Exogenous ochronosis presents as asymptomatic brown-gray or blue-black pigmentation on photoexposed areas or on contact sites. It mainly affects the face and neck [3, 4, 11, 12]. Exogenous ochronosis is classified into three stages [13] (Table 12.2):

Dermatoscopy has been reported to be a promising tool. Charlin et al. [10] described “bluish-gray amorphous areas obliterating the follicular structures.” In contrast, melasma appears as accentuation of the normal pseudo-rete of the face. Other dermatoscopic features include “brown-gray globular, annular, and arciform structures [14],” “speckling [3],” and confetti-like leukoderma, which showed up as structureless areas on the skin [7].

Exogenous ochronosis is histologically confirmed by pigmentary incontinence, solar elastosis, presence of banana-shaped yellow-brown (ochre) fibers in the papillary dermis, and eventual collagen degeneration [10, 15, 16].

Differential diagnosis in adolescents includes post-inflammatory pigmentary alteration, cafe au lait macules, Becker’s nevi, erythema dyschromicum perstans (which resembles dermoscopically), tinea versicolor, and melasma (especially older teenage females on oral contraceptives).

The exact pathogenesis of exogenous ochronosis is unclear. The most widely accepted theory is that of Penneys [17], which proposes that hydroquinone inhibits the local activity of the homogentisic acid oxidase, resulting in accumulation of homogentisic acid, which is polymerized, forming the ochronotic pigment and being deposited in the dermis.

Findlay et al. [2] theorized that with prolonged use of hydroquinone, melanocytes would overcome the bleaching effect of hydroquinone which would then pass down to the papillary dermis to be taken up by fibroblasts, resulting in attachment and polymerization of phenols in elastic fibers.

Another proposal [18] suggests that hydroquinone oxidizes into quinine, forming hydroxylated indoles similar to melanin precursors.

There is currently no reported consistently effective treatment for exogenous ochronosis. Most importantly, creams containing hydroquinone should be identified and stopped. Topical treatment with retinoic acid, azelaic acid, and kojic acid and cryotherapy have been ineffective. Various modalities like dermabrasion and CO₂ laser [19, 20], Q-switched Ruby [21], Q-switched Alexandrite [15], and Q-switched Nd:YAG lasers have shown variable success.

Exogenous ochronosis should be considered in individuals in whom hydroquinone had been used for 6 months without any improvement. Recognition and early cessation of hydroquinone containing creams is the key as an erroneous diagnosis may lead to continuous drug application, leading to worsening of the pigmentation.