Madeha Al-Kelani*, Kutlwano Molema
Hair and Skin Research Laboratory, Division of Dermatology, Department of Medicine Faculty of Health Sciences, University of Cape Town, Anzio Road, Observatory, Cape Town, South Africa.
*Corresponding author: Madeha Al-Kelani, Hair and Skin Research Laboratory, Division of Dermatology, Department of Medicine Faculty of Health Sciences, University of Cape Town, Anzio Road, Observatory, Cape Town, South Africa.
Received: August 01, 2024
Accepted: August 08, 2024
Published: August 21, 2024
Citation: Madeha Al-Kelani, Kutlwano Molema. (2024) “Advancements in Research on Lichen Planopilaris and Frontal Fibrosing Alopecia: Exploring Pathobiological Developments and Translational Prospects.” Journal of Dermatology and Venereology, 2(1); DOI: DOI: 10.61148/JDV/010
Copyright: © 2024 Madeha Al-Kelani. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
Frontal fibrosing alopecia (FFA) and lichen planopilaris (LPP) are primary lymphocytic hair loss disorders predominantly affecting perimenopausal and postmenopausal women. FFA is often regarded as a variant of LPP due to similar histological findings, including perifollicular lymphohistiocytic infiltrate with a lichenoid pattern. Despite an increase in the prevalence of FFA and LPP over the past decade, their etiology and pathophysiology remain unclear.
This review highlights recent findings on the pathogenesis of FFA and LPP, focusing on immunomodulation, neurogenic inflammation, and genetic factors. A prolonged inflammatory response and collapse of immune privilege trigger the loss of epithelial hair follicle stem cells (eHFSCs) and epithelial-mesenchymal transition (EMT), leading to the replacement of healthy hair follicles with fibrous tissue. Familial reports and genome-wide association studies suggest a genetic or epigenetic basis for FFA development.
Current therapeutic options are limited, underscoring the need for further research and cohort studies to elucidate the etiology and improve treatment strategies for these conditions.
frontal fibrosing alopecia; lichen planopilaris; lymphocytic hair loss; perifollicular lymphohistiocytic infiltrate; lichenoid pattern; immune privilege (ip) collapse
1.Introduction:
Frontal fibrosing alopecia (FFA) and Lichen planopilaris (LPP) are inflammatory scarring hair loss disorders primarily affecting premenopausal and postmenopausal women. These forms of primary cicatricial alopecias (PCAs) lead to disfiguring hair loss, significant scalp symptoms, secondary cutaneous morbidity, and severely reduced quality of life (QOL), imposing a substantial psychosocial burden on patients. [1]
FFA is an irreversible primary lymphocytic scarring alopecia first described by Kossard in 1994. [2] Prevalence has increased globally since its initial report. [3] Pathogenesis remains unclear, with proposed factors including hormones (oestrogens, androgens, thyroid hormones); [4] environmental factors (cosmetic products, allergens, chemical exposure, or food); [5,6] UV filters, [7] smoking, [8] neurogenic inflammation, [9] peroxisome proliferator-activated receptor-y PPAR-y
dysfunction, [10] promoting epithelial-to-mesenchymal transition and fibrosis; and genetic predisposition, [11] as evidenced by frequent familial segregation (Figure 1). [12]
Clinically, FFA presents with frontal hairline recession seen in 100% of cases. However, the disease may affect both the occipital and temporal areas, with scarring occurring in up to 96% of individuals. [13-15] Signs of scarring include loss of follicular ostia, local inflammation with perifollicular erythema and scaling, [16] skin pallor accompanied by itching or burning, occasional smooth and lighter than the chronically-sun-exposed forehead, and the lonely hair sign. Scarred hair loss areas on the scalp are pale and show local atrophy with depression of the frontal veins. [17-19] FFA can also involve the eyebrows in up to 50% - 95% of patients and is the primary form of presentation in up to 39% of cases. [20-22] The eyelashes may be affected in 3% of patients, and while other areas, such as the underarms, pubis, and limbs, have a wide range of prevalence ranging from 0 to 77 %. [2,23]
LPP is a prototypical lymphocytic scarring alopecia occurring at the isthmus level and affecting the hair follicle bulge. [24] First described by Pringle in 1895, [25] LPP is considered a follicular variant of lichen planus. [26] It accounts for 40% of primary scarring alopecia. While predominantly affecting women, men can also be affected. [27] The exact cause remains unknown, though Peroxisome Proliferator-Activated Receptor-Gamma (PPAR-γ) dysfunction has been implicated in its pathogenesis PPAR-γ supposedly deletes hair follicle stem cells causing a similar inflammatory reaction that leads to EMT and fibrosis. [28,29] Clinically, LPP predominantly affects the scalp, particularly the vertex, with variable presentation. LPP typically presents with patchy or diffuse hair loss, accompanied by inflammation and scaling around hair follicles, perifollicular erythema and scaling (keratotic spines). The condition progresses toatrophic cicatricial alopecia with loss of follicular ostia. [4] Extracutaneous lichen planus skin lesions may occur in about 50% of cases.13
Figure 1: Different hypothetical triggers, such as cosmetics, sunscreen, or stressful conditions, can cause FFA in potentially genetically susceptible individuals. PPAR-γ/TGF-β pathway plays an essential role in EMT and fibrosis. mTOR signalling works as a modulator of PPAR-γ activity and lipid homeostasis.
2.Pathogenesis:
2.1.Immunomodulation:
Mounting evidence suggests that immune system dysfunction and inflammatory processes contribute to the development of FFA and LPP. [30] Several key immune-mediated pathways and inflammatory signals are likely involved.
2.2. Immune privilege collapse and inflammation in FFA and LPP:
Hair follicles (HFs) have a unique microenvironment with a degree of immune privilege (IP) that protects epithelial hair follicle stem cells (eHFSCs) from immune attack. This IP is maintained by mechanisms like the suppression of MHC class I and II pathways and the expression of immunosuppressive molecules like TGF-β2 and CD200.[31-33] However, in FFA and LPP, histological evidence suggests a breakdown of this immune privilege. Studies have shown reduced expression of key IP-maintaining factors like TGF-β2 and CD200 in affected HFs, while markers of immune activation (MHC class I and II) are increased. This disruption creates a pro-inflammatory state, with infiltration of immune cells like CD8+ cytotoxic T cells and plasmacytoid dendritic cells. The exact trigger for this immune privilege collapse remains unclear, and further research is needed to elucidate the sequence of events and identify the underlying cause of the inflammatory processes observed in FFA and LPP. [30,34,35]
2.3. Epithelial-to- mesenchymal transition (EMT) and Fibrosis:
Epithelial-to-mesenchymal transition (EMT) is a natural process involved in embryonic development, wound healing, and tissue repair. However, it can also contribute to pathological conditions like cancer and fibrosis.[36,37] Scarring and fibrosis are hallmarks of FFA and LPP. [38,39] Simple depletion of epithelial stem cells through apoptosis wouldn't explain this fibrosis, as it would lead to tissue loss, not scarring. Studies suggest EMT might play a role in the development of FFA and LPP fibrosis. Elevated levels of EMT markers such as Snail1, Vimentin, and Fibronectin have been observed in affected hair follicles. [40-42] Researchers have also induced EMT in human hair follicles in the lab using specific growth factors, suggesting EMT may contribute to the conversion of epithelial stem cells into scar-forming fibroblasts in FFA and LPP. [28,43,44]
2.4. Peroxisome Proliferator-Activated Receptor γ (PPARγ) and its Potential Role:
PPARγ is involved in fat metabolism and the health of hair follicle oil glands (sebocytes). [45] Reduced PPARγ activity has been linked to fibrosis. [46] Emerging evidence suggests PPARγ may play a significant role in FFA and LPP development. Changes in fat metabolism and reduced activity in hair follicle structures called peroxisomes have been observed in LPP. [29] These changes might contribute to inflammation by allowing the buildup of pro-inflammatory fats within the follicle. Treatment with pioglitazone, a drug that activates PPARγ, has shown promise in managing LPP. Reduced PPARγ activity has been noted in both affected and unaffected areas of the LPP scalp, suggesting a broader role for this pathway. [26,45,47-49]
The mTOR signalling pathway, which influences hair follicle growth and immune function, is also linked to PPARγ activity. Reduced expression of mTOR pathway proteins has been observed in scalp samples from FFA/LPP patients. More research is needed to identify how the mTOR and PPARγ pathways contribute to FFA and LPP pathogenesis. [50,51] A recent investigation demonstrated that the PPAR-/mTOR signalling pathway in microglia suppresses the expression of tumour necrosis factor (TNF) and interleukin (IL). [52] Additionally, immunohistochemical evaluation of scalp samples from FFA/LPP patients revealed that the expression of all mTOR signalling pathway proteins was reduced in the lesional epidermis of patients. [50] More research is needed to identify how the mTOR and PPAR- pathways, either alone or in combination, contribute to FFA and LPP pathogenesis.
PPARγ activation has been shown to suppress a process called epithelial-to-mesenchymal transition (EMT), which is thought to contribute to scarring in FFA. [28,48] PPARγ agonists may help prevent or reverse EMT, potentially reducing fibrosis. [53-56] Studies have shown that PPAR-γ activation in TGF-β transgenic mice suppresses the TGF-STAT3 and TGF-EGR1 transcriptional activation pathways in various fibrotic disorders, lending credence to the PPAR-γ/TGF- pathway's significance in FFA. [57]
2.5. Genetic and family background:
While the exact genetic cause of FFA and LPP remains unclear, [19,58] there's growing evidence suggesting a genetic predisposition in some cases. [59,60] FFA has been reported in siblings and families, with estimates suggesting a positive family history in 5-8% of cases. Studies have also identified potential links between FFA and specific human leukocyte antigen (HLA) variations.[61-63] This suggests a possible autosomal dominant inheritance pattern with incomplete penetrance, meaning the genetic mutation isn't always expressed in carriers. [64] LPP appears to have a stronger familial link compared to FFA, with documented cases in children and a more even gender distribution. [65,66] Epigenetic factors, which influence gene expression without altering the DNA code itself, might also play a role. [67] Understanding the interplay of genetics and epigenetics in FFA and LPP may provide insights into other hair follicle stem cell disorders. [68]
2.6. Hormonal and neurogenic factors:
While androgens and other hormones are crucial for hair growth, their exact role in FFA and LPP remains uncertain. [69-71] The higher prevalence in postmenopausal women and occasional overlap with androgenetic alopecia (AGA) suggest a possible link to androgens, but evidence is inconclusive. [72,73] The use of 5-alpha reductase inhibitors (5ARIs) has shown mixed benefits. [74-77] Further research is Recent studies suggest a potential role for neurogenic inflammation in FFA. Some patients exhibited increased scalp sweating, and anti-sweat treatments offered temporary relief. However, more research is required to determine if sweating is a cause or consequence of the inflammatory process. [78] However, more research is required to determine if sweating is a cause or consequence of the inflammatory process.
2.7. Environmental Triggers Suspected:
Several factors suggest a possible environmental link to FFA and LPP. [79] The first documented cases of LPP involved follicular spinous eruptions on the scalp associated with generalized lichen planus. Isolated cases link scalp conditions similar to LPP to exposure to chemicals and medications. An increase in reported FFA cases and the location of hair loss on areas exposed to personal care products (PCPs) have led researchers to investigate a connection between FFA and PCPs. [80-82,83] Studies suggest FFA patients may use certain personal care products (PCPs) have led researchers to investigate a connection between FFA and PCPs. [84] Studies suggest FFA patients may use certain PCPs more frequently and might be more sensitive to fragrance ingredients, potentially leading to an immune response. [85,86] Smoking may also be a risk factor for FFA. [87,88] However, more research is needed to confirm these links. Interestingly, the increase in published research on FFA mirrors the rise in reported cases, while LPP research has remained steadier, suggesting a potential role for environmental factors in FFA specifically.
3.Clinical Features:
FFA and LPP, both causing scarring alopecia, can be distinguished by their clinical features. FFA primarily affects postmenopausal women but can also occur in younger individuals and men. [2,3] Similarly, LPP affects both men and women, with a higher prevalence in women. [27] The location of hair loss is a key differentiating factor. FFA typically presents with a receding frontal hairline, potentially extending to the occipital and temporal scalp regions. [13-15] In contrast, LPP manifests as patchy or diffuse hair loss centred on the scalp vertex. [4] Early stages of both conditions may show redness and scaling around remaining hairs. FFA is known for "perifollicular erythema and scaling", [16] while LPP features similar inflammation with "keratotic spines". [4] As the diseases progress, the scalp can become smooth and pale with loss of hair follicles in FFA, and scarring becomes more prominent. [8-10] Eyebrow involvement is common in FFA, affecting up to 95% of patients and sometimes serving as the initial presentation. [21,22] LPP, in its advanced stages, can lead to permanent loss of hair follicles and a smooth, atrophic scalp due to scarring. [13] (Figure 2).
Figure 2: Scarring alopecia: (A) presents FFA with a distinctive clinical pattern of progressive frontotemporal band-like hairline recession and eyebrow loss, (B) presents LPP occurring at the mid-frontal and vertex area of the scalp, (C) FFA histopathology shows perifollicular fibrosis with a moderately dense perifollicular lymphoid cell infiltrate involving several hair follicles. [89] (D) LPP histopathology shows Follicular plugging, hypergranulosis, and dense, band-like perifollicular lymphocytic infiltrate that obscures the infundibular epithelium. [90]
4.Histopathology of FFA and LPP:
FFA exhibits distinct histopathological features depending on the disease progression. The early stages show an inflammatory infiltrate containing lymphocytes and histiocytes surrounding the outer root sheath, accompanied by mild perifollicular fibrosis. As the disease progresses, pilosebaceous units are replaced by scar tissue, leading to decreased hair density and significant perifollicular fibrosis. [19] A key diagnostic feature in the early stages is the presence of a "follicular triad" consisting of vellus, intermediate, and terminal hairs in various growth phases. [18] This triad results from the inflammatory infiltrate preferentially targeting vellus and intermediate hairs, which are more abundant in the frontal hairline and might express specific antigens that attract the inflammatory cells. [17]
Distinguishing FFA from LPP solely based on histological features remains a challenge. While some studies report potential distinguishing factors like eosinophilic necrosis of the outer root sheath and spared interfollicular epidermis in FFA, [21,91] others haven't found consistent differences. [6,21] Similarly, direct immunofluorescence, a technique helpful in diagnosing LPP, hasn't proven reliable for FFA diagnosis due to variable patterns. [22,23] Consequently, current histological evaluation suggests FFA and LPP might be variants within a larger spectrum of lichenoid alopecia. [91] However, despite these similarities, there are notable differences in demographics, clinical presentation, and potentially underlying pathology between FFA and LPP (Table 1)
conducted to treat acne sequelae are a high cost procedural interventions. [2,14] Skin maintenance to improve skin health and skin integrity be the major goal for the patients by receive daily routine skincare. [16] Over-the-counter (OTC) products effectiveness data are limited and it makes clinicians often have difficulty to recommend which products is the most appropriate for the patients, [15] but when it is selected properly, OTC products have the advantages of being effective and convenient. [17]
Case Report:
Five patients present with post inflammatory acne and acne scars on the face after having treatment for their acne problems. These problems occurred right after their acnes were controlled. Redness on their skin sometimes feel uncomfortable and make patients losing their confidence. There is no previous history of treatment for these conditions. There is no history of family members who have acne scars and post inflammatory acne. There is no history of atopy of all the patients. Physical examination results of the patient are within normal limits. All the patients have signed the informed consent.
Dermatologicus status obtained erythema macules and scars typed mostly ice picks and rolling on the both cheeks. We used Clinicians’s Erythema Assesment (CEA) for clinicians and for patients we used Patients Self-Assessment (PSA), Dermatology Life Quality Index (DLQI) and Scale of Generalized Anxiety Disorder (GAD-2). All of the patients feel satisfied with the results using this skincare regimen.
Discussion:
Stratum corneum (SC) as the outermost skin layer is containing ceramides, cholesterol, and free fatty acids, it is in a multilamellar lipid matrix, constituted by corneocytes embedded. The function of skin barrier is determined primarily by stratum corneum integrity. Epidermal barrier impairment caused by exposure from multiple exogenous factors, the SC is continuously active in maintaining a state of physiology function by a self-repair mechanism. [18,19] Keratinocyte hyperproliferation is promoted by an inflammatory cascade triggers the release of tumor necrosis factor (TNF), interleukin (IL)-1 and IL-6 in initial. Epidermal becomes thicker and lead to counter the excessive trans-epidermal water loss (TEWL). [19] Skin injury can also affect the dermis in addition to the epidermal barrier. Cohesiveness of the epithelium can be compromised by disruption of epidermis and dermis. Wound healing consists of a dynamic and interactive process. It has four phases: 1. Hemostasis; 2. Inflammation; 3. Proliferation; and 4. Remodeling. Each other phase can partially overlap. [20,21]
Skin diseases linked with inflammation formed as occasional rashes are the most common problem in dermatology. [22] Macular erythema induced by acne or post inflammatory acne is a transitional lesion for atrophic scars. The development of atrophic scar as one of the acnes sequalae’s pathogenesis is complex, ongoing inflammations appears to be a key underlying cause.[23] Increase in TEWL and decrease in SC capacitance and conductance have been reported as a malfunction SC that leads to scar form. [24]
Medical devices, medicines, and cosmetic products have different mechanisms to promote skin repair. Cosmetic products act in the epidermis which means the active substances in the skincare formulation action is in the inflammatory phase or in the regeneration phase. [25] The substances can act by reducing pro-inflammatory mediators, neutralizing free radical species, or by improving synthesis of collagen or inhibiting its degradation process in the regeneration phase. [25.26] Improvement of skin hydration can be impacted by products which act to improve the skin barrier damage by the moisturizer effect. The ingredients that boost skin structural lipids synthesis, restore the skin barrier directly, or bind and retain water to stratum corneum therefore reducing TEWL make this moisturizer effect. [25-27] Moisturizer can regulate epidermal cytokine and production of growth factor (GF), as a result, it is to be expected that moisturizer may improve scar form. [24]
Acne-induced erythema or post inflammatory acne is often contributing to psychosocial burden and unacceptable cosmetically. [1] Residual scarring from acne also can be linked to psychosocial effects. Acne scars can trigger and exacerbate negative body image and self-esteem to the patients. One of the important parameters in the dermatology field is recognizing acne scars impact to psychosocial well-being. Patients with acne scars experienced occurrence of anxiety, depressive symptoms, even suicidal tendencies. Personal relationship and social participation also impair the DLQI because of the acne scars. [28] We used CEA (table 1) for clinicians and for patients we used PSA (table 2) for the erythema and the DLQ) (table 3) and GAD-2 (table 4) to assess both of skin problems (erythema and scars).
|
|
Score |
Mild |
Mild erythema; define redness |
2 |
Moderate |
Moderate erythema; marked redness |
3 |
Severe |
Severe erythema; fiery redness |
4 |
Table 1: Clinicians’s Erythema Assesment (CEA)
|
|
Score |
Mild |
Somewhat more redness than I prefer |
2 |
Moderate |
More redness than I prefer |
3 |
Severe |
Completely unacceptable redness |
4 |
Table 2: Patients Self-Assessment (PSA)
The aim of this questionnaire is to measure how much your skin problem has affected your life OVER THE LAST WEEK. Please tic (√) one box for each question. |
|||
1. |
Over the last week, how itchy, sore, painful or stinging has your skin been? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
2. |
Over the last week, how embarrassed or self-conscious have you been because of your skin? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
3. |
Over the last week, how much has your Very much skin interfered with you going A lot shopping or looking after your home or A little garden? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
Not relevant |
|
||
4. |
Over the last week, how much has your skin influenced the clothes you wear? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
Not relevant |
|
||
5. |
Over the last week, how much has your skin affected any social or leisure activities? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
Not relevant |
|
||
6. |
Over the last week, how much has your skin made it difficult for you to do any sport? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
Not relevant |
|
||
7. |
Over the last week, has your skin prevented you from working or studying? |
Yes |
|
No |
|
||
Not relevant |
|
||
If "No", over the last week how much has your skin been a problem at work or studying? |
A lot |
|
|
A little |
|
||
Not at all |
|
||
8. |
Over the last week, how much has your skin created problems with your partner or any of your close friends or relatives? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
Not relevant |
|
||
9. |
Over the last week, how much has your skin caused any sexual difficulties? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
Not relevant |
|
||
10. |
Over the last week, how much of a problem has the treatment for your skin been, for example by making your home messy, or by taking up time? |
Very much |
|
A lot |
|
||
A little |
|
||
Not at all |
|
||
Not relevant |
|
Table 3: Dermatology Life Quality Index (DLQI)
Very much |
Scored 3 |
A lot |
Scored 2 |
A little |
Scored 1 |
Not at all |
Scored 0 |
Not relevant |
Scored 0 |
Question unanswered |
Scored 0 |
Question 7: “prevented work or studying” |
Scored 3 |
The scoring of each question is as follows:
The DLQI is calculated by summing the score of each question resulting in a maximum of 30 and a minimum of 0. The higher the score, the more quality of life is impaired.
Meaning of DLQI scores:
• 0 -1 = no effect at all on patient’s life
• 2 – 5 = small effect on patient’s life
• 6 – 10 = moderate effect on patient’s life
• 11 – 20 = very large effect on patient’s life
• 21 – 30 = extremely large effect on patient’s life
|
CEA |
PSA |
||
Before |
After |
Before |
After |
|
Patient 1 |
3 |
2 |
3 |
2 |
Patient 2 |
3 |
2 |
3 |
2 |
Patient 3 |
3 |
2 |
3 |
2 |
Patient 4 |
3 |
2 |
3 |
2 |
Patient 5 |
2 |
0 |
2 |
0 |
Table 4: Generalized Anxiety Disorder Scale (GAD-2)
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6).
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
||
|
|
Before |
After |
|
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
3 |
2 |
|
|
|
3 |
2 |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
3 |
2 |
|
|
|
3 |
2 |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
All the patients clinically had their erythema reduced based on CEA and PSA. It proves that a proper skincare regimen can lead to improvement of patients’ skin problem in this matter are erythema and scars on their skin (table 5 and table 6). |
2 |
0 |
Table 5: Result of Clinicians’s Erythema Assesment (CEA) and Patients Self-Assessment (PSA).
Table 6: Before and after having skincare regimen.
Pictures taken before skincare regimen on day 1 (figure a). Patients were given skincare regimen including facial wash, daily cream and sunscreen for 4 (four) weeks. We repeated taken the pictures 2 weeks on day 14 during the treatment (figure b). Last pictures taken on the fourth week (day 28) of using skincare regimen (figures c). Patients started to feel more comfortable with their skin on the second week, and on the last week, erythema reduced and there was improvement on scar appearances.
Most inflammatory skin diseases’ treatment is dominated by corticosteroid but it is only for short term use because of the side effects. [22] If a cosmetic product is truly capable of repairing skin, it should help the healing process of a damage skin. Pharmaceuticals industries currently use a non-steroidal formula to decrease skin inflammation. In this serial case we treated the patients for 4 (four) weeks with skincare regimen including facial wash, moisturizer and sunblock without any other treatment. They used facial wash and moisturizer twice a day and sunscreen every day. The moisturizer contains active ingredients such as azelaic acid (AZA), β-glucan, Calendula extract and bisabolol.
One of the ingredients known with the ability to regenerate skin is bisabolol. It is reducing the production of pro-inflammatory cytokine and improving skin inflammation. [22.29] As well as the β-glucans, it enhances GF production that are essential for skin, promotes collagen biosynthesis and maintains moisture and elasticity of the skin. Macrophages is activated and it removes cellular debris resulting from oxidative stress, hence speeding up the recovery tissue damage. [30] Another anti-inflammatory, anti-oxidant, a scavenger of harmful free radicals and can inhibit the reactive oxygen species (ROS) production is azelaic acid. Azelaic acid is a natural substance produced by the yeast Malassezia spp.. The effect of AZA has been confirmed in a study conducted by Draelos et al., compared to placebo in 961 patients is more effective 32% vs. 23.5%; p < 0.001. [31]
The plant raw material that has anti-inflammatory activity related to therapeutic indications of medicinal plants has been described in most studies. They also have the ability to regulate lipid synthesis in epidermis. One of them is Calendula officinalis L has anti- inflammatory effects related to the content of flavonoids and derivates of triterpene and there is a lipoxygenase inhibitor from isolated calendula flower that is isorhamnetin 3-glycosides. Faradiol and this flower extract at high concentration was comparable to indomethacin (synthetic drug for anti-inflammation). Calendula officinalis L inhibits cytokines formation to prevent the inflammatory reaction. [32] Topical formulations of Calendula are intended for wound healing and soothing inflamed and/ or damaged skin. [33]
It was reported in a recent researched that 26.2% of the people with acne had anxiety symptoms and the severity of this symptoms found to be associated to the impairment of quality of life.34 Due to this report, the sequalae of acne such as erythema and scarring could possibly affect the psychosocial burden of the patients.
On the result on table 7, the quality of life of 4 patients were in very large effect state on their life, only 1 patient in moderate effect state before they start using the skincare regimen. On the 4th week, their quality of life improved to be in small effect state and moderate effect state in 1 patient and 4 patients, respectively. The result of GAD-2 showed there was improvement in their anxiety disorder based on the scale. Based on the result, there was improvement in patients’ quality of life and the anxiety symptoms were reduced since their skin had an improvement.
|
DLQI |
GAD-2 |
||
Before |
After |
Before |
After |
|
Patient 1 |
8 |
3 |
2 |
1 |
Patient 2 |
16 |
10 |
3 |
2 |
Patient 3 |
13 |
10 |
1 |
0 |
Patient 4 |
11 |
6 |
1 |
0 |
Patient 5 |
15 |
7 |
3 |
1 |
Table 7: Result of Dermatology Life Quality Index (DLQI) and Generalized Anxiety Disorder Scale (GAD-2).
Conclusion:
The sequalae of acne such as scarring and erythema could have a significant impact on physiological and psychosocial effects for patient’s quality of life. Proper clinical assessment has important role to treat these skin problems because the treatment options of both skin problems also challenging and costly. Clinicians should choose the right and proper treatment start from the initial inflammatory phase occurred. Effective treatment in the earlier stage can potentially limit and prevent development of the sequelae. One of treatment options of post inflammatory acne and acne scar is daily skincare that have moisturizing property to help repairing the condition of the sequelae of acne. By using a proper daily routine skincare should have benefits or clinical efficacy lead to reducing inflammatory lesions and scars, and eventually improving skin barrier.
Acknowledgements:
The authors would like to thank all individuals who participated and contributed in this case report.
Declaration of competing interest:
I hereby declare that, to the best of my knowledge, there is no aspect of my current personal or professional state that significantly affect my views regarding the material subject I am presenting.
Ethics statement:
The content presented in this manuscript is solely for educational and informational purposes and does not require ethical approval as per institutional guidelines. All confidential or personal data is used solely for the purposes of this manuscript and has been approved and signed by the patients on informed consent. All sources have been given appropriate credit to respect intellectual property rights and academic integrity.