Abstract
Background:
Seborrheic dermatitis (SD) is the most common concurrent disease in patients with androgenetic alopecia (AGA). There are inadequate data to determine whether there is a relationship between AGA severity and SD severity.
Aim and Objectives:
This study aimed to investigate the presence and the severity of SD in patients with AGA, who were divided into groups based on the severity of AGA.
Patients and Methods:
We evaluated 311 patients aged ≥18 years who were diagnosed with AGA at the dermatology outpatient clinic between April and September 2023. Patients were divided into three groups according to AGA severity. We used the Clinical Severity Score Criteria to determine the severity of SD on the scalp. We subsequently compared the severity scores among the groups based on the severity of AGA.
Results:
The mean age was 41.5 ± 15.2 (range 18–85) years. Of these patients, 74 (23.8%) were female and 237 (76.2%) were male. SD was observed in 131 patients (42.1%). Among those with SD, 19.9% were female and 80.1% were male. As AGA severity increased, the prevalence of SD also increased (P = 0.28). Furthermore, there was a statistically significant difference in the SD scores as the severity of AGA increased (P < 0.001).
Limitations:
Small patient group and cross-sectional design.
Conclusion:
SD may affect the pathophysiology and severity of AGA.
Keywords: Androgenetic alopecia, female pattern alopecia, male androgenetic alopecia, seborrheic dermatitis, severity of disease
Introduction
Androgenetic alopecia (AGA) is a prevalent condition affecting approximately 80% of men and 50% of women throughout their lives, especially those with a genetic predisposition. This condition can have negative effects on the mental and emotional well-being of those affected, leading to issues such as depression and shame.[1] Among the scales used to evaluate AGA, the most well-known and frequently used in practice are the Norwood–Hamilton classification for men and the Ludwig classification for women. However, these classifications have shortcomings, which have led to efforts to improve them.[2] For example, the Norwood–Hamilton classification is neither easy to remember nor comprehensive for every type of baldness seen in women. On the other hand, the Ludwig classification does not have an equivalent for male-pattern hair loss.[3,4] The basic and specific (BASP) classification was developed to address these deficiencies, providing a systematic and gradual approach based on hair loss and quantity.[5]
Seborrheic dermatitis (SD) is a chronic inflammatory skin disease most commonly seen on the scalp and face, where the sebaceous gland is located, with a prevalence rate of approximately 3% in the general population; however, if milder forms are included, it can be said to be even more common.[6] Although there are no definitive data on whether there is a relationship between AGA and SD, studies conducted in areas with SD have shown increased dihydrotestosterone (DHT) production.[7,8] This is important because it supports the idea that increased DHT levels may affect the pathophysiology of both AGA and SD by stimulating the sebaceous glands. Moreover, this hormone contributes to the progression of AGA.[9] The high amount of 5α-reductase in the sebaceous glands and the resulting increase in 5α-DHT synthesis affect hair growth and diameter, potentially explaining the heterogeneity in follicle miniaturization that is typical of AGA.[10,11]
There are insufficient data to establish a relationship between SD and AGA. Therefore, this study aimed to examine the prevalence of SD in patients with AGA and to investigate the relationship between AGA severity and SD severity.
Patients and Methods
This study included 311 patients aged 18 years and older, who were diagnosed with AGA at our dermatology outpatient clinic between April and September 2023. The patients were diagnosed with AGA based mainly on clinical and trichoscopic findings. If conditions that could be confused with AGA, such as frontal fibrosing alopecia, could not be excluded clinically and/or by trichoscopy, the diagnosis of AGA in these patients was confirmed through histopathological examination. Our study included patients with both past and present SD. If the patient had previous SD and did not have it during the examination, the Clinical Severity Score Criteria (CSSC) were calculated as zero.
On admission to the outpatient clinic, all patients underwent clinical examinations. Demographic data, medical history, treatments used for AGA and SD, other medications taken, presence of other diseases, family history, and AGA severity were recorded. In addition, data on the presence of SD on the scalp (past, and present during the examination), CSSC, and duration of SD were recorded. The CSSC score is a system used by dermatologists to assess the severity of dandruff, erythema, and lesions. The total clinical severity score is determined by adding the scores from these three categories, with each category able to score between 0 and 3 points.[12]
Patients (n = 311) were divided into three groups: group 1 (n = 77; Hamilton–Norwood types 1-2 or Ludwig stage 1 or BASP type equivalent to these groups), group 2 (n = 145; Hamilton–Norwood types 3-5 or Ludwig stage 2 or BASP type equivalent to these groups), and group 3 (n = 89; Hamilton–Norwood types 6-7 or Ludwig stage 3, or BASP type equivalent to these groups). The presence and severity of SD were compared across the groups [Table 1].
Table 1.
Presence and severity (assessed by clinical severity score criteria score) of seborrheic dermatitis
| Group 1 (n=77) | Group 2 (n=145) | Group 3 (n=89) | Total (n=311) | P | |
|---|---|---|---|---|---|
| Seborrheic dermatitis | 0.282a | ||||
| Present (n, %) | 27 (35.1%) | 62 (42.8%) | 42 (47.2%) | 131 (42.1%) | |
| Absent (n, %) | 50 (64.9%) | 83 (57.2%) | 47 (52.8%) | 180 (57.9%) | |
|
| |||||
| Androgenetic Alopecia | Clinical severity score criteria (CSSC) score of seborrheic dermatitis Mean score±SD | P | |||
|
| |||||
| Group 1 (n=27) | 3.26±0.90 | <0.001b | |||
| Group 2 (n=62) | 3.79±1.51 | ||||
| Group 3 (n=42) | 4.86±1.61 | ||||
aPearson’s Chi-squared test. bOne-way ANOVA test
This study was approved by the local ethics committee (number: AEŞH-EK1-2023-051). Written informed consent was obtained from all patients.
Statistical analysis
We performed all analyses in our study using version 2.3.28 of the Jamovi program. Descriptive analyses were conducted to calculate the mean, standard deviation, frequency, and minimum and maximum values. We examined the normality distribution of the data using the Shapiro–Wilk and Kolmogorov–Smirnov tests. The Chi-square test was used to analyze categorical variables, whereas the Pearson Chi-square test was used to compare the differences between categorical variables among the groups. The independent t-test and one-way ANOVA tests were used to compare the groups for continuous variables. Spearman’s correlation analysis was performed to investigate the relationship between age, gender, and CSSC score. Based on the 95% confidence interval, a P value of less than 0.05 was considered statistically significant.
Results
The mean age of a total of 311 patients in the study was 41.5 ± 15.2 years (range 18–85). Of these, 74 were women (23.8%) and 237 were men (76.2%). The mean age of women was 42.6 ± 13.6 (19-78) years, and the mean age of men was 41.1 ± 15.8 (18-85) years. While the mean age at disease onset was 31.5 ± 9.4 (15-60) years for AGA, the mean age at onset for SD was 22.6 ± 8.89 (12-65) years. The mean disease duration of AGA was 9.96 ± 9.5 years, and the SD was 20.8 ± 14.1 years. Of the 311 patients, 131 (42.1%) were diagnosed with SD. Among these 131 patients, 26 were women and 105 were men.
The most prevalent comorbidities were hypertension (n = 46, 14.8%), diabetes mellitus (n = 27, 8.7%), hyperlipidemia (n = 26, 8.4%), and coronary artery disease (n = 12, 3.9%). Of the study participants, 104 (33.4%) were smokers and 24 (7.7%) used alcohol. In addition, 217 (69.8%) patients had a family history of AGA and 75 (24.1%) had a history of SD. Body mass index (BMI) calculated according to groups was found to be 24.4 ± 2.93 in group 1, 26.6 ± 3.68 in group 2, and 27.4 ± 3.32 in group 3 (P < 0.001). Hamilton–Norwood, Ludwig, and BASP classifications were used to evaluate the severity of AGA in all patients. The distribution of patients according to AGA severity was as follows: 77, 145, and 89 patients in groups 1, 2, and 3, respectively. The frequency of SD were as follows: group 3 (n = 42, 47.2%), group 2 (n = 62, 42.8%), and group 1 (n = 27, 35.1%). There was no statistically significant difference in the frequency of SD between the groups (P = 0.28; Table 1). As AGA severity increased, a statistically significant increase was observed in CSSC scores (group 3> group 1) (P < 0.001) [Table 1]. The CSSC scores were found to be 3.26 ± 0.90 in group 1, 3.79 ± 1.51 in group 2, and 4.86 ± 1.61 in group 3. The BASP patterns by sex are compared and presented in Table 2. The BASP patterns in men and women were significantly different (P < 0.001). The most common BASP pattern in men was M2V1, whereas that in women was F2 [Table 2]. In the Spearman correlation analysis conducted between age and CSSC score, a Spearman’s rho value of 0.34 was found, indicating a low level of relationship between the two variables (P < 0.001). However, gender and CSSC score showed no significant relationship (P = 0.29).
Table 2.
BASP classification of patients according to gender
| Female (n=74) | Male (n=237) | Total (n=311) | P | |
|---|---|---|---|---|
| BASP classification | <0.001* | |||
| C1 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| C1F2 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| C1V2 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| C1V3 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| C2 | 0.0 (0.0%) | 7.0 (3.0%) | 7.0 (2.3%) | |
| C2F2 | 0.0 (0.0%) | 2.0 (0.8%) | 2.0 (0.6%) | |
| C2F3 | 0.0 (0.0%) | 2.0 (0.8%) | 2.0 (0.6%) | |
| C2V1 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| C2V2 | 0.0 (0.0%) | 13.0 (5.5%) | 13.0 (4.2%) | |
| C2V3 | 0.0 (0.0%) | 9.0 (3.8%) | 9.0 (2.9%) | |
| C3 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| C3F2 | 0.0 (0.0%) | 7.0 (3.0%) | 7.0 (2.3%) | |
| C3F3 | 0.0 (0.0%) | 4.0 (1.7%) | 4.0 (1.3%) | |
| C3V2 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| C3V3 | 0.0 (0.0%) | 8.0 (3.4%) | 8.0 (2.6%) | |
| F1 | 28.0 (37.8%) | 1.0 (0.4%) | 29.0 (9.3%) | |
| F2 | 34.0 (45.9%) | 3.0 (1.3%) | 37.0 (11.9%) | |
| F3 | 8.0 (10.8%) | 0.0 (0.0%) | 8.0 (2.6%) | |
| M0 | 0.0 (0.0%) | 4.0 (1.7%) | 4.0 (1.3%) | |
| M0V1 | 0.0 (0.0%) | 2.0 (0.8%) | 2.0 (0.6%) | |
| M1 | 1.0 (1.4%) | 19.0 (8.0%) | 20.0 (6.4%) | |
| M1F2 | 2.0 (2.7%) | 0.0 (0.0%) | 2.0 (0.6%) | |
| M1V1 | 0.0 (0.0%) | 16.0 (6.8%) | 16.0 (5.1%) | |
| M2 | 0.0 (0.0%) | 11.0 (4.6%) | 11.0 (3.5%) | |
| M2F3 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| M2V1 | 1.0 (1.4%) | 38.0 (16.0%) | 39.0 (12.5%) | |
| M2V2 | 0.0 (0.0%) | 20.0 (8.4%) | 20.0 (6.4%) | |
| M2V3 | 0.0 (0.0%) | 4.0 (1.7%) | 4.0 (1.3%) | |
| M3F1 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| M3F2 | 0.0 (0.0%) | 4.0 (1.7%) | 4.0 (1.3%) | |
| M3F3 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| M3V1 | 0.0 (0.0%) | 1.0 (0.4%) | 1.0 (0.3%) | |
| M3V2 | 0.0 (0.0%) | 6.0 (2.5%) | 6.0 (1.9%) | |
| M3V3 | 0.0 (0.0%) | 9.0 (3.8%) | 9.0 (2.9%) | |
| U1 | 0.0 (0.0%) | 3.0 (1.3%) | 3.0 (1.0%) | |
| U1F3 | 0.0 (0.0%) | 11.0 (4.6%) | 11.0 (3.5%) | |
| U2 | 0.0 (0.0%) | 5.0 (2.1%) | 5.0 (1.6%) | |
| U2F3 | 0.0 (0.0%) | 8.0 (3.4%) | 8.0 (2.6%) | |
| U3 | 0.0 (0.0%) | 2.0 (0.8%) | 2.0 (0.6%) | |
| U3F3 | 0.0 (0.0%) | 8.0 (3.4%) | 8.0 (2.6%) |
*Pearson’s Chi-square test
Discussion
The normal cycle of the hair follicle changes in AGA, resulting in a more prolonged telogen phase and progressively shorter anagen phase. This causes the hair follicle to shrink, leading to shorter, thinner, and less pigmented hair in each hair cycle. Eventually, in the final stage, the follicle is unable to produce hair, resulting in baldness.[13,14] Although there is no clear evidence in the literature, there have been reports of coexisting dandruff and AGA, which can worsen hair loss. In addition, increased hair loss is associated with changes in the proportion of hair in the anagen and telogen phases and the size of the hair shaft, which are believed to worsen the problem.[15,16] Although it is difficult to establish a direct relationship with this situation, the higher severity scores of SD in the AGA patient group indicates that the symptoms are more severe, and support this correlation.
Sawaya et al.[17] conducted a study on a specific androgen-binding protein found in the sebaceous glands of hairy and hairless scalps. Their findings indicated that individuals with bald scalps exhibited a higher binding strength and capacity of this protein compared to those with hair. This result suggests that sebum production is higher in bald areas and may be related to AGA and SD. In another study from Japan, including 23 patients with AGA, the patients’ sebaceous glands and follicle bulge areas were examined. It was seen that the stem cells in the sebaceous glands of these patients did not change, and the sebaceous glands grew above the expected level, suggesting that the sebaceous glands may have a significant share in AGA.[18] Although it remains unclear whether these changes are a cause or consequence of AGA progression, it is hoped that they will prove helpful for the development of future targeted cellular therapies.[19,20] These studies suggest that sebaceous gland-related diseases of the scalp may affect the progression and severity of AGA. SD, the disease investigated in our study, is one of the related conditions.
As SD increases inflammation in the scalp, it may cause telogen effluvium and increase the severity and rate of AGA progression. Therefore, it has been shown that choosing anti-inflammatory treatments (such as shampoos containing cannabidiol) can significantly benefit patients regarding both diseases.[21] In AGA, the use of cannabinoid receptor 1 antagonists rather than agonists from cannabinoid compounds is recommended.[22]
In a study by Jang et al.,[7] which examined 1218 patients with AGA, 606 of 833 men and 276 of 385 women had AGA-related diseases. The most common accompanying disease in both sexes was SD, with a frequency of 51.2% in men and 45.7% in women. This was followed by hypertension (13.4% in men and 11.2% in women) and hyperlipidemia (5.9% in men and 8.0% in women). Our study also found a high prevalence of SD in patients with AGA (42.1%). Hypertension was the most common comorbidity, apart from SD, with a prevalence of 14.8%. These findings are consistent with those reported by Jang et al.
In addition to SD, fibrosing alopecia in pattern distribution (FAPD) is another AGA-related disease. FAPD, whose notification was made for the first time in 2000, is a scarring alopecia exhibiting AGA and lichen planopilaris characteristics.[23] A study examining 188 FAPD patients regarding this disease and AGA reported that FAPD may contribute to the development of AGA. This is believed to be caused by an excessive inflammatory response in the damaged hair follicles. Although there are limited data on the treatment of FAPD, it has been suggested that combining treatments with anti-inflammatory components could be an effective approach to managing the disease.[24]
Dandruff occurs on the scalp because of a decrease in stratum corneum lipids and deterioration of the skin barrier. This combination of hyperproliferation and an impaired scalp barrier leads to changes in corneocyte maturation and the occurrence of a subclinical inflammatory state.[25,26] To address stratum corneum abnormalities, it is not sufficient to simply eliminate the dandruff, and the underlying causes must also be treated. Therefore, ingredients like zinc pyrithione are used in the treatment of SD, as they help normalize epithelial keratinization and sebum production.[25] Considering this information regarding the treatment and prognosis of AGA, it is essential to treat co-occurring scalp diseases, such as SD. Treating SD will be a supportive step in treating alopecias associated with SD, as it will have several positive effects, including reducing inflammation, maintaining control over SD, and improving the scalp–skin barrier. Some genetic changes have also been shown to cause an increase in inflammation in SD.[27] Our study’s significant finding was the higher score of SD observed in the severe AGA group. This suggests that SD may be a factor that increases severity of AGA. Therefore, early diagnosis and appropriate treatment of SD should be implemented to minimize its impact on the progression of alopecia. However, it is substantial to determine whether the correlation between SD severity and AGA is coincidental or a combination of various factors.
Limitations
Small patient group and cross-sectional design. Conducting prospective cohort studies with larger patient groups may provide a more comprehensive understanding of SD in AGA and shed light on its role in AGA pathophysiology.
Conclusion
Seborrheic dermatitis may affect the pathophysiology and severity of AGA. Therefore, the effective treatment and management of SD could have a positive impact on the progression of AGA. More research is needed to clarify the pathophysiology of AGA to fully understand the relationship between AGA and SD.
Conflicts of interest
There are no conflicts of interest.
Use of AI
The authors confirm that there was no use of artificial intelligence (AI).
Funding Statement
Nil.
References
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