To the Editor:
There are many examples of dystrophic calcification in the skin described in the literature. In most of them, the calcium deposits are located in the dermis because involvement of the epidermis by calcium is very rare. The most common form of epidermal involvement by calcium is the transepidermal elimination of the deposits.1–4
We have recently seen an uncommon pattern of calcinosis involving the epidermis in a biopsy from the foot of a 61-year-old man.
The patient was a heavy tobacco smoker and a moderate drinker with a long history of chronic obstructive pulmonary disease, currently controlled by the Pneumology Department with no metabolic unbalance. He had also previously presented with a Dupuytren fibromatosis on the left hand, which had been operated on and resolved by fasciotomy 6 years earlier.
He complained of a painful thickening on the sole of the left foot. The exploration demonstrated a well-demarked, skin-colored, dome-shaped lesion measuring 1 cm in diameter on the plantar side of the metatarsophalangeal joint of the fourth toe. The lesion was excised with the clinical impression of papilloma.
The biopsy showed an acanthotic epidermis with remarkable orthokeratotic hyperkeratosis and hypergranulosis (Fig. 1A). The calcium deposit was located above the granular layer (Fig. 1B), and it was composed of large, coarse, diffuse deposits (Fig. 1C). The lower deposits were thick intracytoplasmic calcium granules coalescing into the large deposits all over the stratum corneum (Fig. 1D). Histochemical stain with von Kossa demonstrated positive granular coarse deposits in the keratin layer with a reinforcement of the cellular boundaries (Fig. 2). Our final diagnosis was calcified heloma durum (clavus).
Because the patient did not show any metabolic alteration, the most feasible mechanism is a dystrophic deposit in an area with marked changes of lichen simplex chronicus. However, we are not aware of any previous dystrophic change in the stratum corneum of the epidermis. We have only found examples of dystrophic calcification in the bursae underneath a heloma.5,6 We are also aware of examples of calcinosis cutis following trauma,7 even showing transepidermal elimination of the calcium.8 However, in such cases, the main deposit was located in the dermis, which was totally absent in our case. In addition, we have seen many examples of dystrophic calcification in the keratin contained within epidermal and follicular cysts, which has been suggested as the origin of scrotal calcinosis.9 However, the calcification in the cyst is probably the result of a favoring milieu, with matrical debris and sulfated mucopolysaccharides derived from exfoliated cells.9
Last, the deposit in our case could not be explained on phylogenetic bases: Animal horns base their hardness on a bone core and on a cover of compact keratin, with no calcium deposits in the latter.10
Following this observation, we additionally performed von Kossa stain in 13 clavi in which there was no evidence of calcium deposits in the hematoxylin–eosin stain (Table 1). To our surprise, a fine granular deposit was found in 4 of them (Fig. 3). Although in von Kossa technique a nonspecific precipitation can sometimes be observed, the latter was excluded by 2 facts: First, the granular deposits were located in the same section plane as the keratin layer (by moving the fine adjustment knob). Second, the granular deposits were exclusively located in the keratin layer (in a nonspecific precipitation, they can be indiscriminately found all over the biopsy).
In conclusion, fine calcium deposits are probably more frequent than we believe in cutaneous clavi. However, they hardly ever coalesce in coarse thick granular deposits as to be easily identified in the hematoxylin–eosin stain.
1. Nakamura Y, Muto M. Subepidermal calcified nodule of the knee with transepidermal elimination of calcium. J Dermatol. 2012;39:965–966.
2. Majima M, Kanai T, Oh-i T. A unique case of cutaneous calcinosis with transepidermal elimination. J Dermatol. 1992;19:306–313.
3. Maroon M, Tyler W, Marks VJ. Calcinosis cutis associated with syringomas: a transepidermal elimination disorder in a patient with Down syndrome. J Am Acad Dermatol. 1990;23(2 pt 2):372–375.
4. Pitt AE, Ethington JE, Troy JL. Self-healing dystrophic calcinosis following trauma with transepidermal elimination. Cutis. 1990;45:28–30.
5. Rubin LM. Calcification of a bursa beneath a heloma durum. J Am Podiatry Assoc. 1967;57:335.
6. Roven MD. Heloma durum with calcified bursa. A case report. J Am Podiatry Assoc. 1968;58:517–518.
7. Sneddon IB, Archibald RM. Traumatic calcinosis of the skin. Br J Dermatol. 1958;70:211–214.
8. Larralde M, Giachetti A, Cáceres MR, et al. Calcinosis cutis following trauma. Pediatr Dermatol. 2005;22:227–229.
9. Shah V, Shet T. Scrotal calcinosis results from calcification of cysts derived from hair follicles: a series of 20 cases evaluating the spectrum of changes resulting in scrotal calcinosis. Am J Dermatopathol. 2007;29:172–175.
10. Hieronymus TL, Witmer LM, Ridgely RC. Structure of white rhinoceros (Ceratotherium simum) horn investigated by X-ray computed tomography and histology with implications for growth and external form. J Morphol. 2006;267:1172–1176.