Evaluation, Symptoms, Influencing Factors, and Prospects of Sensitive Scalp: A Literature Review

Abstract

Sensitive scalp (SSC) is a common but often overlooked dermatological state, characterized by subjective symptoms such as pruritus, tingling, tightness, pain, or burning sensations. Primary SSC typically occurs in the absence of visible clinical inflammation. Numerous studies have suggested that the onset of SSC may be influenced by a variety of intrinsic and extrinsic factors, including physical (ultraviolet radiation, changes in temperature and humidity), chemical (cosmetic ingredients, environmental pollutants), and psychological factors (emotional stress). This article provides a narrative review of the current research on SSC, drawing on literature published between 1963 and 2024 in PubMed, Elsevier, and Web of Science databases. We summarize its hallmark symptoms, available evaluation methods, potential mechanisms, and contributing factors and propose corresponding scalp care recommendations. This review aims to offer theoretical insights into the pathogenesis of SSC and to support the development of effective protective strategies.

1. Introduction

The International Forum for the Study of Itch (IFSI) defines sensitive skin as a syndrome characterized by the occurrence of unpleasant sensations such as stinging, burning, pain, pruritus, and tingling in response to stimuli that should not normally provoke such feelings. These sensations cannot be explained by visible skin lesions attributable to any dermatological disease. The skin may appear normal or present with erythema. Sensitive skin can affect all parts of the body, particularly the face [1]. However, it is not restricted to the face and frequently occurs on other regions such as the hands, scalp, feet, neck, trunk, and back [2]. Due to its thin skin and rich network of sebaceous glands, nerves, and blood vessels, the scalp is particularly prone to sensitivity.

Sensitive scalp (SSC) is defined as the occurrence of abnormal and unpleasant sensory reactions such as pruritus, stinging, tightness, pain, and burning in response to environmental stimuli in the absence of obvious clinical signs of inflammation [3]. While these symptoms are commonly seen in various scalp conditions, it is noteworthy that patients may experience these sensations even without a clear underlying skin disease. In a French epidemiological study on SSC [4], 11.5% of individuals with SSC reported coexisting scalp disorders, such as seborrheic dermatitis, psoriasis, or alopecia, while 88.5% did not present with any known scalp diseases. Although the prevalence of scalp disorders was higher among those with SSC compared to non-sensitive individuals (11.5% vs. 1.1%), these disorders are not considered direct symptoms of scalp sensitivity. An increased degree of scalp sensitivity was associated with a higher likelihood of concurrent scalp diseases. However, the majority of individuals, particularly those with mild to moderate sensitivity, did not exhibit any identifiable dermatological diseases.

In addition, some researchers have classified sensitive scalp into two types: primary sensitive scalp and secondary sensitive scalp [5]. Primary sensitive scalp refers to sensitive symptoms occurring in the absence of known scalp diseases, while secondary sensitive scalp refers to sensitive scalp symptoms associated with existing skin conditions such as seborrheic dermatitis, psoriasis, or hair loss. Although these two types of sensitive scalp share common symptoms, they differ in their etiology and treatment strategies. This review will focus on primary sensitive scalp, in which no dermatologic disease is present, although reference to secondary causes will be made when relevant for context. We will explore the symptoms, current assessment methods, potential pathogenic mechanisms, epidemiological characteristics, and triggering factors of SSC. Through the analysis of existing literature, we will propose management strategies. Furthermore, we will also highlight emerging insights from the fields of lipidomics and microbiomics, aiming to deepen understanding in this area and provide guidance for future research.

2. Symptoms and Evaluation of Sensitive Scalp

The primary symptoms of scalp sensitivity are similar to those observed in sensitive skin on other body sites and commonly include pruritus, stinging, tightness, pain, and burning sensations [2]. Among these, pruritus is the most frequently reported complaint in individuals with SSC. Scalp pruritus may result from various causes. It is now classified into the following categories based on the underlying etiologies [6,7]: dermatological (e.g., seborrheic dermatitis, psoriasis [8,9,10]); neuropathic (diabetic neuropathy [11], postherpetic neuralgia [12], or small fiber neuropathy [13]); systemic (e.g., chronic kidney disease, liver disorders, and hematological malignancies [6]); and psychogenic (e.g., anxiety, delusional parasitosis [14,15]). When no identifiable underlying disease is found, the condition is categorized as pruritus of unknown origin.

SSC is characterized by abnormal or unpleasant sensory reactions. In the absence of identifiable dermatological conditions or specific pathological mechanisms, the associated pruritus is classified as pruritus of unknown origin [1,4]. Individuals with SSC often exhibit a reduced threshold for external stimuli and are more susceptible to environmental triggers such as temperature fluctuations, pollutants, and hair care products [6]. Tingling sensations are believed to result from overstimulation of cutaneous sensory nerve endings, potentially due to underlying neurological conditions or nerve damage [16]. The SSC reacts easily to even minor stimuli, often leading to burning, stinging, or pain. Exposure to irritant chemicals such as shampoos, conditioners, and hair dyes may provoke burning sensations on the scalp. Additionally, a feeling of scalp tightness may be caused by excessive lipid removal and subsequent dryness due to the prolonged use of overly harsh cleansing shampoos [17].

Topical tests such as the capsaicin and lactic acid sting tests are commonly used to evaluate facial sensitive skin. However, due to the presence of hair, these methods are not easily applicable to the scalp [18]. Currently, the evaluation of scalp sensitivity primarily relies on the assessment of subjective symptoms, which remains the main approach for identifying SSC and determining its severity.

Three commonly used subjective evaluation methods for SSC include the four-grade self-assessment scale, the 3S questionnaire, and the 10Q questionnaire. The four-grade self-assessment method classifies sensitivity into four levels (non-sensitive, mildly sensitive, sensitive, and very sensitive) based on the subject’s perception. Although it allows for rapid initial screening, the results are often influenced by the individual’s understanding of what constitutes a “SSC”, thereby limiting objectivity. The 3S questionnaire assesses five key symptoms-pruritus, stinging, tightness, pain, and burning, and evaluates their impact on quality of life using a 0–4 scale. A total score ranging from 0 to 20 is calculated and used to classify the severity: mild (≤8), moderate (9–11), and severe (≥12). This method focuses on quantifying the subjective severity of symptoms and their interference with daily life, offering advantages in standardized scoring and diagnostic stratification [4].

The 10Q questionnaire explores the association between 10 common environmental triggers (e.g., sunlight, heat, dryness, stress) and symptom occurrence [18]. It emphasizes identifying the relationship between specific triggers and symptoms through a trigger exposure frequency score (maximum 50 points), thus highlighting the influence of environmental factors on scalp sensitivity.

A 2016 epidemiological study conducted in China compared the application of these three methods [18]. The 3S questionnaire revealed an age-dependent increase in the prevalence of SSC. Yet, the self-assessment scale seemed to underestimate prevalence in older adults, likely due to differences in self-awareness. Strong correlations were observed between the 3S and 10Q scores, and both identified pruritus as the predominant symptom. However, discrepancies emerged in the evaluation of stinging, tightness, and burning sensations, reflecting the differing emphases of each method.

Overall, current evaluations of SSC remain predominantly subjective. Although advances have been made in symptom stratification and trigger identification, assessment remains constrained by the limitations of self-reporting. These include difficulties in accurately recalling symptom frequency and intensity due to the transient and subjective nature of symptoms. Additionally, cultural differences may influence symptom interpretation and reporting. For instance, emotional stress was reported as a key trigger by 53.03% of participants in a French study [19], compared to only 15.2% in a Korean cohort [20]. These findings highlight the influence of recall bias, cultural variability, and the lack of objective biomarkers in the assessment of SSC.

3. Barrier Function of Sensitive Scalp

As a distinct cutaneous region, the scalp represents one of the body sites with the highest density of hair follicles [21]. Within the dermis, deeply rooted follicles in close association with large sebaceous glands form a symbiotic unit that creates a low-oxygen, high-humidity microenvironment. In parallel, the rich capillary network and the dense distribution of sensory nerve endings constitute a highly sensitive surveillance system [6,22], rendering the scalp particularly responsive to both exogenous and endogenous stimuli. Currently, due to the limited direct research on primary sensitive scalp, much of the discussion is based on extrapolations from studies on other skin conditions. Based on previous studies, such stimuli can activate transient receptor potential vanilloid 1 (TRPV1) channels. This leads to the release of substance P and multiple neuropeptides, triggering neurogenic inflammation and eliciting symptoms of sensitive skin [23,24,25]. Given that SSC is a form of sensitive skin, similar mechanisms may also be involved in the development of SSC. Furthermore, disruption of the scalp barrier may also play a crucial role in the pathogenesis of SSC.

Multiple inflammatory skin diseases have been shown to be closely associated with barrier dysfunction. For instance, in atopic dermatitis (AD), disruption of the stratum corneum structure and intercellular lipid lamellae compromises the permeability barrier [26,27], facilitates penetration of environmental factors, and perpetuates a vicious cycle under the drive of type 2 inflammatory responses [28]. Concurrently, microbial diversity on AD skin is markedly reduced. Pathogens like Staphylococcus aureus colonize abnormally, while commensals decline. This dysbiosis further weakens barrier function and amplifies inflammation [29,30,31]. Seborrheic dermatitis (SD) is characterized by barrier dysfunction in sebum-rich areas [32,33], primarily driven by aberrant interactions between sebum and microbes. Specifically, Malassezia secretes lipases that hydrolyze triglycerides, generating metabolites like oleic acid and arachidonic acid. These metabolites disrupt keratinocyte differentiation and barrier integrity, and simultaneously induce inflammatory responses [34,35,36]. Collectively, these findings highlight the importance of the interplay between sebum, lipid metabolism, and the microbiome in maintaining skin barrier homeostasis. Their imbalance often leads to barrier disruption and exacerbated inflammation.

As one of the areas with the highest sebaceous secretion and follicular density, the scalp barrier is particularly vulnerable to changes in sebum production and the microbiome [37]. Although most of the current evidence on SSC comes from epidemiological studies, existing findings clearly show that SSC is closely associated with scalp barrier dysfunction. Ma et al. (2019) found that SSC is frequently accompanied by increased pH, higher sebum secretion, and microbial dysbiosis, particularly an increase in Propionibacterium and a decrease in microbial diversity [21]. These results strongly suggest that the balance between sebum, lipid metabolism, and the microbiome plays a critical role in maintaining scalp barrier function, and its disruption may be a key factor in the development of SSC symptoms (Figure 1). However, the exact roles of lipid composition and microbial changes in SSC are still not fully understood. Given the close, dynamic interplay between the lipidome and microbiome, combining lipidomics and microbiomics could offer new insights into the mechanisms underlying scalp barrier dysfunction in SSC. Future research could focus on several key areas, including identifying the specific lipidomic profile associated with SSC, examining microbial changes during SSC development, and understanding how these lipid and microbial alterations impair the scalp barrier and promote inflammation at the molecular level. These studies are essential for further elucidating the complex pathophysiology of SSC and could provide a theoretical basis for developing targeted treatments and scalp care products.

4. Epidemiology and Triggers of Sensitive Scalp

Epidemiological studies on SSC indicate that the prevalence generally ranges from 30% to 56%. Most of these studies rely on self-report questionnaires, which are inherently subjective. Differences in regional lifestyle habits, cultural backgrounds, and environmental factors can introduce response bias, potentially affecting the reported prevalence rates. Furthermore, variations in sample size and questionnaire design may contribute to biases in the results. For instance, four-level self-assessment questionnaires tend to overestimate the prevalence, while structured tools, such as the 3S questionnaire, tend to provide more conservative estimates [18]. Although the prevalence estimates vary across studies, the general trends in identifying the factors influencing SSC appear to be consistent.

4.1. Prevalence of Sensitive Scalp by Age and Gender

Further analysis of the epidemiological survey results revealed that the prevalence of SSC varies by age and gender. Several studies have demonstrated that the prevalence of SSC is significantly higher in women than in men. A nationwide survey conducted in France [19] revealed that 47.4% of women reported having SSC, compared to only 40.8% of men (p < 0.05). Subsequent research further confirmed this finding [4], showing that the proportion of SSC in women was 35.56%, which was significantly higher than the 29.10% observed in men. In addition, a cohort study focusing on individuals with hair loss [38] showed that 84.31% of patients with SSC were women, while only 15.69% were men. The higher prevalence in females may be attributed to differences in neural sensitivity, hormonal fluctuations, and more frequent use of cosmetic products. Additionally, elevated anxiety levels in women may enhance pain perception [39].

A significant association also appears to exist between age and the prevalence of SSC. Misery et al. [4] (2011) reported that the prevalence of SSC in the French population increased with age, rising from 23.16% in individuals aged 15–17 years to 39.07% in those aged ≥75 years. This trend was hypothesized to be associated with a reduction in epidermal nerve endings [40] and long-term use of irritating shampoos. Similarly, Ma et al. [18] (2016) observed that in Chinese women, the self-assessed prevalence of SSC peaked at 54.54% in the 30–39 age group, while assessments based on the 3S questionnaire indicated a continuous age-related increase, reaching 57.23% in the 50–60 age group. Burroni et al. (2022) [38] further confirmed that among patients with hair loss, the prevalence of sensitive scalp was highest (49.02%) in individuals over the age of 50. This phenomenon was attributed to the loss of nerve endings [40] and the imbalance of scalp microbiota in the elderly [38]. Collectively, these findings suggest that advancing age may increase the risk of SSC through a combination of neurodegeneration and chronic exposure to irritants. Additionally, in the elderly, sebaceous glands may become enlarged. However, sebum secretion levels tend to decline with age [41,42]. Studies have also shown that the content of stratum corneum lipids decreases in aged skin, particularly ceramides [43], leading to a weakened barrier function. Although TEWL does not increase significantly in aged skin [44,45], the decline in hydration capacity makes it more prone to dryness. Meanwhile, cumulative photoaging damage may impair barrier repair capacity [46], further increasing scalp sensitivity to exogenous stimuli and thereby elevating the risk of developing SSC.

4.2. Psychological Stress and Sensitive Scalp

Psychological stress can also exacerbate symptoms of SSC [47]. A French study reported that 53.03% of patients identified emotional fluctuations as a trigger for their symptoms [19], while a study conducted in China found a significant association between stress and scalp tightness (OR = 3.201, p < 0.001) [18]. Conditions such as anxiety, depression, stress, and emotional dysregulation have been shown to aggravate symptoms of skin sensitivity. This has been confirmed by multiple psychological assessments conducted among patients with sensitive skin [48,49,50,51]. Chronic anxiety may activate the hypothalamic-pituitary-adrenal (HPA) axis and increase the secretion of stress hormones, which impairs stratum corneum hydration, elevates TEWL, and alters the composition of epidermal lipids and structural proteins-ultimately leading to scalp barrier dysfunction [52,53]. In addition, psychological factors may contribute to the onset of trichodynia. About 35.7% of patients with alopecia experience trichodynia as a consequence of anxiety or depression [54]. It should be emphasized that trichodynia is not a component of SSC, but rather an independent syndrome with overlapping symptoms. The two conditions may coexist clinically [5,55].

4.3. Cosmetic Products and Sensitive Scalp

The use of cosmetic products is one of the major triggers of SSC. A study by Brenaut et al. [56] involving 133 women without scalp diseases found that 53.6% of those with SSC used hair conditioners, compared to 40% in the control group. Moreover, the amount of conditioner used was significantly higher in the SSC group than in controls (5.48 ± 5.87 g/application vs. 2.88 ± 3.75 g/application, p = 0.03). In addition, Misery et al. [19] observed that subjects with sensitive or very sensitive scalps were more frequently irritated by shampoo compared to those with slightly sensitive or non-sensitive scalps. The use of hair dyes can also induce scalp issues such as erythema, pruritus, desquamation, allergic reactions, and stinging sensations. In severe cases, it may even lead to scalp disorders like contact dermatitis [57,58,59]. Further studies have shown that common ingredients in hair conditioners, such as preservatives (e.g., isothiazolinones), fragrances, and cationic polymers, may induce contact dermatitis, pruritus, and inflammatory responses by forming residues on the scalp and altering barrier function and the local microenvironment [60,61,62]. In fact, epidemiological and toxicological evidence has shown that certain sensitizing components in scalp cosmetics-such as surfactants, para-phenylenediamine (PPD), fragrance mixtures, and isothiazolinone preservatives (methylchloroisothiazolinone/methylisothiazolinone) can damage the scalp barrier, facilitate allergen penetration, and potentially activate delayed-type hypersensitivity responses [62,63]. Extremes in cleansing habits also negatively affect scalp barrier function. Excessive cleansing can increase TEWL and impair barrier integrity, raising exposure to irritants and triggering scalp sensitivity [19]. Conversely, infrequent cleansing can lead to sebum buildup, increasing the occurrence of flaking, pruritus, and dryness [64]. A study by Kato et al. [65] demonstrated that scalp itchiness and greasiness increased at 72 h after shampooing, but these symptoms can be rapidly relieved by re-washing the scalp.

4.4. Environmental Factors: Physical and Chemical Triggers

Environmental factors are major exogenous triggers of SSC. A study conducted in China [18] revealed that 59.06% of patients identified high temperatures as a primary trigger, while 51.52% reported sensitivity to solar ultraviolet radiation. Notably, sun exposure was significantly associated with burning sensations in individuals with SSC. Both dry air and hot, humid conditions can exacerbate TEWL from the stratum corneum, thereby intensifying pruritus symptoms. Although epidemiological data support the association between these environmental factors and SSC, the underlying mechanisms remain hypothetical and currently lack direct experimental validation. The following are some hypothetical mechanisms proposed based on existing literature, aimed at explaining how environmental factors may potentially exacerbate the symptoms of SSC.

Elevated temperatures markedly enhance sebaceous gland activity. For each 1 °C increase in temperature, the rate of sebum secretion rises by approximately 10% [66]. Excessive sebum production can promote the growth of anaerobic and lipophilic microorganisms. When excessive sebum blocks hair follicles and creates hypoxic conditions, Cutibacterium acnes can overproliferate and release more free fatty acids, potentially triggering inflammatory responses in the scalp [67]. Furthermore, high temperatures and high humidity also facilitate the proliferation of Malassezia species. These yeasts metabolize saturated fatty acids into unsaturated fatty acids such as oleic acid and arachidonic acid. The excessive accumulation of these metabolites can penetrate the compromised barrier, stimulate nerve endings, and induce inflammatory responses [68,69]. Overall, high temperatures promote sebum secretion and alter the skin’s microecological environment. This leads to the accumulation of lipid metabolic products, such as free fatty acids and unsaturated fatty acids, which can stimulate nerve endings and trigger inflammatory responses, exacerbating sensitive scalp symptoms.

Environmental pollutants can affect sebum components on the scalp. Squalene, an important component of sebum, is susceptible to oxidative degradation by environmental pollutants such as ozone, UVA radiation, and cigarette smoke [70,71]. Studies have shown that squalene degradation products, particularly squalene monohydroperoxide (SQOOH), can stimulate keratinocyte proliferation and inflammatory responses [66]. Air pollutants are a complex mixture of airborne particles of varying sizes and chemical compositions, including polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs), nitrogen oxides (NOx), particulate matter (PM), ozone, and cigarette smoke [72]. Exposure to air pollutants can induce oxidative stress in the skin, subsequently disrupting the integrity of the skin barrier by altering TEWL, inflammatory signaling pathways, stratum corneum pH, and the skin microbiome. Prolonged contact of PM with the scalp may contribute to scalp inflammation, pruritus and dryness-symptoms that closely resemble those observed in sensitive scalp conditions [47,73].

Overall, although the relationship between these environmental factors and SSC symptoms is supported by epidemiological studies, the understanding of the underlying mechanisms remains largely hypothetical, with insufficient experimental validation. We hypothesize that environmental factors may exacerbate sensitive scalp symptoms through multiple pathways, including influencing sebum secretion, altering the microbiota, disrupting the skin barrier, and inducing oxidative stress. Future experimental research is expected to further validate these hypotheses and provide a more solid theoretical foundation for the prevention and treatment of sensitive scalp.

A summary of the Triggers is presented in Figure 2 and

Table 1. Epidemiological Factors Affecting Sensitive Scalp: A Summary of Data and Conclusions.

Factor	Epidemiological Data	Conclusion	References
Gender	Higher prevalence in females 47.4% vs. 40.8%, (France, 2008) [19]; 35.56% vs. 29.10% (France, 2011) [4]; 84.31% vs. 15.69% (China, 2016) [18]	The prevalence of sensitive scalp is higher in females	Misery et al., 2008 [19] Misery et al., 2011 [4] Ma et al., 2016 [18]
Age	Prevalence increases with age 23.16% in 15–17 years, 39.07% in ≥75 years (France, 2011) [4]; 54.54% in 30–39 years (China, 2016) [18]; 57.23% in 50–60 years (China, 2016) [18]; 49.02% in people aged 50+ (Italy, 2022) [38]	The prevalence of sensitive scalp increases with age	Misery et al., 2011 [4] Ma et al., 2016 [18] Burroni et al., 2022 [38]
Cosmetic Use	53.6% of females using conditioner reported sensitive scalp symptoms, significantly higher than 40% in controls (France, 2020) [56]	The use of conditioner and shampoo exacerbates sensitive scalp symptoms	Brenaut et al., 2020 [56]
Psychological Factors	53.03% of patients reported emotional fluctuations as a major trigger (French, 2008) [19]	Psychological factors like anxiety and emotional fluctuations exacerbate sensitive scalp symptoms	Misery et al., 2008 [19]
Environmental Factors	59.06% report high temperature as a major trigger; 51.52% report UV exposure as a major trigger (China, 2016) [18]	Environmental factors like high temperature and UV exposure exacerbate sensitive scalp symptoms	Ma et al., 2016 [18]

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5. Management of Sensitive Scalp

The symptoms of SSC are influenced by a variety of endogenous and exogenous factors. As a suboptimal health condition, SSC is often overlooked. However, individuals with scalp sensitivity are more prone to disorders such as alopecia and dermatitis. Therefore, it is essential to establish long-term awareness of protection and care for SSC. Based on current evidence, this article proposes a systematic management approach:

5.1. Cosmetic Use and Cleansing

Cosmetic use and cleansing practices represent major triggers of SSC. Daily care should prioritize mild cleansing products, with amphoteric surfactants or gentle anionic surfactants being preferred [74,75]. In addition, studies have shown that shampoos containing Hamamelis virginiana extract can help alleviate symptoms of sensitive scalp [76]. Maintaining an appropriate hair-washing frequency (once every 1–2 days) helps sustain scalp homeostasis [64]. When using conditioners or similar products containing cationic surfactants, direct contact with the scalp should be avoided and thorough rinsing ensured to minimize residual effects on the barrier [56,77]. Furthermore, the frequency of hair coloring and perming should be reduced to avoid chemical-induced sensitivity [63]. The use of high-temperature styling tools such as flat irons should also be limited, as they may burn the scalp and compromise barrier integrity [78].

5.2. Photoprotection and Environmental Care

Ultraviolet exposure can aggravate symptoms in SSC patients, making photoprotection indispensable. Wearing a sun hat can prevent excessive sun exposure that leads to barrier damage and scalp burning sensations [18,79]. Scalp care should also be adapted to seasonal conditions. In hot and humid environments, products containing sebum-controlling and antimicrobial ingredients may help suppress excessive sebum secretion and the proliferation of Malassezia [80]. In cold or dry seasons, hydration should be reinforced with products containing glycerol, hyaluronic acid, or ceramides to improve stratum corneum hydration [81].

5.3. Psychological Management and Lifestyle

Psychological stress is closely associated with the onset and exacerbation of SSC, while emotional disturbances frequently aggravate symptoms such as scalp tightness and trichodynia. Accordingly, daily management should emphasize the identification and control of stressors [82], as well as maintaining regular sleep–wake cycles and sufficient sleep [83,84], in order to preserve neuroendocrine balance and the stability of the scalp barrier.

5.4. Medical Intervention

If patients present with persistent erythema, scaling, or similar symptoms, they should seek medical attention promptly. When necessary, dermoscopy and other diagnostic tests can help exclude underlying inflammatory or allergic dermatoses, followed by systemic or targeted therapies under medical supervision. Sensitive scalp syndrome primarily refers to primary sensitive scalp symptoms, which occur without any identifiable underlying dermatological conditions. For patients exhibiting noticeable erythema, scaling, or similar clinical signs, secondary sensitive scalp should be considered, which may be associated with scalp disorders such as seborrheic dermatitis.

6. Conclusions

SSC has gained increasing attention in dermatology. The most common symptoms include subjective discomfort such as itching, tingling, or burning sensations, and primary SSC is characterized by the absence of visible scalp lesions. Current assessment methods mainly rely on self-reported questionnaires. Although such tools are useful for preliminary classification, they are highly susceptible to bias. This underscores the urgent need for objective and standardized diagnostic criteria.

At present, most mechanistic insights into SSC are extrapolated from studies on other skin sites and have not been fully validated on the scalp. Despite the incomplete understanding of SSC pathogenesis and the lack of well-established experimental models, existing evidence suggests that alterations in lipid metabolism and imbalances in the scalp microbiota may play crucial roles in its development.

Applications of lipidomics and microbiomics in SSC research remain at an early stage, but these approaches have been widely applied in the study of other skin diseases, such as seborrheic dermatitis and atopic dermatitis, yielding preliminary results [85,86,87,88]. These studies provide valuable insights and directions for research on SSC. Our research group has previously established a comprehensive multi-omics research platform and demonstrated that factors such as gender, anatomical site, and circadian rhythm significantly influence the composition of skin lipids and microbial communities [89,90,91,92,93,94,95,96,97,98,99,100,101,102,103,104,105,106,107]. We believe that these omics-based approaches can offer new perspectives for elucidating the molecular mechanisms underlying SSC. Future studies should focus on characterizing the lipidomic profiles associated with SSC, examining dynamic changes in the scalp microbiota during disease progression, and exploring how alterations in lipids and microbes may modulate scalp barrier function and trigger inflammatory responses through molecular mechanisms. Such advancements will ultimately contribute to precision scalp care and evidence-based management, thereby improving clinical outcomes and quality of life for individuals with sensitive scalp.