**1. Introduction**

Melanin is the natural polymer pigment responsible for imparting color to the skin, hair, and eyes as well as provides the photoprotection of the skin against ultraviolet radiation. It is produced inside the specialized organelles, melanosomes of melanocytes through a complex process called melanogenesis. Although melanin protects the skin from UVB radiation damage, its overproduction leads to the problem of hyperpigmentation and its related disorders. Post-inflammatory disorders,

ephelides, solar lentigines, melasma, etc. are the common diseases of hyperpigmentation. Skin color imperfection due to hyperpigmentation spots on the face causes psychological problems in patients and takes them far from their social life. The public perceptions of tanned skin as being healthy and attractive merged with growing demand of treatment of facial hyperpigmentation provoke huge interest cosmeceutically as well as pharmaceutically [1–4].

Facial hyperpigmentation is a common and emergent concern to the dermatologists today. Treatment for facial hyperpigmentation seems to be difficult as there is no universally accepted treatment for it, and also the efficiency of known active agents is different. Majority of reports concerning the treatment of the disease consist of small series of patients. So, it becomes challenging to evaluate the efficacy of variety of therapy. Moreover, there are various options, but some of them come under growing scrutiny, emphasizing the research into pathogenesis and treatment. Sunscreen, chemical peeling, laser therapy, dermabrasion, topical treatment, cosmetic camouflages, etc. are the different treatment modalities used to treat facial hyperpigmentation. Though they are very effective and instant treatment for hyperpigmentation, its long-term exposure causes various side effects. Persistent erythema, swelling, pain, allergic reactions, herpes recurrence, acne, dyspigmentation, etc. are some of the various after effects associated with these treatment strategies [5–7].

In opposition to the state of affairs with these treatment options, we have the other side with herbal treatment which are nowadays attaining importance due to their low cost and ease of use and are believed to be free from risk of handling them as well as scarcely pollute the environment. Consequently, a dermatological formulation, including active ingredients of strictly natural origin, is designed by a variety of scientist to protect the skin from exogenous and endogenous harmful agents. There are many chemical reactions involving various enzymes that are engaged in melanogenesis. So, there is a wide range of targets or mechanisms against which to screen for skin pigmentation control agents. Active compounds isolated from different plants inhibit melanogenesis with no cytotoxicity by different mechanisms including inhibition of tyrosinase and other related protein expressions, inhibition of tyrosinase activity, inhibition of melanin dispersion and translocation, etc. [8–10].

Hence, the present chapter highlights the commonly occurring hyperpigmentary diseases of the face and their aetiologies. The available treatment options for hyperpigmentation along with the problems associated with them. As there is vast flora available on earth which has valuable medicinal properties, they are used for the treatment of many incurable diseases. Consequently, plants and its products are used for the treatment of hyperpigmentation through different mechanisms of action. Various studies on the use of plants for hyperpigmentation treatment have also been discussed in the present chapter.

#### **2. Biosynthesis of melanin**

Melanin is the end product of complex multistep transformation of amino acid, L-tyrosine. It is the polymorphous and multifunctional biopolymer represented by eumelanin (brown-black melanin), pheomelanin (brown-red melanin), and allomelanin (nitrogen-free melanin). This can be differentiated on the basis of chemical composition and monomer subunit structure of melanin. It has been found that there are four factors involved in melanin formation: (1) tyrosine as substrate, (2) tyrosinase with its coenzyme, (3) molecular oxygen, and (4) dihydroxyphenylalanine (DOPA). Tyrosine is converted into melanin by a series of enzymatic reaction [11–13].

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*On the Intricacies of Facial Hyperpigmentation and the Use of Herbal Ingredients as a Boon…*

Biosynthesis of melanin can be initiated from either the hydroxylation of L-phenylalanine to L-tyrosine or directly from L-tyrosine, which is then hydroxylated to L-dihydroxyphenylalanine (L-DOPA). In the next step, L-DOPA is oxidized to dopaquinone which is common to both eu- and pheomelanogenic pathways. Formation of eumelanin involves transformation of dopaquinone to leukodopachrome, followed by a series of oxidoreduction reactions. Dihydroxyindole (DHI) and DHI carboxylic acid (DHICA) are produced as intermediates, which undergo polymerization to form eumelanin. Pheomelanin synthesis also begins with dopaquinone; this is conjugated to cysteine or glutathione to yield cysteinyldopa and glutathionyldopa, for further transformation into pheomelanin. Mixed melanin contains both eu- and

**3. Hyperpigmentary diseases of the face and their etiology**

Melanocytes are responsible for the synthesis and distribution of melanin pigment, by the process of melanogenesis which involves different stages from embryonic development, melanin synthesis, to its transfer to neighboring keratinocytes. The importance of each of these stages and their mechanisms is evident in clinical defects in the form of hypopigmentation or hyperpigmentation. Exposure of the skin to UV radiation or other exo- and endogenous sources/allergen poses erythema, variation of vascular responses and immunosuppression, formation of inflammatory mediators, or overproduction of melanin which leads to pigmentary

Facial hyperpigmentation is a common and growing concern to the dermatologists today. The difference in structure and function of the skin, as well as the influence of cultural practices, produces variable skin diseases of the face based on skin type. There are many skin conditions quite unique to person skin of color. Some of

Postinflammatory hyperpigmentation (PIH) refers to the darkening of the skin that arises after cutaneous injury or inflammatory eruption. Hyperpigmentation results from the melanocyte's response to the cutaneous insult, which causes increased production of melanin. Acne lesions, scratches, insect bites, ingrown hairs, etc. are among such cutaneous insults. It has been found that patients of darker skin are more susceptible to this pigment alteration. Postinflammatory changes can occur both in the epidermis and dermis of the skin. In epidermal hyperpigmentation, there is an increase in melanin production and/or its transfer to keratinocytes. In dermal postinflammatory hyperpigmentation, a damaged basement membrane allows melanin to enter the dermis, which is then phagocytosed by dermal macrophages, called as melanophages. Macrophages may also migrate into the epidermis, phagocytose melanosomes, and then return to the dermis. Melanin within dermal melanophages

Physical examination of PIH includes small to large hyperpigmented macules and patches of variable size in any distribution. The time required for the normalization of dyspigmentation is unpredictable and depends on many factors including the patient's baseline skin tone, the type and intensity of the injury or inflamma-

*DOI: http://dx.doi.org/10.5772/intechopen.84257*

pheomelanin [12, 14–18].

disorder, i.e. hyperpigmentation [19–21].

**3.1 Postinflammatory hyperpigmentation**

them are summarized here.

may persist for years [22–25].

tion, and the patient's sun exposure habits [22, 24].

*On the Intricacies of Facial Hyperpigmentation and the Use of Herbal Ingredients as a Boon… DOI: http://dx.doi.org/10.5772/intechopen.84257*

Biosynthesis of melanin can be initiated from either the hydroxylation of L-phenylalanine to L-tyrosine or directly from L-tyrosine, which is then hydroxylated to L-dihydroxyphenylalanine (L-DOPA). In the next step, L-DOPA is oxidized to dopaquinone which is common to both eu- and pheomelanogenic pathways. Formation of eumelanin involves transformation of dopaquinone to leukodopachrome, followed by a series of oxidoreduction reactions. Dihydroxyindole (DHI) and DHI carboxylic acid (DHICA) are produced as intermediates, which undergo polymerization to form eumelanin. Pheomelanin synthesis also begins with dopaquinone; this is conjugated to cysteine or glutathione to yield cysteinyldopa and glutathionyldopa, for further transformation into pheomelanin. Mixed melanin contains both eu- and pheomelanin [12, 14–18].
