Year : 2009 | Volume
: 52 | Issue : 3 | Page : 357--359
Melasma: A clinicopathological study of 43 cases
Vermani Sarvjot, Shruti Sharma, Sharmila Mishra, Avninder Singh
Institute of Pathology - ICMR, New Delhi, India
213 -B Sukhdev Vihar, New Delhi - 110 025
Melasma is a symmetrical hypermelanosis of the exposed skin characterized by brown macules on the sun-exposed areas of the skin. The present study was carried out on 43 patients to analyze the correlation between histopathological features with clinical and Wood«SQ»s light examination. The study showed a clinical and histopathological discordance of 16.2%. Solar elastosis (55.8%) was the single most common histological finding apart from increased melanin concentration, epidermal flattening and dermal lymphomononuclear inflammation.
|How to cite this article:|
Sarvjot V, Sharma S, Mishra S, Singh A. Melasma: A clinicopathological study of 43 cases.Indian J Pathol Microbiol 2009;52:357-359
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Sarvjot V, Sharma S, Mishra S, Singh A. Melasma: A clinicopathological study of 43 cases. Indian J Pathol Microbiol [serial online] 2009 [cited 2022 May 18 ];52:357-359
Available from: https://www.ijpmonline.org/text.asp?2009/52/3/357/54993
A blemish-less skin is the desire of all human beings. The psychological impact of pigmentary imperfection provides the impetus for an understanding of the pathology of melasma and its relevance for better therapy.
Melasma is a common, acquired symmetrical hypermelanosis characterized by irregular light to brown macules on the sun-exposed areas of the skin, more common in women and dark-skinned people, especially of Hispanic origin.  Multiple etiological factors have been implicated in the pathogenesis of melasma, which include ultraviolet radiation exposure, pregnancy, contraceptive pills, hormonal replacement therapy and cosmetics, phototoxic and anti-seizure medications. 
This is a light microscopic, histochemical study to evaluate the histopathological features of the pigmentary anomaly of hyperpigmented lesions in 43 cases of melasma along with clinicopathological correlation.
Materials and Methods
Patient consent and clearance from the institutional ethical committee was obtained for this study, wherein 43 patients attending the dermatology outpatient department of Safdarjung Hospital, New Delhi, were included in this study, who had an average duration of symptoms for 1 year and more.
A complete clinical examination was performed for evaluating the characteristic features and extension of the pigmentary disorder. Wood's light examination was carried out and the patients were grouped into epidermal, dermal and mixed types.
With informed consent, a 3 mm punch biopsy from the lesional skin of the patient was taken and the tissue was prepared for light microscopic examination by fixation in 10% formalin and stained with hematoxylin and eosin (H and E) and Masson-Fontana stains.
The melanocyte:keratinocyte ratio was assessed manually by counting the cells in the basal epidermis using an eyepiece pinhole of 1 mm 2 area.
The histopathological and clinical parameters are summarized in [Table 1]. In our study of 43 patients, the age range was 17-45 years (mean 31.1). The male:female ratio was 1:2.5, with duration of symptoms ranging from 2 to 8 years (mean 4.8). The clinical pattern of presentation classified the cases of melasma into centrofacial, malar and mandibular types. The most predominant pattern was centrofacial and was observed in 38/43 (88.4%) of the patients of whom 29/43 (67.4%) were females. Malar and mandibular patterns showed a male predilection.
There was a significant concordance between clinical and histopathological evaluation of the level of pigment. In epidermal melasma, the predominant site of deposition of melanin in sections stained with H&E was in the basal and suprabasal layers [Figure 1]a and was better appreciated on Masson-Fontana stain [Figure 1]b. The increase in the melanocyte to keratinocyte ratio can be appreciated in [Figure 1]c. In the dermal type, the epidermal findings, although similar to the epidermal type, were less conspicuous. The dermal changes consisted of the presence of melanin-laden macrophages in the superficial dermis with or without lymphomononuclear infiltrate [Figure 1]d.
Only 4/21 (19%) patients who were clinically evaluated as epidermal type showed dermal pigment. Three of the 15 (20%) patients with dermal pigment clinically showed epidermal pigment on histopathology. Most patients with mixed type of pigment clinically showed epidermal pigment on histopathology. Biopsy of this category of patients is essential.
Solar elastosis was a predominant finding in 24/43 (55.8%) biopsies and was seen in 9/10 (90%) patients in the age group of 31-40 years.
The mean melanocyte to keratinocyte ratio observed in our study was 1:5 (normal 1:10).
No correlation could be established between basal layer degeneration and melanophages, observed in the dermis.
There is indeed a paucity of published data evaluating the histologic spectrum of melasma. For understanding the pathogenesis of hyperpigmentation in melasma, function of melanocytes, contribution to phenotypical coloration or how genetically predetermined skin color becomes altered to facultative skin color by influence of factors such as sunlight, hormones, inflammation needs to be known.  The morphological features however suggest an increase in the number and activity of melanocytes, melanization, increased transfer and decreased degradation of melanosomes in keratinocytes as essential for development of melasma. ,,
Sanchez et al.  assessed the histopathological features of melasma of 17 patients via Thiersch graft skin biopsies. They reported an increase in both epidermal melanin and melanocytes, basilar vaculopathy and sparse lymphohistiocytic infiltrate. Biopsies were taken from melasmal facial skin lesions. Previous studies have documented that sun-exposed facial skin contains more melanocytes than other sites of the body. ,
Our study, similar to Sanchez et al.  was carried out on 43 patients. We found an increase in the melanin with H&E and Masson-Fontana stains in all the epidermal layers. Epidermal thinning and flattening of the rete ridges were also noted. Solar elastosis was found in 24/43 (55.8%) cases and was more in the reticular dermis. We found a sparse to mild lymphohistiocytic infiltrate in 60% of our cases, which was similar to the studies conducted by Sanchez et al.  Grimes et al.  also found a mild lymphohistiocytic infiltrate in 75% of the biopsies.
Our findings on histopathological features of melasma are in affirmation with the study of Kang et al.  from Korea, who characterized histopathological features of melasma in 56 Korean women using methodologies similar to ours. Skin punch biopsies 2-mm-thick from involved and uninvolved adjacent skin were taken. The concentration of melanin was significantly increased in all epidermal layers in melasmal skin. The staining intensity and number of epidermal melanocytes was also increased in all epidermal layers of melasmal skin. Lesional skin showed more prominent solar elastosis compared with the normal skin, a finding similar to our study. Increased solar elastosis caused by ultraviolet radiation causes peroxidation of lipids in the cellular membrane leading to generation of free radicals, which may stimulate the melanocytes to produce excess melanin.
We found no significant differences in clinical and light microscopy in patients with malar, centrofacial and mandibular types of melasma. Histopathologically, discordance was observed only in clinically suspected mixed type of melasma where, in 7 cases clinically diagnosed as mixed, 6/7 were confirmed to be epidermal and 1/7 were confirmed to be dermal histopathologically.
To summarize, melasma is more common in females than in males in our study and epidermal type was more common than dermal type. Solar elastosis was a predominant finding, suggesting implications of ultraviolet light exposure in the pathogenesis. Till date, the exact pathogenesis of melasma is not known. Hormonal studies have failed to show any significant association with estrogen-progesterone. More recently, the interaction of stem cell factor, c-kit and vascular endothelial growth factor in the dermal fibroblasts have been proposed to affect melanocyte function and needs to be further evaluated to substantiate what actually triggers the hyperpigmentation.
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