinoma simply so they can excise more lesions and charge more. Medicare inspects CPT codes for destruction and excision very diligently as these are among the most commonly used codes by physicians in general. If we’re going to change the name, we’re going to have to educate patients, insurance carriers, malpractice attorneys, and all physicians, not only dermatologists. We’re not advocating any different treatment. We’re just advocating a different name.
Actinic keratosis (AK) is so common — we tend to see it, treat it and move on. We don’t think about the name or why it’s named what it is. (Nor do we tend to think a lot about the biology behind AK.) The name wasn’t chosen because of its biology or pathology but because of its crusty texture. In truth, it’s a misnomer. It’s not a keratosis like a seborrheic keratosis but instead an evolving malignancy. In my opinion, as well as that of many others, it’s time to change the name of this lesion to reflect what it is rather than the way it feels.
AK Beginnings
The history of AK lesions dates back to 1926 when Walter Freudenthal diagnosed these lesions and named them keratoma senilis. Before this, they were often lumped with seborrheic keratoses and were considered hypertrophies of the skin. Other lesions classified as “keratoses” included keratosis palmaris et plantaris, and keratosis pilaris. All of these processes were called keratoses because of their thick, keratotic crusty textures, not because of their biological make-up. Originally, AKs were not thought to be related to skin cancer at all.
The History Behind the Name
In 1958, dermatopathologist, Herman Pinkus was the first person to scientifically describe AKs in the context of their histopathology. He first coined the term actinic keratosis. In the 1960s, Walter Lever referred to AK as squamous cell carcinoma (SCC) in situ, grade 1/2. A quote from his textbook reads, “Actinic keratoses, or squamous cell carcinoma in situ…” In 1979, the term solar keratosis was used, as opposed to AK, to indicate the lesions were caused by UV sunlight versus other types of light or types of rays. In the 1990s, the Health Care Financing Administration (now known as the Centers for Medicare & Medicaid Services) redefined AKs as cosmetic lesions rather than evolving neoplasms. As a consequence, this government body concluded these lesions didn’t require treatment.
As most dermatologists know, in 1999, dermatology achieved a victory when a national coverage policy for solar keratoses with no restrictions on treatment became effective. Many dermatologists spent a significant amount of time in Washington lobbying and trying to educate decision-makers about AKs and the need to treat them. Today, insurance carriers and many patients understand that AKs lie on a neoplastic spectrum and that they require management and some type of treatment.
Clinical Background
Regarding the science of the neoplastic transformation, UVB is the main culprit. It causes the formation of thymidine cyclobutane dimers in DNA, which result in genetic mutations that lead to altered protein synthesis. The primary site of these mutations is at the p53 gene, which is a tumor suppressor gene. If that gene is mutated, the growth and proliferation of neoplastic cells occurs. This gene mutation is seen in 53% of AKs and in 69% of SCCs. These numbers are quite similar, which is strong evidence the two represent the same process at different stages of evolution. Virtually all cutaneous SCCs that involve the dermis develop from AKs. If you examine cutaneous SCC under the microscope, more than 90% will have features of actinic keratosis overlying or to the side of the cancer in the dermis. Also, virtually all cutaneous SCCs develop secondary to longstanding sun damage. This is analogous to melanoma in situ, which if left untreated, may evolve into invasive melanoma involving the dermis. In the majority of invasive melanomas, there is evidence of melanoma in situ in the epidermis. Like AK in some cases, melanoma in situ progresses and in some cases it doesn’t.
Even though AK and SCC represent the same disease in different stages, we give it a different name when it’s in an early stage. This used to be the situation in melanoma, but now we refer to early intraepidermal melanoma as melanoma in situ. This leads to definitive treatment and has been a boon to patients and physicians alike. What is the incidence of solar keratosis progressing to involve the dermis as squamous cell carcinoma? We don’t know the exact number, and it would be impossible to determine. There are too many of these lesions to study all of them. The likelihood of an individual solar keratosis giving rise to SCC has been estimated at 0.75% to 0.96% per person per year. It may not seem like a lot, but if you take this number and extrapolate it over the total number of lesions out there, they range anywhere from 13% to 20% over a 10-year period. That’s a significant number. So, if we don’t treat these lesions or manage them in some fashion, we run the risk of patients developing serious complications. It’s not a cosmetic disease at any stage of the game.
Finally, the progression of AK to SCC is analogous to epithelial neoplasms that develop in other organs such as intra-epithelial neoplasia of the uterine cervix progressing to cervical carcinoma. It’s well recognized by our colleagues in gynecology that early intraepithelial neoplasia is just that — evolving cancer. This is even recognized by Medicare and other carriers. Although we don’t have a test to detect SCC early, such as a Pap smear helps to detect early malignancies of the cervix, we do need to diagnose AKs early and appropriately treat them to prevent their evolution to invasive SCC. What’s In A Name? To better reflect its insidious nature maybe it’s time to re-name this lesion. Others have suggested a name change to solar keratotic type of squamous cell carcinoma in situ.
We previously suggested “keratinocytic intraepithelial neoplasia” and a system to grade the lesions. While this may not be popular from a clinical point of view, it’s valuable for research studies because you can quantitate the extent of involved epidermis as well as cytologic atypia. Nevertheless, both of these names emphasize the point that this is a neoplasm and not simply a benign cosmetic process. While some have objected to renaming AKs to indicate they’re evolving cancers because it may “alarm” patients, in my opinion, it’s important to point out that these lesions are neoplasms. I want my patients who have solar keratoses to understand they’ve been exposed excessively to the sun to the point that neoplastic transformation has taken place on their body. I want them to get the message loud and clear that they’re now at risk and that the next neoplasm to develop might be more serious. To me renaming AK to reflect its more serious nature is an opportunity to talk with patients about the fact that they have a condition that’s going to eventually worsen if they don’t start taking better care of themselves. It might be a wake-up call to some of our baby-boomer patients.
Final Thoughts
I’m not sure what the new name for AKs should be. In some settings, people are actually using the term solar keratotic squamous cell carcinoma in situ. I’m not against that terminology but I don’t think all the clinicians given those diagnoses know what to do with it yet and if this is the term we choose, we will need to couple it with an educational program. I’ve seen cases of wide excisions performed on lesions that would be routinely called AK both clinically and histologically. On the other hand, I’ve had some dermatologists say that if the name is changed to squamous cell carcinoma in situ regardless of the subtype, it creates a situation of medico-legal liability for the physician if the lesion is not excised or treated more aggressively. It’s an important consideration, and guidelines to specifically point out the rational approaches to treating these lesions will need to be developed as well. Finally, we don’t want a situation where governmental agencies or insurers claim that dermatologists are calling these lesions squamous cell carcinoma simply so they can excise more lesions and charge more. Medicare inspects CPT codes for destruction and excision very diligently as these are among the most commonly used codes by physicians in general. If we’re going to change the name, we’re going to have to educate patients, insurance carriers, malpractice attorneys, and all physicians, not only dermatologists. We’re not advocating any different treatment. We’re just advocating a different name.
Actinic keratosis (AK) is so common — we tend to see it, treat it and move on. We don’t think about the name or why it’s named what it is. (Nor do we tend to think a lot about the biology behind AK.) The name wasn’t chosen because of its biology or pathology but because of its crusty texture. In truth, it’s a misnomer. It’s not a keratosis like a seborrheic keratosis but instead an evolving malignancy. In my opinion, as well as that of many others, it’s time to change the name of this lesion to reflect what it is rather than the way it feels.
AK Beginnings
The history of AK lesions dates back to 1926 when Walter Freudenthal diagnosed these lesions and named them keratoma senilis. Before this, they were often lumped with seborrheic keratoses and were considered hypertrophies of the skin. Other lesions classified as “keratoses” included keratosis palmaris et plantaris, and keratosis pilaris. All of these processes were called keratoses because of their thick, keratotic crusty textures, not because of their biological make-up. Originally, AKs were not thought to be related to skin cancer at all.
The History Behind the Name
In 1958, dermatopathologist, Herman Pinkus was the first person to scientifically describe AKs in the context of their histopathology. He first coined the term actinic keratosis. In the 1960s, Walter Lever referred to AK as squamous cell carcinoma (SCC) in situ, grade 1/2. A quote from his textbook reads, “Actinic keratoses, or squamous cell carcinoma in situ…” In 1979, the term solar keratosis was used, as opposed to AK, to indicate the lesions were caused by UV sunlight versus other types of light or types of rays. In the 1990s, the Health Care Financing Administration (now known as the Centers for Medicare & Medicaid Services) redefined AKs as cosmetic lesions rather than evolving neoplasms. As a consequence, this government body concluded these lesions didn’t require treatment.
As most dermatologists know, in 1999, dermatology achieved a victory when a national coverage policy for solar keratoses with no restrictions on treatment became effective. Many dermatologists spent a significant amount of time in Washington lobbying and trying to educate decision-makers about AKs and the need to treat them. Today, insurance carriers and many patients understand that AKs lie on a neoplastic spectrum and that they require management and some type of treatment.
Clinical Background
Regarding the science of the neoplastic transformation, UVB is the main culprit. It causes the formation of thymidine cyclobutane dimers in DNA, which result in genetic mutations that lead to altered protein synthesis. The primary site of these mutations is at the p53 gene, which is a tumor suppressor gene. If that gene is mutated, the growth and proliferation of neoplastic cells occurs. This gene mutation is seen in 53% of AKs and in 69% of SCCs. These numbers are quite similar, which is strong evidence the two represent the same process at different stages of evolution. Virtually all cutaneous SCCs that involve the dermis develop from AKs. If you examine cutaneous SCC under the microscope, more than 90% will have features of actinic keratosis overlying or to the side of the cancer in the dermis. Also, virtually all cutaneous SCCs develop secondary to longstanding sun damage. This is analogous to melanoma in situ, which if left untreated, may evolve into invasive melanoma involving the dermis. In the majority of invasive melanomas, there is evidence of melanoma in situ in the epidermis. Like AK in some cases, melanoma in situ progresses and in some cases it doesn’t.
Even though AK and SCC represent the same disease in different stages, we give it a different name when it’s in an early stage. This used to be the situation in melanoma, but now we refer to early intraepidermal melanoma as melanoma in situ. This leads to definitive treatment and has been a boon to patients and physicians alike. What is the incidence of solar keratosis progressing to involve the dermis as squamous cell carcinoma? We don’t know the exact number, and it would be impossible to determine. There are too many of these lesions to study all of them. The likelihood of an individual solar keratosis giving rise to SCC has been estimated at 0.75% to 0.96% per person per year. It may not seem like a lot, but if you take this number and extrapolate it over the total number of lesions out there, they range anywhere from 13% to 20% over a 10-year period. That’s a significant number. So, if we don’t treat these lesions or manage them in some fashion, we run the risk of patients developing serious complications. It’s not a cosmetic disease at any stage of the game.
Finally, the progression of AK to SCC is analogous to epithelial neoplasms that develop in other organs such as intra-epithelial neoplasia of the uterine cervix progressing to cervical carcinoma. It’s well recognized by our colleagues in gynecology that early intraepithelial neoplasia is just that — evolving cancer. This is even recognized by Medicare and other carriers. Although we don’t have a test to detect SCC early, such as a Pap smear helps to detect early malignancies of the cervix, we do need to diagnose AKs early and appropriately treat them to prevent their evolution to invasive SCC. What’s In A Name? To better reflect its insidious nature maybe it’s time to re-name this lesion. Others have suggested a name change to solar keratotic type of squamous cell carcinoma in situ.
We previously suggested “keratinocytic intraepithelial neoplasia” and a system to grade the lesions. While this may not be popular from a clinical point of view, it’s valuable for research studies because you can quantitate the extent of involved epidermis as well as cytologic atypia. Nevertheless, both of these names emphasize the point that this is a neoplasm and not simply a benign cosmetic process. While some have objected to renaming AKs to indicate they’re evolving cancers because it may “alarm” patients, in my opinion, it’s important to point out that these lesions are neoplasms. I want my patients who have solar keratoses to understand they’ve been exposed excessively to the sun to the point that neoplastic transformation has taken place on their body. I want them to get the message loud and clear that they’re now at risk and that the next neoplasm to develop might be more serious. To me renaming AK to reflect its more serious nature is an opportunity to talk with patients about the fact that they have a condition that’s going to eventually worsen if they don’t start taking better care of themselves. It might be a wake-up call to some of our baby-boomer patients.
Final Thoughts
I’m not sure what the new name for AKs should be. In some settings, people are actually using the term solar keratotic squamous cell carcinoma in situ. I’m not against that terminology but I don’t think all the clinicians given those diagnoses know what to do with it yet and if this is the term we choose, we will need to couple it with an educational program. I’ve seen cases of wide excisions performed on lesions that would be routinely called AK both clinically and histologically. On the other hand, I’ve had some dermatologists say that if the name is changed to squamous cell carcinoma in situ regardless of the subtype, it creates a situation of medico-legal liability for the physician if the lesion is not excised or treated more aggressively. It’s an important consideration, and guidelines to specifically point out the rational approaches to treating these lesions will need to be developed as well. Finally, we don’t want a situation where governmental agencies or insurers claim that dermatologists are calling these lesions squamous cell carcinoma simply so they can excise more lesions and charge more. Medicare inspects CPT codes for destruction and excision very diligently as these are among the most commonly used codes by physicians in general. If we’re going to change the name, we’re going to have to educate patients, insurance carriers, malpractice attorneys, and all physicians, not only dermatologists. We’re not advocating any different treatment. We’re just advocating a different name.
