2012.3-24.Andre Nanta

DOI: 10.7241/ourd.20123.60                                                                                  article in PDF
Our Dermatol Online. 2012; 3(3): 241-242
Date of submission: 27.02.2012 / acceptance: 16.03.2012
Conflicts of interest: None

Khalid Al Aboud

Pathology Department, Wake Forest University, Winston-Salem, NC, USA

Corresponding author: Dr. Khalid Al Aboud     e-mail:amoa65@hotmail.com



Nevus of Nanta
A nevus of Nanta lesion is characterized by the presence of cutaneous ossification (osteoma cutis) of an existing melanocytic nevus [1-4]. It is postulated that secondary ossification is the consequence of folliculitis, trauma, or neoplastic proliferation, which may induce the dermal fibroblasts to differentiate into osteoblasts [1]. Histologically, the osteomas are composed of well-formed bony spicules with prominent cement lines and calcification. They may demonstrate osteoblasts, osteoclasts, and osteocytes and occasionally may even demonstrate bone marrow elements [2]. Notably, nevus of Nanta has a higher prevalence in women than in men, possibly due to the effect of estrogen stimulation on osteoblasts within the lesion. Of clinical significance, melanoma can occur in association with nevus of Nanta [4]. Using skeletal bone formation as a guide, two mechanisms of bone formation can be expected in the skin. First, enchondral ossification, which occurs in most of the long bones of the skeleton, involves a cartilaginous template that is subsequently ossified and replaced. Or more commonly, membranous bone formation is a result of direct bone formation without the cartilaginous anlage [2]. The osteomas in nevus of Nanta usually occur at the base of the melanocytic proliferation occurring maily in the intradermal nevus but may rarely occur with nevi with junctional activities. In one series of 74 cases of primary and secondary cutaneous ossification, nevus of Nanta represented 26% (19 of 74) of the total osteomas identified and was the single most common lesion with osteoma formation [2].
André Nanta (1883-1963)
André Nanta, French dermatologist, born in 31 May, 1883 [5,6]. He descended from Franche-Comte ancestary. He spent his childhood in toulous. He rapidely ascended into his medical field and become a professor of universities in 1934 [5]. He had multiple interest and contributions in dermatology. He presented a thesis on lymphodermia and myelodermia. He had a special interest in deep fungal infection and made several trips to Algeria for this purpose. This interest in mycosis led him to isolate a special strain in fungus named with his name; aspergillus nantae [5]. He worked also on cutaneous lipidosis, and eosinophilic granuloma [7] (Nanta- Gadrat disease). The Nanta name also remains attached to osteo-nevus described in 1911. He also contributed with his students Bazex and Dupré in understanding of congenital skin disorders [5]. He had several scientific assignments and he had been a president of Société Française de Dermatologie. André Nanta died on 27 May 1963 [5.6].
Figure 1. André Nanta (1883-1963). With permission from
reference number 5
1. Abessi B, Meyer DR, Carlson JA: Osteoma cutis (nevus of nanta) of the eyebrow. Ophthal Plast Reconstr Surg. 2012; 28: 74-75. 2. Conlin PA, Jimenez-Quintero LP, Rapini RP: Osteomas of the skin revisited: a clinicopathologic review of 74 cases. Am J Dermatopathol. 2002; 24: 479-483. 3. Weedon D: Chapter 32 Lentigines, Nevi, and Melanomas. Weedon’s skin pathology. 3ed edn. 2010. Elsevier limited. P710-756. 4. Culver W, Burgdorf WH: Malignant melanoma arising in a nevus of Nanta. J Cutan Pathol. 1993; 20: 375–377. 5. Bouissou X, Bazex J: History of Dermatology in Toulouse. In: Wallach D, Tilles G, eds. Dermatology in France. Privat: Pierre Fabre Dermo-Cosmetique; 2002: 669-680. http://www2.biusante.parisdescartes.fr/livanc/?p=670&cote=extwall00001&do=page Accessed Feb 25, 2012. 6. Cabre J: [In memoriam André Nanta (1883-1963)]. Hautarzt. 1964; 15: 97. 7. Nanta, Gadrat, Bazex, Charouleau: [Eosinophilic granuloma of maxilla]. Sang. 1952; 23: 360-363.



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