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Zygomatic implants are used to restore function in patients with highly edentulous atrophic maxillae, in which it is not possible to place conventional implants. The aim of this paper is to present a case of bilateral cutaneous fistula after placement of zygomatic implants and the treatment performed to resolve the condition, as well as to establish a hypothesis regarding the etiology of these lesions. Presented is a 59-year-old woman with an atrophic edentulous maxilla who received four zygomatic implants. At 8 months and 31 months after implant placement on the right and left sides, respectively, the patient developed inflammatory lesions in the lateral aspect of both orbits that evolved toward developing a fistula within weeks. The patient underwent surgery in both cases. Complications of zygomatic implants are relatively common but rarely involve the loss or removal of implants. In this case, the patient retained her implants, and several months after resection of both fistulae, the patient is asymptomatic without recurrence of the lesions. The probable cause of the occurrence of the fistula could be an accumulation of sinus mucosa remnants, periosteum, and bone particles at the malar level as a result of poor irrigation at the time of implant placement.

The clinical criteria for the diagnosis of urticarial vasculitis lack accuracy, according to previous studies. The aim of the study was to assess the accuracy of a clinical and a clinical-dermoscopic model for the differential diagnosis of chronic spontaneous urticaria (CSU) and urticarial vasculitis (UV). Dermoscopic images of lesions with histopathologically confirmed diagnosis of CSU and UV were evaluated for the presence of selected criteria (purpuric patches/globules (PG) and red linear vessels). Clinical criteria of CSU and UV were also registered. Univariate and adjusted odds ratios were calculated. Multivariate regression analyses were conducted separately for clinical variables (clinical diagnostic model) and for both clinical and dermoscopic variables (clinical-dermoscopic diagnostic model). 108 patients with CSU and 27 patients with UV were included in the study. The clinical-dermoscopic model notably showed higher diagnostic sensitivity than the clinical approach (63% vs. 44%). Dermoscopic purpuric patches/globules (PG) was the variable that better discriminated UV, increasing by 19-fold the odds for this diagnosis. In conclusion, dermoscopy helps the clinical discrimination between CSU and UV. The visualization of dermoscopic PG may contribute to optimize decisions regarding biopsy in patients with urticarial rashes.

D IFFERENT CLINICAL FORMS OF PURPURA are the result of either noninflammatory or inflammatory changes within or around the blood vessel walls. Dermoscopy helps in distinguishing between these forms beyond the standard examination. The basic dermoscopic patterns are (1) homogeneous, (2) mottled, (3) perifollicular (with purpuric halos), and (4) epidermal purpuric. The homogeneous purpuric pattern characterizes a noninflammatory form of purpura, such as bleeding diathesis (Figure 1 shows the lesions on a patient with acenocoumarol overdose), or vessel wall or supporting stroma abnormalities, such as senile or steroid purpura (Figure 2). This pattern consists of wide, homogeneous, structureless purpuric areas. The mottled purpuric pattern suggests a purpuric lesion of the inflammatory type, such as leukocytoclastic vasculitis (LV) (Figure 3) and pigmented purpuric dermatosis (PPD) (Figure 4). This pattern consists of multiple small, speckled, blurred purpuric blotches (Figure 3) and/or more defined purpuric globules (PGs) over a purple and, later, orange-brown background (Figure 4). Some variations of this basic pattern can be recognized according to the intensity of the background, the presence of necrosis, and the presence of other vascular structures. Purpuric globules may appear as an isolated finding (Figure 3) or surrounding a larger purpuric background. The background color may obscure the globules if it is prominent or when large tissue necrosis is present. Necrotic lesions are seen as whitish blue patches (Figure5 shows LV lesions) or as eroded areas with hemorrhagic crusts in the context of the purpuric areas (Figure6 shows LV lesions). Vascular structures are usually obscured in purpuric lesions, but PGs may be surrounded by linear vessels in some cases of urticaria vasculitis (Figure 7), in some forms of PPD, and in insectbite reactions or by glomerularlike vessels in patients with associated venous stasis (Figure 8). The perifollicular dermoscopic pattern of scurvy consists of purpuric halos centered by hair follicles (Figure 9). “Corkscrew hairs” and follicular hyperkeratosis can also be visualized under the dermatoscope. Other purpuric patterns include purpuric or black blood spots of subcorneal and subungual hemorrhage (Figure 10) and hemorrhagic crusts over eroded lesions (Figure 11 shows lesions of eczema). Histopathologically, the homogeneous and the mottled purpuric patterns correspond to extravasated erythrocytes in the dermis, either with capillaries devoid of inflammatory cells (the homogeneous pattern) or with variable inflammatory changes (the mottled pattern). The dermal erythrocyte extravasation that is related to PGs of LV is secondary to fibrinoid degeneration of small blood vessels, with a mixed neutrophilic infiltrate. In contrast, PGs of PPD are related to variable amounts of erythrocytes, lymphocytes, and siderophages surrounding swollen blood vessels within the upper part of the dermis, with or without epidermal changes. Differences in the color of the background partially reflect the condition of the extravasated erythrocytes (intact erythrocytes in purple lesions or siderophages in yellow lesions).