Skin sensitization caused by cosmetics, including quasi-drugs, is an extremely serious problem and can become a health hazard. Although several in vitro methods for skin sensitization have been established by the Organization for Economic Cooperation and Development (OECD), no practical method for predicting skin sensitization potency has been found which can serve as an alternative to animal testing. In this study, an in silico model is developed which predicts skin sensitization potency by combining in vitro OECD test guidelines and information of the physical properties of chemicals to evaluate hair dye ingredients without animal testing. A dataset published by Cosmetics Europe was used to develop the in silico model. The EC3 value of the mouse local lymph node assay (LLNA), which is used as an indicator of skin sensitization potency, was the objective variable; in vitro test values, physical properties, and chemical information obtained from the molecular descriptor calculation software MOE constituted the explanatory variables. CatBoost was adopted as the machine-learning approach. Bandrowski’s base (BB), a trimer of the typical oxidative dye para-phenylenediamine (pPD), was used as the test material. In the predictive model, the mean-predicted EC3 value for BB was 0.33%, which meant a strong sensitizer. Furthermore, it was lower than the mean model prediction EC3 value (0.66%) of pPD, which is considered weaker sensitization potency than BB in LLNA. This indicates that BB was correctly predicted as a stronger skin sensitizer than pPD in the proposed in silico model.

It is well known that the generation of reactive oxygen species (ROS) is increased in aged cells, however, there have been no reports on ROS levels in replicative senescent normal human epidermal keratinocytes (NHEKs). In this study, we investigated the mechanism of increased ROS generation in replicative senescent NHEKs using long-term cultured NHEKs. We defined primary NHEKs cultured for 27 days as aged NHEKs since they express various senescence markers and have decreased proliferation, and compared them with young NHEKs cultured for 13 days that did not show any senescence traits. The number of mitochondria in aged NHEKs increased along with cell enlargement due to aging but the mitochondrial density per protein content was not significantly different from that of young NHEKs. However, the ability to produce ATP was significantly decreased in aged NHEKs compared to young NHEKs. On the other hand, the amount of superoxide that was produced by mitochondria was not significantly different between young and aged NHEKs, and the amount of Mn-SOD (superoxide dismutase), which catalyzes superoxide to hydrogen peroxide, was significantly increased in aged NHEKs compared to young NHEKs. In addition, when hydrogen peroxide was added to the culture medium of young and of aged NHEKs, the scavenging rate was unexpectedly higher in aged NHEKs than in young NHEKs. Furthermore, the amounts of hydroxyl radicals derived from hydrogen peroxide, and Fe²⁺, which catalyzes the reaction, were both higher in aged NHEKs than in young NHEKs. These results suggested that some hydrogen peroxide that had not been eliminated by catalase or glutathione peroxidase is converted to hydroxyl radicals by Fe²⁺, which may contribute to the increased generation of ROS in replicative senescent NHEKs.

Recently, various kinds of non-surgical treatments for sagging face has come into our aesthetic medical market. Although these treatments are less effective compared with surgical procedures, we can get natural-looking rejuvenating results by understanding how the face change with aging and using energy-based devices, injectables and threads. With aging, laxity and/or atrophy occur in not only skin but also subcutaneous fat, fascia, retaining ligament and bone. As a result, we can see aged appearance. Therefore, in treatment, it is necessary to improve aging changes according to both laxity and atrophy, while always considering which region and which layer should be changed.

Basically, energy-based devices have tightening effect by heating, and cannot improve atrophic change. It is better to combine injectables and threads. However, age-related change of facial appearance does not stop and progress. We should not hang up on getting temporary result. It is important to keep youthful appearance for a long time.

Sagging, which is a ptosis of the skin formed under the influence of gravity, progresses with aging, causes morphological changes of the face, and gives a strong impression of aged appearance, so that it is a great matter of concern to people worldwide. However, until recently, cosmetics R&D has been targeting skin surface wrinkles, which appear on the superficial region on the skin, instead of the morphological change of the face, sagging. Therefore, we tried to refocus R&D in the cosmetic field toward sagging, in order to help people suffering from lower quality of life (QOL) due to this issue. But, since sagging was a novel field, we first needed to establish the fundamental basis for sagging research from scratch, including definitions of sagging, evaluation systems for extent of sagging, and so on. Through this program, we have clarified the actual situation of sagging of the face, such as how it progresses with aging, gender differences, and relationships with other signs of aged appearance. Further, we have identified a variety of critical contributors to the aging-related occurrence of sagging, such as deterioration of the dermal layer, impairment of mimetic muscles, loss of characteristic structure in facial skin (anchoring structure), loss of integrity of the lower dermal layer (dermal cavitation), and so on. Further, we characterized various regulation systems of dermal layer condition that influence resistance to sagging, including regulation of the dermal layer by the subcutaneous adipose layer, and the dermal cell network as a crucial controller of dermal cell aging. Based on these findings, we have established a variety of cosmetic approaches to ameliorate sagging. In this review, I would like to introduce cosmetics R&D focused on sagging in facial skin.

Allergic contact dermatitis from products used on the scalp causes symptoms not only on the scalp, but also on the face, neck, and back. Some products, such as oxidative hair dye, produce a generalized contact dermatitis syndrome. It is difficult for dermatologists to recognize that dermatitis on the face is allergic contact dermatitis caused by products used on the head. The continued treatment with topical tacrolimus ointment or topical steroids, without excluding the causes of the exacerbation, may lead to the development of additional skin diseases such as rosacea-like dermatitis. There are also cases of delayed allergic contact dermatitis caused by oxidative hair dye, which may lead to anaphylactic symptoms after repeated exposure. It is extremely important to diagnose allergic contact dermatitis before it becomes severe and to eliminate allergens from the patient’s life.

Patch testing is most useful in finding the cause. Even if the patch test is positive for a product, if the causative allergen cannot be determined, there remains the possibility that symptoms will not improve even if the patient changes the products they use. In addition, patch testing with the product may give false-negative results, so it is advisable to patch test the allergen at the same time along with the product. Japanese baseline series and cosmetics-related allergens are applied, but it is difficult to obtain cosmetics-related patch test allergens in Japan. Even commercially available allergens may give false-negative results depending on the reagent. It would be more diagnostic if raw materials could be provided by the manufacturer of the product that tested positive in the patch test.

In this paper, we will provide specific examples of cases of contact dermatitis caused by products used on the scalp and describe the problems involved in diagnosing allergic contact dermatitis and determining its cause.

Skin disorders caused by skin care products and cleansers, especially allergic contact dermatitis, are described from 2 cases, interviews, symptoms, examination, diagnosis, and daily life guidance until the identification of the causative agent.

A detailed medical interview is necessary in order to perform an accurate examination, identify the causative allergen, make a diagnosis, and provide daily life guidance. If allergic contact dermatitis caused by skin care products or detergents is suspected from the interview, a skin test is performed to identify the causative allergen. Daily life guidance is to provide information on avoidance of causative allergens, methods of confirming causative allergens, and alternatives. Prevention of recurrence is of utmost importance.

Case 1 was diagnosed as allergic contact dermatitis due to beeswax, methylisothiazolinone, propynyl butylcarbamate iodide, and perfume during cleanser. Case 2 was diagnosed as paraben-induced allergic contact dermatitis.