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Microtox and Mesotox
The terms when they mention one of these terms.
Let’s settle the nomenclature confusion. In this column, I define and outline suggested terminology based on studies and my 15 years of experience using neuromodulators. If any readers or colleagues disagree, please write to me and we can discuss the alternatives in a subsequent article; if you agree, please also write to me so we can collaboratively correct the discrepancies in the literature accordingly.
The term mesotherapy, originating from the Greek “mesos” referring to the early embryonic mesoderm, was identified in the 1950’s by Dr. Michel Pistor, a French physician who administered drugs intradermally. The term was defined as a minimally invasive technique by which drugs or bioactive substances are given in small quantities through dermal micropunctures. Drugs administered intradermally diffuse very slowly and therefore, stay in the tissue longer than those administered intramuscularly.
Thus, Mesotox is defined not by the concentration of the neuromodulator or location, but by the depth of injection in the superficial dermis. It can be delivered through individual injections or through a microneedling pen.
Microtox refers to the dilution of the neuromodulator at concentrations below the proposed dilution guidelines of the manufacturer: Less than 2.5 U per 0.1 mL for onabotulinumtoxinA (OBA), incobotulinumtoxinA (IBA), and prabotulinumtoxinA (PBA); and less than 10 U per 0.1 mL for abobotulinumtoxinA (ABO), This method allows for the injection of superficial cutaneous muscles softening the dynamic rhytids without complete paralysis.
Mesotox is widely used off label for facial lifting, reduction in skin laxity or crepiness, flushing of rosacea, acne, hyperhidrosis of the face, keloids, seborrhea, neck rejuvenation, contouring of the mandibular border, and scalp oiliness. Based on a review of articles using this technique, dilution methods were less than 2.5 U per 1 mL (OBA, IBA) and less than 10 U per 0.1 mL (ABO) depth of injection was the superficial to mid-dermis with injection points 0.5 cm to 1 cm apart.
In a study by Atwa and colleagues, 25 patients with mild facial skin laxity received intradermal Botox-A on one side and saline on the other. This split face study showed a highly significant difference with facial lifting on the treated side. Mesotox injection points vary based on the clinical indication and area being treated.
The treatment of dynamic muscles using standard neuromodulator dosing protocols include the treatment of the glabella, crow’s feet, forehead lines, masseter hypertrophy, bunny lines, gummy smile, perioral lines, mentalis hypertonia, platysmal bands, and marionette lines.
However, hyperdilute neuromodulators or Microtox can effectively be used alone or in combination with standard dosing for the following off-label uses. Used in combination with standard dosing of the forehead lines, I use Microtox in the lateral brow to soften the frontalis muscle without dropping the brow in patients with a low-set brow or lid laxity. I also use it for the jelly roll of the eyes and to open the aperture of the eyes. Along the nose, Microtox can also be used to treat a sagging nasal tip, decrease the width of the ala, and treat overactive facial muscles adjacent to the nose resulting in an overactive nasolabial fold.
Similarly, Microtox can be used to treat lateral smile lines and downward extensions of the crow’s feet. In all of the aforementioned treatment areas, I recommend approximately 0.5-1 U of toxin in each area divided at 1-cm intervals.Mesotox and Microtox are both highly effective strategies to treat the aging face. However, the nomenclature is not interchangeable. I propose that the term Mesotox be used only to articulate or define the superficial injection of a neuromodulator for the improvement of the skin that does not involve the injection into or paralysis of a cutaneous muscle (“tox” being used generically for all neuromodulators). I also propose that the term Microtox should be used to define the dilution of a neuromodulator beyond the manufacturer-recommended dilution protocols – used for the paralysis of a cutaneous muscle. In addition, I recommend that the terms MicroBotox and MesoBotox no longer be used. These procedures all have risks, and adverse events associated with Microtox and Mesotox are similar to those of any neuromodulator injection at FDA-recommended maximum doses, and dilution and storage protocols and proper injection techniques need to be followed. Expertise and training is crucial and treatment by a board-certified dermatologist or plastic surgeon is imperative.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to her at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Awaida CJ et al. Plast Reconstr Surg. 2018 Sep;142(3):640-9.
Calvani F et al. Plast Surg (Oakv). 2019 May;27(2):156-61.
Iranmanesh B et al. J Cosmet Dermatol. 2022 Oct;21(10):4160-70.
Kandhari R et al. J Cutan Aesthet Surg. 2022 Apr-Jun;15(2):101-7.
Lewandowski M et al. Molecules. 2022 May 13;27(10):3143.
Mammucari M et al. Eur Rev Med Pharmacol Sci. 2011 Jun;15(6):682-94.
Park KY et al. Ann Dermatol. 2018 Dec;30(6):688-93.
Pistor M. Chir Dent Fr. 1976;46:59-60.
Rho NK, Gil YC. Toxins (Basel). 2021 Nov 19;13(11):817.
Wu WTL. Plast Reconstr Surg. 2015 Nov;136(5 Suppl):92S-100S.
Zhang H et al. Clin Cosmet Investig Dermatol. 2021 Apr 30;14:407-17.
The terms when they mention one of these terms.
Let’s settle the nomenclature confusion. In this column, I define and outline suggested terminology based on studies and my 15 years of experience using neuromodulators. If any readers or colleagues disagree, please write to me and we can discuss the alternatives in a subsequent article; if you agree, please also write to me so we can collaboratively correct the discrepancies in the literature accordingly.
The term mesotherapy, originating from the Greek “mesos” referring to the early embryonic mesoderm, was identified in the 1950’s by Dr. Michel Pistor, a French physician who administered drugs intradermally. The term was defined as a minimally invasive technique by which drugs or bioactive substances are given in small quantities through dermal micropunctures. Drugs administered intradermally diffuse very slowly and therefore, stay in the tissue longer than those administered intramuscularly.
Thus, Mesotox is defined not by the concentration of the neuromodulator or location, but by the depth of injection in the superficial dermis. It can be delivered through individual injections or through a microneedling pen.
Microtox refers to the dilution of the neuromodulator at concentrations below the proposed dilution guidelines of the manufacturer: Less than 2.5 U per 0.1 mL for onabotulinumtoxinA (OBA), incobotulinumtoxinA (IBA), and prabotulinumtoxinA (PBA); and less than 10 U per 0.1 mL for abobotulinumtoxinA (ABO), This method allows for the injection of superficial cutaneous muscles softening the dynamic rhytids without complete paralysis.
Mesotox is widely used off label for facial lifting, reduction in skin laxity or crepiness, flushing of rosacea, acne, hyperhidrosis of the face, keloids, seborrhea, neck rejuvenation, contouring of the mandibular border, and scalp oiliness. Based on a review of articles using this technique, dilution methods were less than 2.5 U per 1 mL (OBA, IBA) and less than 10 U per 0.1 mL (ABO) depth of injection was the superficial to mid-dermis with injection points 0.5 cm to 1 cm apart.
In a study by Atwa and colleagues, 25 patients with mild facial skin laxity received intradermal Botox-A on one side and saline on the other. This split face study showed a highly significant difference with facial lifting on the treated side. Mesotox injection points vary based on the clinical indication and area being treated.
The treatment of dynamic muscles using standard neuromodulator dosing protocols include the treatment of the glabella, crow’s feet, forehead lines, masseter hypertrophy, bunny lines, gummy smile, perioral lines, mentalis hypertonia, platysmal bands, and marionette lines.
However, hyperdilute neuromodulators or Microtox can effectively be used alone or in combination with standard dosing for the following off-label uses. Used in combination with standard dosing of the forehead lines, I use Microtox in the lateral brow to soften the frontalis muscle without dropping the brow in patients with a low-set brow or lid laxity. I also use it for the jelly roll of the eyes and to open the aperture of the eyes. Along the nose, Microtox can also be used to treat a sagging nasal tip, decrease the width of the ala, and treat overactive facial muscles adjacent to the nose resulting in an overactive nasolabial fold.
Similarly, Microtox can be used to treat lateral smile lines and downward extensions of the crow’s feet. In all of the aforementioned treatment areas, I recommend approximately 0.5-1 U of toxin in each area divided at 1-cm intervals.Mesotox and Microtox are both highly effective strategies to treat the aging face. However, the nomenclature is not interchangeable. I propose that the term Mesotox be used only to articulate or define the superficial injection of a neuromodulator for the improvement of the skin that does not involve the injection into or paralysis of a cutaneous muscle (“tox” being used generically for all neuromodulators). I also propose that the term Microtox should be used to define the dilution of a neuromodulator beyond the manufacturer-recommended dilution protocols – used for the paralysis of a cutaneous muscle. In addition, I recommend that the terms MicroBotox and MesoBotox no longer be used. These procedures all have risks, and adverse events associated with Microtox and Mesotox are similar to those of any neuromodulator injection at FDA-recommended maximum doses, and dilution and storage protocols and proper injection techniques need to be followed. Expertise and training is crucial and treatment by a board-certified dermatologist or plastic surgeon is imperative.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to her at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Awaida CJ et al. Plast Reconstr Surg. 2018 Sep;142(3):640-9.
Calvani F et al. Plast Surg (Oakv). 2019 May;27(2):156-61.
Iranmanesh B et al. J Cosmet Dermatol. 2022 Oct;21(10):4160-70.
Kandhari R et al. J Cutan Aesthet Surg. 2022 Apr-Jun;15(2):101-7.
Lewandowski M et al. Molecules. 2022 May 13;27(10):3143.
Mammucari M et al. Eur Rev Med Pharmacol Sci. 2011 Jun;15(6):682-94.
Park KY et al. Ann Dermatol. 2018 Dec;30(6):688-93.
Pistor M. Chir Dent Fr. 1976;46:59-60.
Rho NK, Gil YC. Toxins (Basel). 2021 Nov 19;13(11):817.
Wu WTL. Plast Reconstr Surg. 2015 Nov;136(5 Suppl):92S-100S.
Zhang H et al. Clin Cosmet Investig Dermatol. 2021 Apr 30;14:407-17.
The terms when they mention one of these terms.
Let’s settle the nomenclature confusion. In this column, I define and outline suggested terminology based on studies and my 15 years of experience using neuromodulators. If any readers or colleagues disagree, please write to me and we can discuss the alternatives in a subsequent article; if you agree, please also write to me so we can collaboratively correct the discrepancies in the literature accordingly.
The term mesotherapy, originating from the Greek “mesos” referring to the early embryonic mesoderm, was identified in the 1950’s by Dr. Michel Pistor, a French physician who administered drugs intradermally. The term was defined as a minimally invasive technique by which drugs or bioactive substances are given in small quantities through dermal micropunctures. Drugs administered intradermally diffuse very slowly and therefore, stay in the tissue longer than those administered intramuscularly.
Thus, Mesotox is defined not by the concentration of the neuromodulator or location, but by the depth of injection in the superficial dermis. It can be delivered through individual injections or through a microneedling pen.
Microtox refers to the dilution of the neuromodulator at concentrations below the proposed dilution guidelines of the manufacturer: Less than 2.5 U per 0.1 mL for onabotulinumtoxinA (OBA), incobotulinumtoxinA (IBA), and prabotulinumtoxinA (PBA); and less than 10 U per 0.1 mL for abobotulinumtoxinA (ABO), This method allows for the injection of superficial cutaneous muscles softening the dynamic rhytids without complete paralysis.
Mesotox is widely used off label for facial lifting, reduction in skin laxity or crepiness, flushing of rosacea, acne, hyperhidrosis of the face, keloids, seborrhea, neck rejuvenation, contouring of the mandibular border, and scalp oiliness. Based on a review of articles using this technique, dilution methods were less than 2.5 U per 1 mL (OBA, IBA) and less than 10 U per 0.1 mL (ABO) depth of injection was the superficial to mid-dermis with injection points 0.5 cm to 1 cm apart.
In a study by Atwa and colleagues, 25 patients with mild facial skin laxity received intradermal Botox-A on one side and saline on the other. This split face study showed a highly significant difference with facial lifting on the treated side. Mesotox injection points vary based on the clinical indication and area being treated.
The treatment of dynamic muscles using standard neuromodulator dosing protocols include the treatment of the glabella, crow’s feet, forehead lines, masseter hypertrophy, bunny lines, gummy smile, perioral lines, mentalis hypertonia, platysmal bands, and marionette lines.
However, hyperdilute neuromodulators or Microtox can effectively be used alone or in combination with standard dosing for the following off-label uses. Used in combination with standard dosing of the forehead lines, I use Microtox in the lateral brow to soften the frontalis muscle without dropping the brow in patients with a low-set brow or lid laxity. I also use it for the jelly roll of the eyes and to open the aperture of the eyes. Along the nose, Microtox can also be used to treat a sagging nasal tip, decrease the width of the ala, and treat overactive facial muscles adjacent to the nose resulting in an overactive nasolabial fold.
Similarly, Microtox can be used to treat lateral smile lines and downward extensions of the crow’s feet. In all of the aforementioned treatment areas, I recommend approximately 0.5-1 U of toxin in each area divided at 1-cm intervals.Mesotox and Microtox are both highly effective strategies to treat the aging face. However, the nomenclature is not interchangeable. I propose that the term Mesotox be used only to articulate or define the superficial injection of a neuromodulator for the improvement of the skin that does not involve the injection into or paralysis of a cutaneous muscle (“tox” being used generically for all neuromodulators). I also propose that the term Microtox should be used to define the dilution of a neuromodulator beyond the manufacturer-recommended dilution protocols – used for the paralysis of a cutaneous muscle. In addition, I recommend that the terms MicroBotox and MesoBotox no longer be used. These procedures all have risks, and adverse events associated with Microtox and Mesotox are similar to those of any neuromodulator injection at FDA-recommended maximum doses, and dilution and storage protocols and proper injection techniques need to be followed. Expertise and training is crucial and treatment by a board-certified dermatologist or plastic surgeon is imperative.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to her at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Awaida CJ et al. Plast Reconstr Surg. 2018 Sep;142(3):640-9.
Calvani F et al. Plast Surg (Oakv). 2019 May;27(2):156-61.
Iranmanesh B et al. J Cosmet Dermatol. 2022 Oct;21(10):4160-70.
Kandhari R et al. J Cutan Aesthet Surg. 2022 Apr-Jun;15(2):101-7.
Lewandowski M et al. Molecules. 2022 May 13;27(10):3143.
Mammucari M et al. Eur Rev Med Pharmacol Sci. 2011 Jun;15(6):682-94.
Park KY et al. Ann Dermatol. 2018 Dec;30(6):688-93.
Pistor M. Chir Dent Fr. 1976;46:59-60.
Rho NK, Gil YC. Toxins (Basel). 2021 Nov 19;13(11):817.
Wu WTL. Plast Reconstr Surg. 2015 Nov;136(5 Suppl):92S-100S.
Zhang H et al. Clin Cosmet Investig Dermatol. 2021 Apr 30;14:407-17.
Vision loss may be a risk with PRP facial injections
A systematic review was recently conducted by Wu and colleagues examining the risk of blindness associated with platelet-rich plasma (PRP) injection. In dermatology, PRP is used more commonly now than 5 years ago to promote hair growth with injections on the scalp, as an adjunct to microneedling procedures, and sometimes – in a similar way to facial fillers – to improve volume loss, and skin tone and texture (particularly to the tear trough region).
Total unilateral blindness occurred in all cases. In one of the seven reported cases, the patient experienced recovery of vision after 3 months, but with some residual deficits noted on the ophthalmologist examination. In this case, the patient was evaluated and treated by an ophthalmologist within 3 hours of symptom onset.
In addition, four cases were reported from Venezuela, one from the United States, one from the United Kingdom, and one from Malaysia. Similar to reports of blindness with facial fillers, the most common injection site reported with this adverse effect was the glabella (five cases);
Other reports involved injections of the forehead (two), followed by the nasolabial fold (one), lateral canthus (one), and temporomandibular joint (one). Two of the seven patients received injections at more than one site, resulting in the total number of injections reported (10) being higher than the number of patients.
The risk of blindness is inherent with deep injection into a vessel that anastomoses with the blood supply to the eye. No mention was made as to whether PRP or platelet-rich fibrin was used. Other details are lacking from the original articles as to injection technique and whether or not cannula injection was used. No treatment was attempted in four of seven cases.
As plasma is native to the arteries and dissolves in the blood stream naturally, the mechanism as to why retinal artery occlusion or blindness would occur is not completely clear. One theory is that it is volume related and results from the speed of injection, causing a large rapid bolus that temporarily occludes or compresses an involved vessel.
Another theory is that damage to the vessel results from the injection itself or injection technique, leading to a clotting cascade and clot of the involved vessel with subsequent retrograde flow or blockade of the retinal artery. But if this were the case, we would expect to hear about more cases of clots leading to vascular occlusion or skin necrosis, which does not typically occur or we do not hear about.
Details about proper collection materials and technique or mixing with some other materials are also unknown in these cases, thus leaving the possibility that a more occlusive material may have been injected, as opposed to the fluid-like composition of the typical PRP preparation.With regards to risk with scalp PRP injection, the frontal scalp does receive blood supply from the supratrochlear artery that anastomoses with the angular artery of the face – both of which anastomose with the retinal artery (where occlusion would occur via back flow). The scalp tributaries are small and far enough away from the retina at that point that risk of back flow the to retinal artery should be minimal. Additionally, no reports of vascular occlusion from PRP scalp injection leading to skin necrosis have ever been reported. Of note, this is also not a risk that has been reported with the use of PRP with microneedling procedures, where PRP is placed on top of the skin before, during and after microneedling.
Anything that occludes the blood supply to the eye, whether it be fat, filler, or PRP, has an inherent risk of blindness. As there is no reversal agent or designated treatment for PRP occlusion, care must be taken to minimize risk, including awareness of anatomy and avoidance of injection into high risk areas, and cannula use where appropriate. Gentle, slow, low-volume administration, and when possible, use of a retrograde injection technique, may also be helpful.
Dr. Wesley and Lily Talakoub, MD, are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
A systematic review was recently conducted by Wu and colleagues examining the risk of blindness associated with platelet-rich plasma (PRP) injection. In dermatology, PRP is used more commonly now than 5 years ago to promote hair growth with injections on the scalp, as an adjunct to microneedling procedures, and sometimes – in a similar way to facial fillers – to improve volume loss, and skin tone and texture (particularly to the tear trough region).
Total unilateral blindness occurred in all cases. In one of the seven reported cases, the patient experienced recovery of vision after 3 months, but with some residual deficits noted on the ophthalmologist examination. In this case, the patient was evaluated and treated by an ophthalmologist within 3 hours of symptom onset.
In addition, four cases were reported from Venezuela, one from the United States, one from the United Kingdom, and one from Malaysia. Similar to reports of blindness with facial fillers, the most common injection site reported with this adverse effect was the glabella (five cases);
Other reports involved injections of the forehead (two), followed by the nasolabial fold (one), lateral canthus (one), and temporomandibular joint (one). Two of the seven patients received injections at more than one site, resulting in the total number of injections reported (10) being higher than the number of patients.
The risk of blindness is inherent with deep injection into a vessel that anastomoses with the blood supply to the eye. No mention was made as to whether PRP or platelet-rich fibrin was used. Other details are lacking from the original articles as to injection technique and whether or not cannula injection was used. No treatment was attempted in four of seven cases.
As plasma is native to the arteries and dissolves in the blood stream naturally, the mechanism as to why retinal artery occlusion or blindness would occur is not completely clear. One theory is that it is volume related and results from the speed of injection, causing a large rapid bolus that temporarily occludes or compresses an involved vessel.
Another theory is that damage to the vessel results from the injection itself or injection technique, leading to a clotting cascade and clot of the involved vessel with subsequent retrograde flow or blockade of the retinal artery. But if this were the case, we would expect to hear about more cases of clots leading to vascular occlusion or skin necrosis, which does not typically occur or we do not hear about.
Details about proper collection materials and technique or mixing with some other materials are also unknown in these cases, thus leaving the possibility that a more occlusive material may have been injected, as opposed to the fluid-like composition of the typical PRP preparation.With regards to risk with scalp PRP injection, the frontal scalp does receive blood supply from the supratrochlear artery that anastomoses with the angular artery of the face – both of which anastomose with the retinal artery (where occlusion would occur via back flow). The scalp tributaries are small and far enough away from the retina at that point that risk of back flow the to retinal artery should be minimal. Additionally, no reports of vascular occlusion from PRP scalp injection leading to skin necrosis have ever been reported. Of note, this is also not a risk that has been reported with the use of PRP with microneedling procedures, where PRP is placed on top of the skin before, during and after microneedling.
Anything that occludes the blood supply to the eye, whether it be fat, filler, or PRP, has an inherent risk of blindness. As there is no reversal agent or designated treatment for PRP occlusion, care must be taken to minimize risk, including awareness of anatomy and avoidance of injection into high risk areas, and cannula use where appropriate. Gentle, slow, low-volume administration, and when possible, use of a retrograde injection technique, may also be helpful.
Dr. Wesley and Lily Talakoub, MD, are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
A systematic review was recently conducted by Wu and colleagues examining the risk of blindness associated with platelet-rich plasma (PRP) injection. In dermatology, PRP is used more commonly now than 5 years ago to promote hair growth with injections on the scalp, as an adjunct to microneedling procedures, and sometimes – in a similar way to facial fillers – to improve volume loss, and skin tone and texture (particularly to the tear trough region).
Total unilateral blindness occurred in all cases. In one of the seven reported cases, the patient experienced recovery of vision after 3 months, but with some residual deficits noted on the ophthalmologist examination. In this case, the patient was evaluated and treated by an ophthalmologist within 3 hours of symptom onset.
In addition, four cases were reported from Venezuela, one from the United States, one from the United Kingdom, and one from Malaysia. Similar to reports of blindness with facial fillers, the most common injection site reported with this adverse effect was the glabella (five cases);
Other reports involved injections of the forehead (two), followed by the nasolabial fold (one), lateral canthus (one), and temporomandibular joint (one). Two of the seven patients received injections at more than one site, resulting in the total number of injections reported (10) being higher than the number of patients.
The risk of blindness is inherent with deep injection into a vessel that anastomoses with the blood supply to the eye. No mention was made as to whether PRP or platelet-rich fibrin was used. Other details are lacking from the original articles as to injection technique and whether or not cannula injection was used. No treatment was attempted in four of seven cases.
As plasma is native to the arteries and dissolves in the blood stream naturally, the mechanism as to why retinal artery occlusion or blindness would occur is not completely clear. One theory is that it is volume related and results from the speed of injection, causing a large rapid bolus that temporarily occludes or compresses an involved vessel.
Another theory is that damage to the vessel results from the injection itself or injection technique, leading to a clotting cascade and clot of the involved vessel with subsequent retrograde flow or blockade of the retinal artery. But if this were the case, we would expect to hear about more cases of clots leading to vascular occlusion or skin necrosis, which does not typically occur or we do not hear about.
Details about proper collection materials and technique or mixing with some other materials are also unknown in these cases, thus leaving the possibility that a more occlusive material may have been injected, as opposed to the fluid-like composition of the typical PRP preparation.With regards to risk with scalp PRP injection, the frontal scalp does receive blood supply from the supratrochlear artery that anastomoses with the angular artery of the face – both of which anastomose with the retinal artery (where occlusion would occur via back flow). The scalp tributaries are small and far enough away from the retina at that point that risk of back flow the to retinal artery should be minimal. Additionally, no reports of vascular occlusion from PRP scalp injection leading to skin necrosis have ever been reported. Of note, this is also not a risk that has been reported with the use of PRP with microneedling procedures, where PRP is placed on top of the skin before, during and after microneedling.
Anything that occludes the blood supply to the eye, whether it be fat, filler, or PRP, has an inherent risk of blindness. As there is no reversal agent or designated treatment for PRP occlusion, care must be taken to minimize risk, including awareness of anatomy and avoidance of injection into high risk areas, and cannula use where appropriate. Gentle, slow, low-volume administration, and when possible, use of a retrograde injection technique, may also be helpful.
Dr. Wesley and Lily Talakoub, MD, are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
Low-dose oral minoxidil for the treatment of alopecia
Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.
Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.
Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.
In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3
To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.
Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).
In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.
Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.
Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.
Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.
Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.
Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.
Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.
Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.
Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.
Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.
In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3
To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.
Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).
In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.
Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.
Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.
Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.
Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.
Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.
Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.
Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.
Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.
Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.
In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3
To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.
Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).
In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub had no relevant disclosures.
References
Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.
Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.
Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.
Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.
Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.
Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.
Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.
How does radiofrequency microneedling work?
Technology in the field of aesthetic dermatology continues to advance over time. Microneedling, largely used to improve textural changes of the skin associated with photoaging and acne scarring, has evolved over time from the use of dermarollers and microneedling skin pens to energy-based devices that deliver radiofrequency (RF) energy though microneedles that are used today.
.
Unlike prior radiofrequency energy-based devices that deliver radiofrequency energy on the skin surface to allow bulk thermal energy (or heat) to stimulate collagen remodeling and tissue tightening, RF microneedling devices deliver the same RF or thermal energy via needles. RF, measured in Hertz (Hz) is part of the electromagnetic spectrum, with most devices delivering thermal energy at around 1-2 MHz, which is less than most typical RF only devices (at around 4-6 MHz), but with potentially more precise depth and delivery. For comparison, the RF of household electrical currents are around 60 Hz; traditional electrosurgical units, 50Hz -300 kHz; AM radio, 500 KHz; and microwaves, 2500 MHz.
When delivered to the skin, RF energy produces a change in the electrical charge of the skin, resulting in movement of electrons. The impedance (or resistance) of the tissue to the electron movement is what generates heat. Different factors, including tissue thickness, pressure applied to the tissue, hydration, bipolar versus monopolar delivery, and the number of needles are several factors than can affect the impedance.
Bipolar RF means that the current passes between two electrodes, whereas monopolar RF means that the electrical current is between an active treatment electrode and a passive grounding electrode (or grounding pad typically placed on the patient’s back). With bipolar RF, the current is limited to the area between the two electrodes. The depth of penetration is half of the distance between the electrodes, thus resulting in shallow (but potentially more aggressive) tissue heating. With monopolar RF, deeper tissue penetration occurs that is also often less uncomfortable to the patient.
The desired result of the energy delivery is collagen remodeling and strengthening of elastin. RF microneedling and microneedling in general may also have potential for use in enhancing topical product delivery.
Depending on the device, settings can be tailored to affect the energy delivery, including the type of needle (insulated vs. uninsulated vs. semi-insulated), Hz, number of needles, depth of needles, and time of exposure. In general, insulated needle tips provide less heat accumulation and potential injury to the skin surface, whereas uninsulated needles allow for more heat accumulation. Insulated needles, longer time of exposure, and lower energies (Hz) are safer options for darker skin types and those who hyperpigment easily.
Immediately after treatment, expected clinical endpoints can include erythema, edema, and possibly pinpoint bleeding that may last approximately several days to 2 weeks depending on the intensity of treatment. Potential side effects include infection, pigmentary alteration, folliculitis, prolonged grid marks, and scarring. Contraindications to treatment include having a pacemaker, history of keloid formation, active skin infections, prior gold threads in the treatment area, pregnancy and breastfeeding, metal implants in the treatment area, embedded electronic devices that cannot be turned off, isotretinoin use in the past 6 months, and allergy to any of the components of treatment.
Caution should be taken with tattoos in the treatment area or grounding pad (including cosmetic tattoos as tattoo ink may often contain metals that may absorb some of the heat, increasing the risk for injury or extrusion of the ink), a history of cold sores or herpes simplex virus in the treatment area (if so, a prophylactic antiviral would be indicated prior to treatment), use of topical retinoids in the past 7 days, having received neurotoxin or fillers in the prior 2 weeks, autoimmune disease, bleeding disorders, neuropathy, and history of poor healing.
Depending on the device and area being treated, most RF microneedling treatments require two to five treatments, typically 4-6 weeks apart. If improvement is seen, it may be noticeable after one to two treatments, and as with laser resurfacing, continued improvement may be noticeable over the following 6-12 months post treatment.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. Dr. Wesley has no relevant disclosures.
Technology in the field of aesthetic dermatology continues to advance over time. Microneedling, largely used to improve textural changes of the skin associated with photoaging and acne scarring, has evolved over time from the use of dermarollers and microneedling skin pens to energy-based devices that deliver radiofrequency (RF) energy though microneedles that are used today.
.
Unlike prior radiofrequency energy-based devices that deliver radiofrequency energy on the skin surface to allow bulk thermal energy (or heat) to stimulate collagen remodeling and tissue tightening, RF microneedling devices deliver the same RF or thermal energy via needles. RF, measured in Hertz (Hz) is part of the electromagnetic spectrum, with most devices delivering thermal energy at around 1-2 MHz, which is less than most typical RF only devices (at around 4-6 MHz), but with potentially more precise depth and delivery. For comparison, the RF of household electrical currents are around 60 Hz; traditional electrosurgical units, 50Hz -300 kHz; AM radio, 500 KHz; and microwaves, 2500 MHz.
When delivered to the skin, RF energy produces a change in the electrical charge of the skin, resulting in movement of electrons. The impedance (or resistance) of the tissue to the electron movement is what generates heat. Different factors, including tissue thickness, pressure applied to the tissue, hydration, bipolar versus monopolar delivery, and the number of needles are several factors than can affect the impedance.
Bipolar RF means that the current passes between two electrodes, whereas monopolar RF means that the electrical current is between an active treatment electrode and a passive grounding electrode (or grounding pad typically placed on the patient’s back). With bipolar RF, the current is limited to the area between the two electrodes. The depth of penetration is half of the distance between the electrodes, thus resulting in shallow (but potentially more aggressive) tissue heating. With monopolar RF, deeper tissue penetration occurs that is also often less uncomfortable to the patient.
The desired result of the energy delivery is collagen remodeling and strengthening of elastin. RF microneedling and microneedling in general may also have potential for use in enhancing topical product delivery.
Depending on the device, settings can be tailored to affect the energy delivery, including the type of needle (insulated vs. uninsulated vs. semi-insulated), Hz, number of needles, depth of needles, and time of exposure. In general, insulated needle tips provide less heat accumulation and potential injury to the skin surface, whereas uninsulated needles allow for more heat accumulation. Insulated needles, longer time of exposure, and lower energies (Hz) are safer options for darker skin types and those who hyperpigment easily.
Immediately after treatment, expected clinical endpoints can include erythema, edema, and possibly pinpoint bleeding that may last approximately several days to 2 weeks depending on the intensity of treatment. Potential side effects include infection, pigmentary alteration, folliculitis, prolonged grid marks, and scarring. Contraindications to treatment include having a pacemaker, history of keloid formation, active skin infections, prior gold threads in the treatment area, pregnancy and breastfeeding, metal implants in the treatment area, embedded electronic devices that cannot be turned off, isotretinoin use in the past 6 months, and allergy to any of the components of treatment.
Caution should be taken with tattoos in the treatment area or grounding pad (including cosmetic tattoos as tattoo ink may often contain metals that may absorb some of the heat, increasing the risk for injury or extrusion of the ink), a history of cold sores or herpes simplex virus in the treatment area (if so, a prophylactic antiviral would be indicated prior to treatment), use of topical retinoids in the past 7 days, having received neurotoxin or fillers in the prior 2 weeks, autoimmune disease, bleeding disorders, neuropathy, and history of poor healing.
Depending on the device and area being treated, most RF microneedling treatments require two to five treatments, typically 4-6 weeks apart. If improvement is seen, it may be noticeable after one to two treatments, and as with laser resurfacing, continued improvement may be noticeable over the following 6-12 months post treatment.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. Dr. Wesley has no relevant disclosures.
Technology in the field of aesthetic dermatology continues to advance over time. Microneedling, largely used to improve textural changes of the skin associated with photoaging and acne scarring, has evolved over time from the use of dermarollers and microneedling skin pens to energy-based devices that deliver radiofrequency (RF) energy though microneedles that are used today.
.
Unlike prior radiofrequency energy-based devices that deliver radiofrequency energy on the skin surface to allow bulk thermal energy (or heat) to stimulate collagen remodeling and tissue tightening, RF microneedling devices deliver the same RF or thermal energy via needles. RF, measured in Hertz (Hz) is part of the electromagnetic spectrum, with most devices delivering thermal energy at around 1-2 MHz, which is less than most typical RF only devices (at around 4-6 MHz), but with potentially more precise depth and delivery. For comparison, the RF of household electrical currents are around 60 Hz; traditional electrosurgical units, 50Hz -300 kHz; AM radio, 500 KHz; and microwaves, 2500 MHz.
When delivered to the skin, RF energy produces a change in the electrical charge of the skin, resulting in movement of electrons. The impedance (or resistance) of the tissue to the electron movement is what generates heat. Different factors, including tissue thickness, pressure applied to the tissue, hydration, bipolar versus monopolar delivery, and the number of needles are several factors than can affect the impedance.
Bipolar RF means that the current passes between two electrodes, whereas monopolar RF means that the electrical current is between an active treatment electrode and a passive grounding electrode (or grounding pad typically placed on the patient’s back). With bipolar RF, the current is limited to the area between the two electrodes. The depth of penetration is half of the distance between the electrodes, thus resulting in shallow (but potentially more aggressive) tissue heating. With monopolar RF, deeper tissue penetration occurs that is also often less uncomfortable to the patient.
The desired result of the energy delivery is collagen remodeling and strengthening of elastin. RF microneedling and microneedling in general may also have potential for use in enhancing topical product delivery.
Depending on the device, settings can be tailored to affect the energy delivery, including the type of needle (insulated vs. uninsulated vs. semi-insulated), Hz, number of needles, depth of needles, and time of exposure. In general, insulated needle tips provide less heat accumulation and potential injury to the skin surface, whereas uninsulated needles allow for more heat accumulation. Insulated needles, longer time of exposure, and lower energies (Hz) are safer options for darker skin types and those who hyperpigment easily.
Immediately after treatment, expected clinical endpoints can include erythema, edema, and possibly pinpoint bleeding that may last approximately several days to 2 weeks depending on the intensity of treatment. Potential side effects include infection, pigmentary alteration, folliculitis, prolonged grid marks, and scarring. Contraindications to treatment include having a pacemaker, history of keloid formation, active skin infections, prior gold threads in the treatment area, pregnancy and breastfeeding, metal implants in the treatment area, embedded electronic devices that cannot be turned off, isotretinoin use in the past 6 months, and allergy to any of the components of treatment.
Caution should be taken with tattoos in the treatment area or grounding pad (including cosmetic tattoos as tattoo ink may often contain metals that may absorb some of the heat, increasing the risk for injury or extrusion of the ink), a history of cold sores or herpes simplex virus in the treatment area (if so, a prophylactic antiviral would be indicated prior to treatment), use of topical retinoids in the past 7 days, having received neurotoxin or fillers in the prior 2 weeks, autoimmune disease, bleeding disorders, neuropathy, and history of poor healing.
Depending on the device and area being treated, most RF microneedling treatments require two to five treatments, typically 4-6 weeks apart. If improvement is seen, it may be noticeable after one to two treatments, and as with laser resurfacing, continued improvement may be noticeable over the following 6-12 months post treatment.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. Dr. Wesley has no relevant disclosures.
Understanding filler reversal with hyaluronidase
Hyaluronic acid is the most common filler used in the United States for cosmetic procedures. . However, there has been little research and there are no formal clinical guidelines on its use. Hyaluronidase is approved by the Food and Drug Administration for several indications, but its use in cosmetic procedures is off-label.
Hyaluronic acid filler complications can be local and transient or delayed and/or dangerous. Local reactions generally improve over time or respond to symptomatic care. But granulomatous reactions, misplaced injection, adverse aesthetic outcomes, and vascular occlusion are some of the detrimental outcomes that require immediate treatment, often using hyaluronidase, a naturally occurring enzyme that degrades hyaluronic acid.
Hyaluronic acid products vary in concentration, cross-linking, type of cross-linker used, and particle size, and therefore display different degradation patterns with hyaluronidase. The three hyaluronidase products available also vary in concentration, source, and enzyme activity. Hyaluronidase has a half-life of 2 minutes but has a duration of action of 24-48 hours depending on the product used.
In an interesting study by Casabona G et al., the dose and activity of five hyaluronidase products available worldwide were used to degrade five different fillers (Juvederm Volbella, Voluma, and Ultraplus; Belotero, and Belotero Balance) with various concentrations and cross-linking in human skin. The results showed that the Vycross products (Juvederm Voluma) are the least sensitive to hyaluronidase and require the greatest concentration of hyaluronidase and a longer time for dissolution requiring up to three times more hyaluronidase to degrade the same volume of other hyaluronic acid products.
In addition, the ovine hyaluronidase product marketed in the United States as Vitrase had the greatest activity against the range of hyaluronic acids used in the trial. Higher concentrations of hyaluronidase also could produce type-I hypersensitivity reactions and angioedema in susceptible patients as evidenced by eosinophilic tissue reactions at concentrations greater than 300 IU.
Hyaluronidase is stored at cool temperatures (35-46° F). It can be reconstituted with saline, water, or bacteriostatic saline for reducing injection site pain; however, it should not be mixed with local anesthetic. The volume of diluent used depends on the surface area treated and ranges from 1 mL to 10 mL. Smaller volumes are used for more concentrated local injection and larger volumes for more precise dosing.
For impending necrosis, hyaluronidase should be used within minutes to hours of blanching of the skin and the area should be flooded every 30 minutes until the tissue has reperfused. Depending on the type of filler used, the volume of injection varies and the area should continually be injected and tissue response observed. A high-dosed large-volume protocol allows the tissue perfusion to gradually infiltrate the vessel walls. Recommendations are 2 mL of bacteriostatic saline diluted with a vial of hyaluronidase. Retrobulbar injection of hyaluronidase within minutes of retinal artery occlusion in doses of 150-200 units in 2-4 mL of diluent into the inferolateral orbit by an experienced ophthalmologist or oculoplastic surgeon is recommended.
Although there is no consensus, there are various clinical studies using hyaluronidase dilutions varying between 5 and 30 units to break down 0.1mg/mL of hyaluronic acid for the reversal of facial hyaluronic acid fillers. In my clinical experience, the recommendation is that, apart from necrosis, the concentration used is titrated to clinical efficacy, which can also be done over multiple appointments every 48 hours until the desired outcome is achieved.
Complications from hyaluronidase injection include local tissue erythema, edema, pain, allergic reactions, and anaphylaxis. An intradermal patch test of 10-20 units of hyaluronidase in the forearm can be done in patients with a history of allergy to hyaluronidase, which, in people with sensitivity, results in a wheal within 30 minutes of injection. If a patient has a positive patch test, hyaluronidase cannot be used. In addition, a history of allergic reactions to bees may pose a heightened reaction to hyaluronidase and is a contraindication to use.
It is recommended that any practitioner using hyaluronic acid fillers keep 2-3 vials of hyaluronidase available at all times in the event of a vascular emergency. Stability, storage, and expiration dates should also be monitored closely.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub has no relevant disclosures.
References
Casabona G et al. Dermatol Surg. 2018 Nov;44 Suppl 1:S42-S50.
DeLorenzi C. Aesthet Surg J. 2017 Jul 1;37(7):814-25.
Juhász MLW et al. Dermatol Surg. 2017 Jun;43(6):841-7.
King M. J Clin Aesthet Dermatol. 2016 Nov; 9(11):E6–8.
Kim M et al. J Clin Aesthet Dermatol. 2018 Jun;11(6):E61-8.
Hyaluronic acid is the most common filler used in the United States for cosmetic procedures. . However, there has been little research and there are no formal clinical guidelines on its use. Hyaluronidase is approved by the Food and Drug Administration for several indications, but its use in cosmetic procedures is off-label.
Hyaluronic acid filler complications can be local and transient or delayed and/or dangerous. Local reactions generally improve over time or respond to symptomatic care. But granulomatous reactions, misplaced injection, adverse aesthetic outcomes, and vascular occlusion are some of the detrimental outcomes that require immediate treatment, often using hyaluronidase, a naturally occurring enzyme that degrades hyaluronic acid.
Hyaluronic acid products vary in concentration, cross-linking, type of cross-linker used, and particle size, and therefore display different degradation patterns with hyaluronidase. The three hyaluronidase products available also vary in concentration, source, and enzyme activity. Hyaluronidase has a half-life of 2 minutes but has a duration of action of 24-48 hours depending on the product used.
In an interesting study by Casabona G et al., the dose and activity of five hyaluronidase products available worldwide were used to degrade five different fillers (Juvederm Volbella, Voluma, and Ultraplus; Belotero, and Belotero Balance) with various concentrations and cross-linking in human skin. The results showed that the Vycross products (Juvederm Voluma) are the least sensitive to hyaluronidase and require the greatest concentration of hyaluronidase and a longer time for dissolution requiring up to three times more hyaluronidase to degrade the same volume of other hyaluronic acid products.
In addition, the ovine hyaluronidase product marketed in the United States as Vitrase had the greatest activity against the range of hyaluronic acids used in the trial. Higher concentrations of hyaluronidase also could produce type-I hypersensitivity reactions and angioedema in susceptible patients as evidenced by eosinophilic tissue reactions at concentrations greater than 300 IU.
Hyaluronidase is stored at cool temperatures (35-46° F). It can be reconstituted with saline, water, or bacteriostatic saline for reducing injection site pain; however, it should not be mixed with local anesthetic. The volume of diluent used depends on the surface area treated and ranges from 1 mL to 10 mL. Smaller volumes are used for more concentrated local injection and larger volumes for more precise dosing.
For impending necrosis, hyaluronidase should be used within minutes to hours of blanching of the skin and the area should be flooded every 30 minutes until the tissue has reperfused. Depending on the type of filler used, the volume of injection varies and the area should continually be injected and tissue response observed. A high-dosed large-volume protocol allows the tissue perfusion to gradually infiltrate the vessel walls. Recommendations are 2 mL of bacteriostatic saline diluted with a vial of hyaluronidase. Retrobulbar injection of hyaluronidase within minutes of retinal artery occlusion in doses of 150-200 units in 2-4 mL of diluent into the inferolateral orbit by an experienced ophthalmologist or oculoplastic surgeon is recommended.
Although there is no consensus, there are various clinical studies using hyaluronidase dilutions varying between 5 and 30 units to break down 0.1mg/mL of hyaluronic acid for the reversal of facial hyaluronic acid fillers. In my clinical experience, the recommendation is that, apart from necrosis, the concentration used is titrated to clinical efficacy, which can also be done over multiple appointments every 48 hours until the desired outcome is achieved.
Complications from hyaluronidase injection include local tissue erythema, edema, pain, allergic reactions, and anaphylaxis. An intradermal patch test of 10-20 units of hyaluronidase in the forearm can be done in patients with a history of allergy to hyaluronidase, which, in people with sensitivity, results in a wheal within 30 minutes of injection. If a patient has a positive patch test, hyaluronidase cannot be used. In addition, a history of allergic reactions to bees may pose a heightened reaction to hyaluronidase and is a contraindication to use.
It is recommended that any practitioner using hyaluronic acid fillers keep 2-3 vials of hyaluronidase available at all times in the event of a vascular emergency. Stability, storage, and expiration dates should also be monitored closely.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub has no relevant disclosures.
References
Casabona G et al. Dermatol Surg. 2018 Nov;44 Suppl 1:S42-S50.
DeLorenzi C. Aesthet Surg J. 2017 Jul 1;37(7):814-25.
Juhász MLW et al. Dermatol Surg. 2017 Jun;43(6):841-7.
King M. J Clin Aesthet Dermatol. 2016 Nov; 9(11):E6–8.
Kim M et al. J Clin Aesthet Dermatol. 2018 Jun;11(6):E61-8.
Hyaluronic acid is the most common filler used in the United States for cosmetic procedures. . However, there has been little research and there are no formal clinical guidelines on its use. Hyaluronidase is approved by the Food and Drug Administration for several indications, but its use in cosmetic procedures is off-label.
Hyaluronic acid filler complications can be local and transient or delayed and/or dangerous. Local reactions generally improve over time or respond to symptomatic care. But granulomatous reactions, misplaced injection, adverse aesthetic outcomes, and vascular occlusion are some of the detrimental outcomes that require immediate treatment, often using hyaluronidase, a naturally occurring enzyme that degrades hyaluronic acid.
Hyaluronic acid products vary in concentration, cross-linking, type of cross-linker used, and particle size, and therefore display different degradation patterns with hyaluronidase. The three hyaluronidase products available also vary in concentration, source, and enzyme activity. Hyaluronidase has a half-life of 2 minutes but has a duration of action of 24-48 hours depending on the product used.
In an interesting study by Casabona G et al., the dose and activity of five hyaluronidase products available worldwide were used to degrade five different fillers (Juvederm Volbella, Voluma, and Ultraplus; Belotero, and Belotero Balance) with various concentrations and cross-linking in human skin. The results showed that the Vycross products (Juvederm Voluma) are the least sensitive to hyaluronidase and require the greatest concentration of hyaluronidase and a longer time for dissolution requiring up to three times more hyaluronidase to degrade the same volume of other hyaluronic acid products.
In addition, the ovine hyaluronidase product marketed in the United States as Vitrase had the greatest activity against the range of hyaluronic acids used in the trial. Higher concentrations of hyaluronidase also could produce type-I hypersensitivity reactions and angioedema in susceptible patients as evidenced by eosinophilic tissue reactions at concentrations greater than 300 IU.
Hyaluronidase is stored at cool temperatures (35-46° F). It can be reconstituted with saline, water, or bacteriostatic saline for reducing injection site pain; however, it should not be mixed with local anesthetic. The volume of diluent used depends on the surface area treated and ranges from 1 mL to 10 mL. Smaller volumes are used for more concentrated local injection and larger volumes for more precise dosing.
For impending necrosis, hyaluronidase should be used within minutes to hours of blanching of the skin and the area should be flooded every 30 minutes until the tissue has reperfused. Depending on the type of filler used, the volume of injection varies and the area should continually be injected and tissue response observed. A high-dosed large-volume protocol allows the tissue perfusion to gradually infiltrate the vessel walls. Recommendations are 2 mL of bacteriostatic saline diluted with a vial of hyaluronidase. Retrobulbar injection of hyaluronidase within minutes of retinal artery occlusion in doses of 150-200 units in 2-4 mL of diluent into the inferolateral orbit by an experienced ophthalmologist or oculoplastic surgeon is recommended.
Although there is no consensus, there are various clinical studies using hyaluronidase dilutions varying between 5 and 30 units to break down 0.1mg/mL of hyaluronic acid for the reversal of facial hyaluronic acid fillers. In my clinical experience, the recommendation is that, apart from necrosis, the concentration used is titrated to clinical efficacy, which can also be done over multiple appointments every 48 hours until the desired outcome is achieved.
Complications from hyaluronidase injection include local tissue erythema, edema, pain, allergic reactions, and anaphylaxis. An intradermal patch test of 10-20 units of hyaluronidase in the forearm can be done in patients with a history of allergy to hyaluronidase, which, in people with sensitivity, results in a wheal within 30 minutes of injection. If a patient has a positive patch test, hyaluronidase cannot be used. In addition, a history of allergic reactions to bees may pose a heightened reaction to hyaluronidase and is a contraindication to use.
It is recommended that any practitioner using hyaluronic acid fillers keep 2-3 vials of hyaluronidase available at all times in the event of a vascular emergency. Stability, storage, and expiration dates should also be monitored closely.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at dermnews@mdedge.com. Dr. Talakoub has no relevant disclosures.
References
Casabona G et al. Dermatol Surg. 2018 Nov;44 Suppl 1:S42-S50.
DeLorenzi C. Aesthet Surg J. 2017 Jul 1;37(7):814-25.
Juhász MLW et al. Dermatol Surg. 2017 Jun;43(6):841-7.
King M. J Clin Aesthet Dermatol. 2016 Nov; 9(11):E6–8.
Kim M et al. J Clin Aesthet Dermatol. 2018 Jun;11(6):E61-8.
20th anniversary and history of cosmetic botulinum toxin type A
The timeline of botulinum toxin discovery began with deadly outbreaks related to contaminated food across Europe in the late 1700s, the largest of which occurred in 1793 in Wildebrad, in southern Germany. In 1811, “prussic acid” was named as the culprit in what was referred to as sausage poisoning. Between 1817 and 1822, German physician Justinus Kerner noted that the active substance interrupted signals from motor nerves to muscles, but spared sensory and cognitive abilities, accurately describing botulism. He hypothesized that this substance could possibly be used as treatment for medical conditions when ingested orally. It wasn’t until 1895 that microbiologist Emile Pierre Van Ermengem, a professor of bacteriology in Belgium, identified the bacterium responsible as Bacillus botulinus, later renamed C. botulinum.
In 1905, it was discovered that C. botulinum produced a substance that affected neurotransmitter function, and between 1895 and 1915, seven toxin serotypes were recognized. In 1928, Herman Sommer, PhD, at the Hooper Foundation, at the University of California, San Francisco, isolated the most potent serotype: botulinum toxin type A (BoNT-A).
In 1946, Carl Lamanna and James Duff developed concentration and crystallization techniques that were subsequently used by Edward Schantz, PhD, at Fort Detrick, Md., for a possible biologic weapon. In 1972, Dr. Schantz took his research to the University of Wisconsin, where he produced a large batch of BoNT-A that remained in clinical use until December 1997.
In the late 1960s and early 1970s, an ophthalmologist in San Francisco, Alan Scott, MD, began animal studies with BoNT-A supplied by Dr. Schantz, as a possible treatment for strabismus, publishing his first report of BoNT-A in primates in 1973. In 1978, the Food and Drug Administration granted approval to begin testing small amounts of the toxin in human volunteers. In 1980, a landmark paper was published demonstrating that BoNT-A corrects gaze misalignment in humans. By 1989, it was approved as Oculinum by the FDA for the treatment of strabismus and blepharospasm.
Keen clinical observation and a serendipitous discovery led to botulinum toxin’s first uses for cosmetic purposes. In the mid-1980s, Jean Carruthers, MD, an ophthalmologist in Vancouver, noted an unexpected concomitant improvement of glabellar rhytids in a patient treated with BoNT for blepharospasm. The result of the treatment was a more serene, untroubled expression. Dr. Carruthers discussed the observation with her dermatologist spouse, Alastair Carruthers, MD, who was attempting to use soft tissue–augmenting agents available at the time to soften forehead wrinkles. Intrigued by the possibilities, the Carruthers subsequently injected a small amount of BoNT-A between the eyebrows of their assistant, Cathy Bickerton Swann, also now known as “patient zero” and awaited the results.
Seventeen additional patients followed, aged 34-51, who collectively, would become part of the first report on the efficacy of BoNT-A for cosmetic use – for the treatment of glabellar frown lines – published in 1992.
Between 1992 and 1997, the popularity of off-label use of BoNT-A grew so rapidly that Allergan’s supply temporarily ran out. By 2002, safety and efficacy profiles of use in medical conditions such as strabismus, blepharospasm, hemifacial spasm, cervical dystonia, cerebral palsy, poststroke spasticity, hyperhidrosis, headache, and back pain had been well-established, facilitating the comfort and use for cosmetic purposes.
By 2002, open-label studies of more than 800 patients confirmed the efficacy and safety of BoNT for the treatment of dynamic facial rhytids. And in April 2002, the FDA granted approval of BoNT for the nonsurgical reduction of glabellar rhytids. The rest, some would say, is history. On this 20th-year anniversary of the approval of botulinum toxin for cosmetic use, special recognition is given here for the physicians and scientists who were astute enough to make this discovery, as botulinum toxin use remains one of the most popular and effective nonsurgical cosmetic procedures today.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. Dr. Wesley disclosed that she has been a clinical investigator and consultant for Botox manufacturer Allergan in the past, and manufacturers of other brands of botulinum toxins available for cosmetic use; Dysport (Galderma), Xeomin (Merz), and Jeuveau (Evolus). Dr. Talakoub had no disclosures.
Reference
“Botulinum Toxin: Procedures in Cosmetic Dermatology Series 3rd Edition” (Philadelphia: Saunders Elsevier, 2013)
The timeline of botulinum toxin discovery began with deadly outbreaks related to contaminated food across Europe in the late 1700s, the largest of which occurred in 1793 in Wildebrad, in southern Germany. In 1811, “prussic acid” was named as the culprit in what was referred to as sausage poisoning. Between 1817 and 1822, German physician Justinus Kerner noted that the active substance interrupted signals from motor nerves to muscles, but spared sensory and cognitive abilities, accurately describing botulism. He hypothesized that this substance could possibly be used as treatment for medical conditions when ingested orally. It wasn’t until 1895 that microbiologist Emile Pierre Van Ermengem, a professor of bacteriology in Belgium, identified the bacterium responsible as Bacillus botulinus, later renamed C. botulinum.
In 1905, it was discovered that C. botulinum produced a substance that affected neurotransmitter function, and between 1895 and 1915, seven toxin serotypes were recognized. In 1928, Herman Sommer, PhD, at the Hooper Foundation, at the University of California, San Francisco, isolated the most potent serotype: botulinum toxin type A (BoNT-A).
In 1946, Carl Lamanna and James Duff developed concentration and crystallization techniques that were subsequently used by Edward Schantz, PhD, at Fort Detrick, Md., for a possible biologic weapon. In 1972, Dr. Schantz took his research to the University of Wisconsin, where he produced a large batch of BoNT-A that remained in clinical use until December 1997.
In the late 1960s and early 1970s, an ophthalmologist in San Francisco, Alan Scott, MD, began animal studies with BoNT-A supplied by Dr. Schantz, as a possible treatment for strabismus, publishing his first report of BoNT-A in primates in 1973. In 1978, the Food and Drug Administration granted approval to begin testing small amounts of the toxin in human volunteers. In 1980, a landmark paper was published demonstrating that BoNT-A corrects gaze misalignment in humans. By 1989, it was approved as Oculinum by the FDA for the treatment of strabismus and blepharospasm.
Keen clinical observation and a serendipitous discovery led to botulinum toxin’s first uses for cosmetic purposes. In the mid-1980s, Jean Carruthers, MD, an ophthalmologist in Vancouver, noted an unexpected concomitant improvement of glabellar rhytids in a patient treated with BoNT for blepharospasm. The result of the treatment was a more serene, untroubled expression. Dr. Carruthers discussed the observation with her dermatologist spouse, Alastair Carruthers, MD, who was attempting to use soft tissue–augmenting agents available at the time to soften forehead wrinkles. Intrigued by the possibilities, the Carruthers subsequently injected a small amount of BoNT-A between the eyebrows of their assistant, Cathy Bickerton Swann, also now known as “patient zero” and awaited the results.
Seventeen additional patients followed, aged 34-51, who collectively, would become part of the first report on the efficacy of BoNT-A for cosmetic use – for the treatment of glabellar frown lines – published in 1992.
Between 1992 and 1997, the popularity of off-label use of BoNT-A grew so rapidly that Allergan’s supply temporarily ran out. By 2002, safety and efficacy profiles of use in medical conditions such as strabismus, blepharospasm, hemifacial spasm, cervical dystonia, cerebral palsy, poststroke spasticity, hyperhidrosis, headache, and back pain had been well-established, facilitating the comfort and use for cosmetic purposes.
By 2002, open-label studies of more than 800 patients confirmed the efficacy and safety of BoNT for the treatment of dynamic facial rhytids. And in April 2002, the FDA granted approval of BoNT for the nonsurgical reduction of glabellar rhytids. The rest, some would say, is history. On this 20th-year anniversary of the approval of botulinum toxin for cosmetic use, special recognition is given here for the physicians and scientists who were astute enough to make this discovery, as botulinum toxin use remains one of the most popular and effective nonsurgical cosmetic procedures today.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. Dr. Wesley disclosed that she has been a clinical investigator and consultant for Botox manufacturer Allergan in the past, and manufacturers of other brands of botulinum toxins available for cosmetic use; Dysport (Galderma), Xeomin (Merz), and Jeuveau (Evolus). Dr. Talakoub had no disclosures.
Reference
“Botulinum Toxin: Procedures in Cosmetic Dermatology Series 3rd Edition” (Philadelphia: Saunders Elsevier, 2013)
The timeline of botulinum toxin discovery began with deadly outbreaks related to contaminated food across Europe in the late 1700s, the largest of which occurred in 1793 in Wildebrad, in southern Germany. In 1811, “prussic acid” was named as the culprit in what was referred to as sausage poisoning. Between 1817 and 1822, German physician Justinus Kerner noted that the active substance interrupted signals from motor nerves to muscles, but spared sensory and cognitive abilities, accurately describing botulism. He hypothesized that this substance could possibly be used as treatment for medical conditions when ingested orally. It wasn’t until 1895 that microbiologist Emile Pierre Van Ermengem, a professor of bacteriology in Belgium, identified the bacterium responsible as Bacillus botulinus, later renamed C. botulinum.
In 1905, it was discovered that C. botulinum produced a substance that affected neurotransmitter function, and between 1895 and 1915, seven toxin serotypes were recognized. In 1928, Herman Sommer, PhD, at the Hooper Foundation, at the University of California, San Francisco, isolated the most potent serotype: botulinum toxin type A (BoNT-A).
In 1946, Carl Lamanna and James Duff developed concentration and crystallization techniques that were subsequently used by Edward Schantz, PhD, at Fort Detrick, Md., for a possible biologic weapon. In 1972, Dr. Schantz took his research to the University of Wisconsin, where he produced a large batch of BoNT-A that remained in clinical use until December 1997.
In the late 1960s and early 1970s, an ophthalmologist in San Francisco, Alan Scott, MD, began animal studies with BoNT-A supplied by Dr. Schantz, as a possible treatment for strabismus, publishing his first report of BoNT-A in primates in 1973. In 1978, the Food and Drug Administration granted approval to begin testing small amounts of the toxin in human volunteers. In 1980, a landmark paper was published demonstrating that BoNT-A corrects gaze misalignment in humans. By 1989, it was approved as Oculinum by the FDA for the treatment of strabismus and blepharospasm.
Keen clinical observation and a serendipitous discovery led to botulinum toxin’s first uses for cosmetic purposes. In the mid-1980s, Jean Carruthers, MD, an ophthalmologist in Vancouver, noted an unexpected concomitant improvement of glabellar rhytids in a patient treated with BoNT for blepharospasm. The result of the treatment was a more serene, untroubled expression. Dr. Carruthers discussed the observation with her dermatologist spouse, Alastair Carruthers, MD, who was attempting to use soft tissue–augmenting agents available at the time to soften forehead wrinkles. Intrigued by the possibilities, the Carruthers subsequently injected a small amount of BoNT-A between the eyebrows of their assistant, Cathy Bickerton Swann, also now known as “patient zero” and awaited the results.
Seventeen additional patients followed, aged 34-51, who collectively, would become part of the first report on the efficacy of BoNT-A for cosmetic use – for the treatment of glabellar frown lines – published in 1992.
Between 1992 and 1997, the popularity of off-label use of BoNT-A grew so rapidly that Allergan’s supply temporarily ran out. By 2002, safety and efficacy profiles of use in medical conditions such as strabismus, blepharospasm, hemifacial spasm, cervical dystonia, cerebral palsy, poststroke spasticity, hyperhidrosis, headache, and back pain had been well-established, facilitating the comfort and use for cosmetic purposes.
By 2002, open-label studies of more than 800 patients confirmed the efficacy and safety of BoNT for the treatment of dynamic facial rhytids. And in April 2002, the FDA granted approval of BoNT for the nonsurgical reduction of glabellar rhytids. The rest, some would say, is history. On this 20th-year anniversary of the approval of botulinum toxin for cosmetic use, special recognition is given here for the physicians and scientists who were astute enough to make this discovery, as botulinum toxin use remains one of the most popular and effective nonsurgical cosmetic procedures today.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. Dr. Wesley disclosed that she has been a clinical investigator and consultant for Botox manufacturer Allergan in the past, and manufacturers of other brands of botulinum toxins available for cosmetic use; Dysport (Galderma), Xeomin (Merz), and Jeuveau (Evolus). Dr. Talakoub had no disclosures.
Reference
“Botulinum Toxin: Procedures in Cosmetic Dermatology Series 3rd Edition” (Philadelphia: Saunders Elsevier, 2013)
Acid series: Trichloroacetic acid
– yet can be one of the most dangerous treatments in the hands of an untrained user.
TCA, in a clear colorless solution, is available in concentrations up to 100%, and has not been associated with allergic reactions or systemic toxicity. The available concentrations include those used for superficial depth peels (10%-30%), medium depth peels (35%-50%), and deep peels (greater than 50%).
TCA causes coagulation of the cellular membrane of epidermal proteins in the epidermis and, depending on the concentration, the dermis, which results in frosting of the skin. Repair of the epidermal cells induces resurfacing of the skin and neocollagenesis. TCA can be combined with other acids, including glycolic acid (Coleman peel), Jessner solution (Monheit peel), and solid CO2 (Brody peel). It has also been combined with lactic acid, mandelic acid, and salicylic acid in combination peels of various concentrations.
Although there are many studies, case reports, and textbooks related to this topic and the applications, combinations and treatment options for TCA peels, it is important to highlight here how many of these solutions – at high concentrations – are available directly to consumers, med spas, and the general public through online websites, including Amazon and overseas sites. Over the last 15 years, I have seen complications of this acid alone in people who have bought TCA online, related to applications not just on the face but on the body, neck, eyes, vaginal, and anal areas. Pigmentation, erosions, ulcers, and strictures are just some of the possible complications that occur not just with a more concentrated solution, but more often from application errors, aggressive layering of the acid, allowing the acid to sit on the skin too long, and improper tissue prepping and posttreatment skin care.
TCA can be an untamable acid, with little control over the depth of penetration even in the most controlled situations. The inability to be neutralize TCA creates an environment in which the depth of penetration and tissue coagulation is not a precise science. Once applied, the tissue reaction cannot be “stopped” or rapidly reversed making it highly variable in its mechanism. Patients of all skin types have the potential to develop complications as the epidermal and dermal thickness, moisture content, sebum production, and pigmentation are highly varied between individuals.
In my opinion, it is a dangerous product to have on the market – not just for the untrained medical providers using it but for estheticians and the general public who now can buy TCA anywhere.
But with effective training, reliable sourcing and appropriate preparation of the patient’s skin, however, a TCA peel can be a highly effective tool for difficult-to-treat dermatological problems, such as scarring and xanthelasma.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. She has no relevant disclosures. Write to them at dermnews@mdedge.com.
– yet can be one of the most dangerous treatments in the hands of an untrained user.
TCA, in a clear colorless solution, is available in concentrations up to 100%, and has not been associated with allergic reactions or systemic toxicity. The available concentrations include those used for superficial depth peels (10%-30%), medium depth peels (35%-50%), and deep peels (greater than 50%).
TCA causes coagulation of the cellular membrane of epidermal proteins in the epidermis and, depending on the concentration, the dermis, which results in frosting of the skin. Repair of the epidermal cells induces resurfacing of the skin and neocollagenesis. TCA can be combined with other acids, including glycolic acid (Coleman peel), Jessner solution (Monheit peel), and solid CO2 (Brody peel). It has also been combined with lactic acid, mandelic acid, and salicylic acid in combination peels of various concentrations.
Although there are many studies, case reports, and textbooks related to this topic and the applications, combinations and treatment options for TCA peels, it is important to highlight here how many of these solutions – at high concentrations – are available directly to consumers, med spas, and the general public through online websites, including Amazon and overseas sites. Over the last 15 years, I have seen complications of this acid alone in people who have bought TCA online, related to applications not just on the face but on the body, neck, eyes, vaginal, and anal areas. Pigmentation, erosions, ulcers, and strictures are just some of the possible complications that occur not just with a more concentrated solution, but more often from application errors, aggressive layering of the acid, allowing the acid to sit on the skin too long, and improper tissue prepping and posttreatment skin care.
TCA can be an untamable acid, with little control over the depth of penetration even in the most controlled situations. The inability to be neutralize TCA creates an environment in which the depth of penetration and tissue coagulation is not a precise science. Once applied, the tissue reaction cannot be “stopped” or rapidly reversed making it highly variable in its mechanism. Patients of all skin types have the potential to develop complications as the epidermal and dermal thickness, moisture content, sebum production, and pigmentation are highly varied between individuals.
In my opinion, it is a dangerous product to have on the market – not just for the untrained medical providers using it but for estheticians and the general public who now can buy TCA anywhere.
But with effective training, reliable sourcing and appropriate preparation of the patient’s skin, however, a TCA peel can be a highly effective tool for difficult-to-treat dermatological problems, such as scarring and xanthelasma.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. She has no relevant disclosures. Write to them at dermnews@mdedge.com.
– yet can be one of the most dangerous treatments in the hands of an untrained user.
TCA, in a clear colorless solution, is available in concentrations up to 100%, and has not been associated with allergic reactions or systemic toxicity. The available concentrations include those used for superficial depth peels (10%-30%), medium depth peels (35%-50%), and deep peels (greater than 50%).
TCA causes coagulation of the cellular membrane of epidermal proteins in the epidermis and, depending on the concentration, the dermis, which results in frosting of the skin. Repair of the epidermal cells induces resurfacing of the skin and neocollagenesis. TCA can be combined with other acids, including glycolic acid (Coleman peel), Jessner solution (Monheit peel), and solid CO2 (Brody peel). It has also been combined with lactic acid, mandelic acid, and salicylic acid in combination peels of various concentrations.
Although there are many studies, case reports, and textbooks related to this topic and the applications, combinations and treatment options for TCA peels, it is important to highlight here how many of these solutions – at high concentrations – are available directly to consumers, med spas, and the general public through online websites, including Amazon and overseas sites. Over the last 15 years, I have seen complications of this acid alone in people who have bought TCA online, related to applications not just on the face but on the body, neck, eyes, vaginal, and anal areas. Pigmentation, erosions, ulcers, and strictures are just some of the possible complications that occur not just with a more concentrated solution, but more often from application errors, aggressive layering of the acid, allowing the acid to sit on the skin too long, and improper tissue prepping and posttreatment skin care.
TCA can be an untamable acid, with little control over the depth of penetration even in the most controlled situations. The inability to be neutralize TCA creates an environment in which the depth of penetration and tissue coagulation is not a precise science. Once applied, the tissue reaction cannot be “stopped” or rapidly reversed making it highly variable in its mechanism. Patients of all skin types have the potential to develop complications as the epidermal and dermal thickness, moisture content, sebum production, and pigmentation are highly varied between individuals.
In my opinion, it is a dangerous product to have on the market – not just for the untrained medical providers using it but for estheticians and the general public who now can buy TCA anywhere.
But with effective training, reliable sourcing and appropriate preparation of the patient’s skin, however, a TCA peel can be a highly effective tool for difficult-to-treat dermatological problems, such as scarring and xanthelasma.
Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. She has no relevant disclosures. Write to them at dermnews@mdedge.com.
Mercury and other risks of cosmetic skin lighteners
Skin hyperpigmentation – whether it is caused by postinflammatory hyperpigmentation from acne or trauma to the skin, melasma, autoimmune disorders, or disorders of pigmentation – is a condition where treatment is commonly sought after in dermatology offices. Topical products used to fade hyperpigmented areas of the skin have long been used around the world, and because of safety concerns, regulations aimed at reducing potential harm or adverse effects caused by certain ingredients in these products are increasing in different countries.
For example, while extremely effective at treating most forms of hyperpigmentation, hydroquinone has been definitively linked to ochronosis, kojic acid has been linked to contact dermatitis in humans, and acid peels and retinoids are associated with irritant dermatitis, disruption of the skin barrier, and photosensitivity. In animal studies, licorice root extract has been linked to endocrine and other organ system irregularities.
Kojic acid was banned in Japan in 2003, and subsequently in South Korea and Switzerland because of concerns over animal studies indicating that its fungal metabolite might be carcinogenic (. Hydroquinone is classified as a drug and has been banned for use in cosmetic products in Japan, the European Union, Australia, and several African nations since at least 2006 because of concerns over adrenal gland dysregulation and high levels of mercury in hydroquinone products in those countries. In Africa specifically, South Africa banned all but 2% hydroquinone in 1983, the Ivory Coast banned all skin whitening creams in 2015, and in 2016, Ghana initiated a ban on certain skin products containing hydroquinone.
The United States followed suit in February 2020 with the Food and Drug Administration introducing a ban on all OTC hydroquinone-containing products because of concerns over carcinogenicity in animal studies (which has not been shown in human studies to date). The “Coronavirus Aid, Relief, and Economic Security” (CARES) Act signed in March 2020 then made the changes effective by halting the sale of OTC hydroquinone products in the United States as of September 2020.
Mercury concerns
Despite these bans, hydroquinone continues to be sold in cosmetics and OTC products around the world and online. And despite being banned or limited in these products, in particular. Mercury has been used in cosmetic products as a skin lightening agent (on its own) and as a preservative.
Mercury has been shown to be carcinogenic, neurotoxic, as well as cytotoxic to the renal and endocrine systems, causes reproductive toxicity, and may be bioaccumulative in wildlife and humans. There is particular concern regarding the risks of exposure in pregnant women and babies because of potential harm to the developing brain and nervous system. Initial signs and symptoms of mercury poisoning include irritability, shyness, tremors, changes in vision or hearing, memory problems, depression, numbness and tingling in the hands, feet, or around the mouth.
Organizations such as the Zero Mercury Working Group (ZMWG) – an international coalition of public interest environmental and health nongovernmental organizations from more than 55 countries, focused on eliminating the use, release, and exposure to mercury – have been working to help ensure safety and mercury levels are below the threshold deemed allowable in hydroquinone-containing products.
On March 10, the ZMWG published the results of a new study demonstrating that skin lighteners containing mercury are still being sold online, despite bans and safety concerns. Ebay, Amazon, Shopee, Jiji, and Flipkart are among the websites still selling high mercury–containing skin lightener products. Some of them were the same offenders selling the banned products in 2019. Of the 271 online products tested from 17 countries, nearly half contained over 1 ppm of mercury, which is the legal limit that has been established by most governments and the Minamata Convention on Mercury. Based on their packaging, the majority of these products were manufactured in Asia, most often in Pakistan (43%), Thailand (8%), China (6%), and Taiwan (4%), according to the report.
In ZMWG’s prior publications, mercury concentrations reported in some of these products ranged from 93 ppm to over 16,000 ppm. Even higher concentrations have been reported by other entities. And according to a World Health Organization November 2019 report, mercury-containing skin lightening products have been manufactured in many countries and areas, including Bangladesh, China, Dominican Republic Hong Kong SAR (China), Jamaica, Lebanon, Malaysia, Mexico, Pakistan, Philippines, Republic of Korea, Thailand, and the United States. According to the ZMWG, 137 countries have committed to the Minamata Convention to phase out and limit mercury, including in cosmetics.
Despite bans on some of these products, consumers in the United States and other countries with bans and restrictions are still at risk of exposure to mercury-containing skin lighteners because of online sales. Hopefully, the work of the ZMWG and similar entities will continue to help limit potentially harmful exposures to mercury, while maintaining access to safe and effective methods to treat hyperpigmentation.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
Skin hyperpigmentation – whether it is caused by postinflammatory hyperpigmentation from acne or trauma to the skin, melasma, autoimmune disorders, or disorders of pigmentation – is a condition where treatment is commonly sought after in dermatology offices. Topical products used to fade hyperpigmented areas of the skin have long been used around the world, and because of safety concerns, regulations aimed at reducing potential harm or adverse effects caused by certain ingredients in these products are increasing in different countries.
For example, while extremely effective at treating most forms of hyperpigmentation, hydroquinone has been definitively linked to ochronosis, kojic acid has been linked to contact dermatitis in humans, and acid peels and retinoids are associated with irritant dermatitis, disruption of the skin barrier, and photosensitivity. In animal studies, licorice root extract has been linked to endocrine and other organ system irregularities.
Kojic acid was banned in Japan in 2003, and subsequently in South Korea and Switzerland because of concerns over animal studies indicating that its fungal metabolite might be carcinogenic (. Hydroquinone is classified as a drug and has been banned for use in cosmetic products in Japan, the European Union, Australia, and several African nations since at least 2006 because of concerns over adrenal gland dysregulation and high levels of mercury in hydroquinone products in those countries. In Africa specifically, South Africa banned all but 2% hydroquinone in 1983, the Ivory Coast banned all skin whitening creams in 2015, and in 2016, Ghana initiated a ban on certain skin products containing hydroquinone.
The United States followed suit in February 2020 with the Food and Drug Administration introducing a ban on all OTC hydroquinone-containing products because of concerns over carcinogenicity in animal studies (which has not been shown in human studies to date). The “Coronavirus Aid, Relief, and Economic Security” (CARES) Act signed in March 2020 then made the changes effective by halting the sale of OTC hydroquinone products in the United States as of September 2020.
Mercury concerns
Despite these bans, hydroquinone continues to be sold in cosmetics and OTC products around the world and online. And despite being banned or limited in these products, in particular. Mercury has been used in cosmetic products as a skin lightening agent (on its own) and as a preservative.
Mercury has been shown to be carcinogenic, neurotoxic, as well as cytotoxic to the renal and endocrine systems, causes reproductive toxicity, and may be bioaccumulative in wildlife and humans. There is particular concern regarding the risks of exposure in pregnant women and babies because of potential harm to the developing brain and nervous system. Initial signs and symptoms of mercury poisoning include irritability, shyness, tremors, changes in vision or hearing, memory problems, depression, numbness and tingling in the hands, feet, or around the mouth.
Organizations such as the Zero Mercury Working Group (ZMWG) – an international coalition of public interest environmental and health nongovernmental organizations from more than 55 countries, focused on eliminating the use, release, and exposure to mercury – have been working to help ensure safety and mercury levels are below the threshold deemed allowable in hydroquinone-containing products.
On March 10, the ZMWG published the results of a new study demonstrating that skin lighteners containing mercury are still being sold online, despite bans and safety concerns. Ebay, Amazon, Shopee, Jiji, and Flipkart are among the websites still selling high mercury–containing skin lightener products. Some of them were the same offenders selling the banned products in 2019. Of the 271 online products tested from 17 countries, nearly half contained over 1 ppm of mercury, which is the legal limit that has been established by most governments and the Minamata Convention on Mercury. Based on their packaging, the majority of these products were manufactured in Asia, most often in Pakistan (43%), Thailand (8%), China (6%), and Taiwan (4%), according to the report.
In ZMWG’s prior publications, mercury concentrations reported in some of these products ranged from 93 ppm to over 16,000 ppm. Even higher concentrations have been reported by other entities. And according to a World Health Organization November 2019 report, mercury-containing skin lightening products have been manufactured in many countries and areas, including Bangladesh, China, Dominican Republic Hong Kong SAR (China), Jamaica, Lebanon, Malaysia, Mexico, Pakistan, Philippines, Republic of Korea, Thailand, and the United States. According to the ZMWG, 137 countries have committed to the Minamata Convention to phase out and limit mercury, including in cosmetics.
Despite bans on some of these products, consumers in the United States and other countries with bans and restrictions are still at risk of exposure to mercury-containing skin lighteners because of online sales. Hopefully, the work of the ZMWG and similar entities will continue to help limit potentially harmful exposures to mercury, while maintaining access to safe and effective methods to treat hyperpigmentation.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
Skin hyperpigmentation – whether it is caused by postinflammatory hyperpigmentation from acne or trauma to the skin, melasma, autoimmune disorders, or disorders of pigmentation – is a condition where treatment is commonly sought after in dermatology offices. Topical products used to fade hyperpigmented areas of the skin have long been used around the world, and because of safety concerns, regulations aimed at reducing potential harm or adverse effects caused by certain ingredients in these products are increasing in different countries.
For example, while extremely effective at treating most forms of hyperpigmentation, hydroquinone has been definitively linked to ochronosis, kojic acid has been linked to contact dermatitis in humans, and acid peels and retinoids are associated with irritant dermatitis, disruption of the skin barrier, and photosensitivity. In animal studies, licorice root extract has been linked to endocrine and other organ system irregularities.
Kojic acid was banned in Japan in 2003, and subsequently in South Korea and Switzerland because of concerns over animal studies indicating that its fungal metabolite might be carcinogenic (. Hydroquinone is classified as a drug and has been banned for use in cosmetic products in Japan, the European Union, Australia, and several African nations since at least 2006 because of concerns over adrenal gland dysregulation and high levels of mercury in hydroquinone products in those countries. In Africa specifically, South Africa banned all but 2% hydroquinone in 1983, the Ivory Coast banned all skin whitening creams in 2015, and in 2016, Ghana initiated a ban on certain skin products containing hydroquinone.
The United States followed suit in February 2020 with the Food and Drug Administration introducing a ban on all OTC hydroquinone-containing products because of concerns over carcinogenicity in animal studies (which has not been shown in human studies to date). The “Coronavirus Aid, Relief, and Economic Security” (CARES) Act signed in March 2020 then made the changes effective by halting the sale of OTC hydroquinone products in the United States as of September 2020.
Mercury concerns
Despite these bans, hydroquinone continues to be sold in cosmetics and OTC products around the world and online. And despite being banned or limited in these products, in particular. Mercury has been used in cosmetic products as a skin lightening agent (on its own) and as a preservative.
Mercury has been shown to be carcinogenic, neurotoxic, as well as cytotoxic to the renal and endocrine systems, causes reproductive toxicity, and may be bioaccumulative in wildlife and humans. There is particular concern regarding the risks of exposure in pregnant women and babies because of potential harm to the developing brain and nervous system. Initial signs and symptoms of mercury poisoning include irritability, shyness, tremors, changes in vision or hearing, memory problems, depression, numbness and tingling in the hands, feet, or around the mouth.
Organizations such as the Zero Mercury Working Group (ZMWG) – an international coalition of public interest environmental and health nongovernmental organizations from more than 55 countries, focused on eliminating the use, release, and exposure to mercury – have been working to help ensure safety and mercury levels are below the threshold deemed allowable in hydroquinone-containing products.
On March 10, the ZMWG published the results of a new study demonstrating that skin lighteners containing mercury are still being sold online, despite bans and safety concerns. Ebay, Amazon, Shopee, Jiji, and Flipkart are among the websites still selling high mercury–containing skin lightener products. Some of them were the same offenders selling the banned products in 2019. Of the 271 online products tested from 17 countries, nearly half contained over 1 ppm of mercury, which is the legal limit that has been established by most governments and the Minamata Convention on Mercury. Based on their packaging, the majority of these products were manufactured in Asia, most often in Pakistan (43%), Thailand (8%), China (6%), and Taiwan (4%), according to the report.
In ZMWG’s prior publications, mercury concentrations reported in some of these products ranged from 93 ppm to over 16,000 ppm. Even higher concentrations have been reported by other entities. And according to a World Health Organization November 2019 report, mercury-containing skin lightening products have been manufactured in many countries and areas, including Bangladesh, China, Dominican Republic Hong Kong SAR (China), Jamaica, Lebanon, Malaysia, Mexico, Pakistan, Philippines, Republic of Korea, Thailand, and the United States. According to the ZMWG, 137 countries have committed to the Minamata Convention to phase out and limit mercury, including in cosmetics.
Despite bans on some of these products, consumers in the United States and other countries with bans and restrictions are still at risk of exposure to mercury-containing skin lighteners because of online sales. Hopefully, the work of the ZMWG and similar entities will continue to help limit potentially harmful exposures to mercury, while maintaining access to safe and effective methods to treat hyperpigmentation.
Dr. Wesley and Dr. Lily Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
Mandelic acid
Acids peels are used to elicit a chemical exfoliation of the skin by hydrolyzing amide bonds between keratinocytes, reducing corneocyte adhesion, as well as inducing an inflammatory reaction stimulating tissue remodeling. Release of cytokines such as interleukin (IL)-1 and IL-6 by keratinocytes activates fibroblasts to increase the production of matrix metalloproteinases. These are involved in the production of hyaluronic acid and new collagen formation.
Mandelic acid was derived from bitter almonds (mandel is the German word for almond). It is a white powder originally used as an antibiotic for the treatment of urinary tract infections. Its antibacterial properties make it an excellent product for the topical treatment of acne, as well as for use in topical preparations to treat hyperpigmentation and photoaging. In cosmetic use, mandelic acid is a slow acting chemical peel that can be used in all skin types, including sensitive and rosacea-prone skin, as well as skin of color. Its large molecular size allows for the slow penetration of the acid on the skin and thus it can be carefully titrated.
Studies have shown its efficacy in reducing sebum content, acne, acne scarring, and hyperpigmentation. In clinical practice however, the most effective use of this acid is on sensitive skin. It is a great tool for clinicians to use as an effective exfoliant in less acid tolerant skin types. In commercially available concentrations of 5%-45%, mandelic acid can be used alone or in combination with other beta hydroxy peels, depending on the indication.
Most dermatologists and patients prefer in-office peels that induce noticeable peeling and resurfacing of the skin. Mandelic acid is one of the largest alpha hydroxy acids, a lipophilic acid that penetrates the skin slowly and uniformly, making it an ideal peel in sensitive or aging and thin skin types. Although many mandelic acid peels are available, however, there is a paucity of studies comparing their benefits and efficacies.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1. Wójcik A et al. Dermatol Alergol. 2013 Jun;30(3):140-5.
2. Soleymani T et al. J Clin Aesthet Dermatol. 2018;11(8):21-8.
Acids peels are used to elicit a chemical exfoliation of the skin by hydrolyzing amide bonds between keratinocytes, reducing corneocyte adhesion, as well as inducing an inflammatory reaction stimulating tissue remodeling. Release of cytokines such as interleukin (IL)-1 and IL-6 by keratinocytes activates fibroblasts to increase the production of matrix metalloproteinases. These are involved in the production of hyaluronic acid and new collagen formation.
Mandelic acid was derived from bitter almonds (mandel is the German word for almond). It is a white powder originally used as an antibiotic for the treatment of urinary tract infections. Its antibacterial properties make it an excellent product for the topical treatment of acne, as well as for use in topical preparations to treat hyperpigmentation and photoaging. In cosmetic use, mandelic acid is a slow acting chemical peel that can be used in all skin types, including sensitive and rosacea-prone skin, as well as skin of color. Its large molecular size allows for the slow penetration of the acid on the skin and thus it can be carefully titrated.
Studies have shown its efficacy in reducing sebum content, acne, acne scarring, and hyperpigmentation. In clinical practice however, the most effective use of this acid is on sensitive skin. It is a great tool for clinicians to use as an effective exfoliant in less acid tolerant skin types. In commercially available concentrations of 5%-45%, mandelic acid can be used alone or in combination with other beta hydroxy peels, depending on the indication.
Most dermatologists and patients prefer in-office peels that induce noticeable peeling and resurfacing of the skin. Mandelic acid is one of the largest alpha hydroxy acids, a lipophilic acid that penetrates the skin slowly and uniformly, making it an ideal peel in sensitive or aging and thin skin types. Although many mandelic acid peels are available, however, there is a paucity of studies comparing their benefits and efficacies.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1. Wójcik A et al. Dermatol Alergol. 2013 Jun;30(3):140-5.
2. Soleymani T et al. J Clin Aesthet Dermatol. 2018;11(8):21-8.
Acids peels are used to elicit a chemical exfoliation of the skin by hydrolyzing amide bonds between keratinocytes, reducing corneocyte adhesion, as well as inducing an inflammatory reaction stimulating tissue remodeling. Release of cytokines such as interleukin (IL)-1 and IL-6 by keratinocytes activates fibroblasts to increase the production of matrix metalloproteinases. These are involved in the production of hyaluronic acid and new collagen formation.
Mandelic acid was derived from bitter almonds (mandel is the German word for almond). It is a white powder originally used as an antibiotic for the treatment of urinary tract infections. Its antibacterial properties make it an excellent product for the topical treatment of acne, as well as for use in topical preparations to treat hyperpigmentation and photoaging. In cosmetic use, mandelic acid is a slow acting chemical peel that can be used in all skin types, including sensitive and rosacea-prone skin, as well as skin of color. Its large molecular size allows for the slow penetration of the acid on the skin and thus it can be carefully titrated.
Studies have shown its efficacy in reducing sebum content, acne, acne scarring, and hyperpigmentation. In clinical practice however, the most effective use of this acid is on sensitive skin. It is a great tool for clinicians to use as an effective exfoliant in less acid tolerant skin types. In commercially available concentrations of 5%-45%, mandelic acid can be used alone or in combination with other beta hydroxy peels, depending on the indication.
Most dermatologists and patients prefer in-office peels that induce noticeable peeling and resurfacing of the skin. Mandelic acid is one of the largest alpha hydroxy acids, a lipophilic acid that penetrates the skin slowly and uniformly, making it an ideal peel in sensitive or aging and thin skin types. Although many mandelic acid peels are available, however, there is a paucity of studies comparing their benefits and efficacies.
Dr. Lily Talakoub and Dr. Naissan O. Wesley are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1. Wójcik A et al. Dermatol Alergol. 2013 Jun;30(3):140-5.
2. Soleymani T et al. J Clin Aesthet Dermatol. 2018;11(8):21-8.
Clay minerals and the skin
Natural clay from the earth and its minerals, imperative for survival of life on our planet, have been used for medicinal purposes for thousands of years. , and for some, the environmental and sustainability viewpoint that minerals will not harm the environment after disposal.
Clay minerals namely consist of silica, alumina, and/or magnesia, and sometimes varying degrees of iron, sodium, potassium, calcium, and water. Depending on the type of clay, as many as 75 trace minerals may be present.
Ochre
The first uses of ochre, or natural clay earth pigment, are thought to be by Homo erectus and Homo neanderthalensis who used ochre with water to soothe irritations, heal wounds, and clean skin. The theory is that they mimicked some animals who instinctively used clay/mud/minerals in this manner.
The first recorded use of medicinal clay is on Mesopotamian clay tablets, dating to about 2500 B.C. The ancient Egyptian physicians used clays as anti-inflammatory agents and antiseptics. Clay was also used as a preservative during mummification.
Throughout history, clay has been used for dermatologic purposes. Aristotle (384-322 BC) made one of the first references to deliberately eating clay, earth, or soil by humans for therapeutic and religious purposes. Later, Marco Polo described in his travels seeing Muslim pilgrims cure fevers by ingesting “pink earth.”
The ochres have also long been found in indigenous and aboriginal art, and in current day Namibia, the Himba tribe have used Otjize paste (bright red clay consisting of butterfat, red ochre, and sometimes herbs) for their characteristic hairstyles and makeup, as well as for skin protection and as a soap replacement. Otjize is sacred to the culture and ethnic identity, signifying the beauty of their hair and skin and a sense of oneness with their surroundings (the earth). There are also many instances of religious, folklore, or mythological references of creation of life or creation of humankind from clay.
Dermatologic uses
The most common uses of clay in dermatology are for treatment of acne and in spa or cosmeceutical preparations to purportedly draw out dirt, impurities, or toxins.
Clay minerals are most commonly formed from prolonged chemical weathering of silicate-bearing rocks. Clay can also be formed from hydrothermal or volcanic activity. Chemical weathering takes place mainly by acid hydrolysis resulting from low concentrations of carbonic acid, dissolved in rainwater or released by plant roots. Clays differ in composition and structure depending upon the source. Simplistically, clay is structured in two layers, organized in various shapes, with varying minerals and electrical charges. The electric charge of clay allows the adsorption of various minerals, water, heavy and radioactive metals, free radicals, and other potentially unwanted byproducts of metabolic activity. With antibacterial properties and adsorptive properties, clay is often used to dry out acne or oily skin and/or to improve the appearance of large pores.
Bentonite clay
Bentonite clay is one of the most common forms of clay used in topical skin products. Bentonite clay, formed after volcanic ash has weathered and aged in the presence of water, is named after a formation called Benton Shale in the western United States. Bentonite has a strong negative electromagnetic charge and when mixed with water it swells like a sponge and can absorb 40-50 times its weight.
There are several types of Bentonite clay, named from the dominant element found within: Sodium bentonite, calcium bentonite, aluminum bentonite, and potassium bentonite are the most common. Bentonite clay is most commonly found in off-white or green colors.
Kaolin and red clay
Typically white or nearly white to sometimes gray in color, kaolin clay is one of the other most common types of clay used in skin care. While the minerals of the kaolin group display a relatively small specific surface area, compared with those of other clay groups, they can still adsorb small molecules, proteins, bacteria, and viruses on the surface of their particles.
Red clay, also sometimes seen in skin care, takes on its color because of a higher content of iron oxides.
In a 2011 study, Valenti et al. evaluated the impact of daily application of clay and retinoic acid 0.025% on the skin of rats.After 7 days, skin where clay had been applied showed a significant increase in collagen fibers, compared with control skin, while areas where retinoic acid had been applied did not show a significant increase in collagen fibers, compared with control skin.2
A recently published study claims that pH and its interaction with the clay particle surface charge may neutralize and impact properties – including antibacterial properties – of clay and is more significant than previously thought.3 The authors emphasize the dangers of this possibility with unregulated marketing and unsubstantiated bioceutical claims of products that contain clay. Many clay-based skin care products on the market today include other ingredients such as acids (for example salicylic acid, lactic acid, and malic acid) that may potentially counteract this issue and help enhance the targeted efficacy of the product.
The types and characteristics of all types of clay go beyond the scope of this column, but as demonstrated throughout history, clay may have a role in medicinal and dermatologic care, the research of which is still ongoing and is important in our understanding of how this earthly compound can affect our bodies.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1: Moraes JDD et al. Int J Pharm. 2017 Dec 20;534(1-2):213-219. doi: 10.1016/j.ijpharm.2017.10.031.
2: Valenti DMZ et al. Clin Exp Dermatol. 2012 Mar;37(2):164-8. doi: 10.1111/j.1365-2230.2011.04216.x
3. Incledion A et al. Biomolecules. 2021 Jan 5;11(1):58. doi: 10.3390/biom11010058.
Natural clay from the earth and its minerals, imperative for survival of life on our planet, have been used for medicinal purposes for thousands of years. , and for some, the environmental and sustainability viewpoint that minerals will not harm the environment after disposal.
Clay minerals namely consist of silica, alumina, and/or magnesia, and sometimes varying degrees of iron, sodium, potassium, calcium, and water. Depending on the type of clay, as many as 75 trace minerals may be present.
Ochre
The first uses of ochre, or natural clay earth pigment, are thought to be by Homo erectus and Homo neanderthalensis who used ochre with water to soothe irritations, heal wounds, and clean skin. The theory is that they mimicked some animals who instinctively used clay/mud/minerals in this manner.
The first recorded use of medicinal clay is on Mesopotamian clay tablets, dating to about 2500 B.C. The ancient Egyptian physicians used clays as anti-inflammatory agents and antiseptics. Clay was also used as a preservative during mummification.
Throughout history, clay has been used for dermatologic purposes. Aristotle (384-322 BC) made one of the first references to deliberately eating clay, earth, or soil by humans for therapeutic and religious purposes. Later, Marco Polo described in his travels seeing Muslim pilgrims cure fevers by ingesting “pink earth.”
The ochres have also long been found in indigenous and aboriginal art, and in current day Namibia, the Himba tribe have used Otjize paste (bright red clay consisting of butterfat, red ochre, and sometimes herbs) for their characteristic hairstyles and makeup, as well as for skin protection and as a soap replacement. Otjize is sacred to the culture and ethnic identity, signifying the beauty of their hair and skin and a sense of oneness with their surroundings (the earth). There are also many instances of religious, folklore, or mythological references of creation of life or creation of humankind from clay.
Dermatologic uses
The most common uses of clay in dermatology are for treatment of acne and in spa or cosmeceutical preparations to purportedly draw out dirt, impurities, or toxins.
Clay minerals are most commonly formed from prolonged chemical weathering of silicate-bearing rocks. Clay can also be formed from hydrothermal or volcanic activity. Chemical weathering takes place mainly by acid hydrolysis resulting from low concentrations of carbonic acid, dissolved in rainwater or released by plant roots. Clays differ in composition and structure depending upon the source. Simplistically, clay is structured in two layers, organized in various shapes, with varying minerals and electrical charges. The electric charge of clay allows the adsorption of various minerals, water, heavy and radioactive metals, free radicals, and other potentially unwanted byproducts of metabolic activity. With antibacterial properties and adsorptive properties, clay is often used to dry out acne or oily skin and/or to improve the appearance of large pores.
Bentonite clay
Bentonite clay is one of the most common forms of clay used in topical skin products. Bentonite clay, formed after volcanic ash has weathered and aged in the presence of water, is named after a formation called Benton Shale in the western United States. Bentonite has a strong negative electromagnetic charge and when mixed with water it swells like a sponge and can absorb 40-50 times its weight.
There are several types of Bentonite clay, named from the dominant element found within: Sodium bentonite, calcium bentonite, aluminum bentonite, and potassium bentonite are the most common. Bentonite clay is most commonly found in off-white or green colors.
Kaolin and red clay
Typically white or nearly white to sometimes gray in color, kaolin clay is one of the other most common types of clay used in skin care. While the minerals of the kaolin group display a relatively small specific surface area, compared with those of other clay groups, they can still adsorb small molecules, proteins, bacteria, and viruses on the surface of their particles.
Red clay, also sometimes seen in skin care, takes on its color because of a higher content of iron oxides.
In a 2011 study, Valenti et al. evaluated the impact of daily application of clay and retinoic acid 0.025% on the skin of rats.After 7 days, skin where clay had been applied showed a significant increase in collagen fibers, compared with control skin, while areas where retinoic acid had been applied did not show a significant increase in collagen fibers, compared with control skin.2
A recently published study claims that pH and its interaction with the clay particle surface charge may neutralize and impact properties – including antibacterial properties – of clay and is more significant than previously thought.3 The authors emphasize the dangers of this possibility with unregulated marketing and unsubstantiated bioceutical claims of products that contain clay. Many clay-based skin care products on the market today include other ingredients such as acids (for example salicylic acid, lactic acid, and malic acid) that may potentially counteract this issue and help enhance the targeted efficacy of the product.
The types and characteristics of all types of clay go beyond the scope of this column, but as demonstrated throughout history, clay may have a role in medicinal and dermatologic care, the research of which is still ongoing and is important in our understanding of how this earthly compound can affect our bodies.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1: Moraes JDD et al. Int J Pharm. 2017 Dec 20;534(1-2):213-219. doi: 10.1016/j.ijpharm.2017.10.031.
2: Valenti DMZ et al. Clin Exp Dermatol. 2012 Mar;37(2):164-8. doi: 10.1111/j.1365-2230.2011.04216.x
3. Incledion A et al. Biomolecules. 2021 Jan 5;11(1):58. doi: 10.3390/biom11010058.
Natural clay from the earth and its minerals, imperative for survival of life on our planet, have been used for medicinal purposes for thousands of years. , and for some, the environmental and sustainability viewpoint that minerals will not harm the environment after disposal.
Clay minerals namely consist of silica, alumina, and/or magnesia, and sometimes varying degrees of iron, sodium, potassium, calcium, and water. Depending on the type of clay, as many as 75 trace minerals may be present.
Ochre
The first uses of ochre, or natural clay earth pigment, are thought to be by Homo erectus and Homo neanderthalensis who used ochre with water to soothe irritations, heal wounds, and clean skin. The theory is that they mimicked some animals who instinctively used clay/mud/minerals in this manner.
The first recorded use of medicinal clay is on Mesopotamian clay tablets, dating to about 2500 B.C. The ancient Egyptian physicians used clays as anti-inflammatory agents and antiseptics. Clay was also used as a preservative during mummification.
Throughout history, clay has been used for dermatologic purposes. Aristotle (384-322 BC) made one of the first references to deliberately eating clay, earth, or soil by humans for therapeutic and religious purposes. Later, Marco Polo described in his travels seeing Muslim pilgrims cure fevers by ingesting “pink earth.”
The ochres have also long been found in indigenous and aboriginal art, and in current day Namibia, the Himba tribe have used Otjize paste (bright red clay consisting of butterfat, red ochre, and sometimes herbs) for their characteristic hairstyles and makeup, as well as for skin protection and as a soap replacement. Otjize is sacred to the culture and ethnic identity, signifying the beauty of their hair and skin and a sense of oneness with their surroundings (the earth). There are also many instances of religious, folklore, or mythological references of creation of life or creation of humankind from clay.
Dermatologic uses
The most common uses of clay in dermatology are for treatment of acne and in spa or cosmeceutical preparations to purportedly draw out dirt, impurities, or toxins.
Clay minerals are most commonly formed from prolonged chemical weathering of silicate-bearing rocks. Clay can also be formed from hydrothermal or volcanic activity. Chemical weathering takes place mainly by acid hydrolysis resulting from low concentrations of carbonic acid, dissolved in rainwater or released by plant roots. Clays differ in composition and structure depending upon the source. Simplistically, clay is structured in two layers, organized in various shapes, with varying minerals and electrical charges. The electric charge of clay allows the adsorption of various minerals, water, heavy and radioactive metals, free radicals, and other potentially unwanted byproducts of metabolic activity. With antibacterial properties and adsorptive properties, clay is often used to dry out acne or oily skin and/or to improve the appearance of large pores.
Bentonite clay
Bentonite clay is one of the most common forms of clay used in topical skin products. Bentonite clay, formed after volcanic ash has weathered and aged in the presence of water, is named after a formation called Benton Shale in the western United States. Bentonite has a strong negative electromagnetic charge and when mixed with water it swells like a sponge and can absorb 40-50 times its weight.
There are several types of Bentonite clay, named from the dominant element found within: Sodium bentonite, calcium bentonite, aluminum bentonite, and potassium bentonite are the most common. Bentonite clay is most commonly found in off-white or green colors.
Kaolin and red clay
Typically white or nearly white to sometimes gray in color, kaolin clay is one of the other most common types of clay used in skin care. While the minerals of the kaolin group display a relatively small specific surface area, compared with those of other clay groups, they can still adsorb small molecules, proteins, bacteria, and viruses on the surface of their particles.
Red clay, also sometimes seen in skin care, takes on its color because of a higher content of iron oxides.
In a 2011 study, Valenti et al. evaluated the impact of daily application of clay and retinoic acid 0.025% on the skin of rats.After 7 days, skin where clay had been applied showed a significant increase in collagen fibers, compared with control skin, while areas where retinoic acid had been applied did not show a significant increase in collagen fibers, compared with control skin.2
A recently published study claims that pH and its interaction with the clay particle surface charge may neutralize and impact properties – including antibacterial properties – of clay and is more significant than previously thought.3 The authors emphasize the dangers of this possibility with unregulated marketing and unsubstantiated bioceutical claims of products that contain clay. Many clay-based skin care products on the market today include other ingredients such as acids (for example salicylic acid, lactic acid, and malic acid) that may potentially counteract this issue and help enhance the targeted efficacy of the product.
The types and characteristics of all types of clay go beyond the scope of this column, but as demonstrated throughout history, clay may have a role in medicinal and dermatologic care, the research of which is still ongoing and is important in our understanding of how this earthly compound can affect our bodies.
Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at dermnews@mdedge.com. They had no relevant disclosures.
References
1: Moraes JDD et al. Int J Pharm. 2017 Dec 20;534(1-2):213-219. doi: 10.1016/j.ijpharm.2017.10.031.
2: Valenti DMZ et al. Clin Exp Dermatol. 2012 Mar;37(2):164-8. doi: 10.1111/j.1365-2230.2011.04216.x
3. Incledion A et al. Biomolecules. 2021 Jan 5;11(1):58. doi: 10.3390/biom11010058.
