Abstract

Propionibacterium acnes: (P. acnes) produce Porphyrins; however, fluorescence measurement of Porphyrins from Ultraviolet-A (UVA) images has failed to establish a correlation. Acne clinical research and imaging has ignored the spectral excitation-emission characteristics and the exact pattern of the Porphyrins synthesized by P. acnes. In this exploratory study, for the first time, the possible relationships of Coproporphyrin III (CpIII) and Protoporphyrin IX (PpIX) fluorescence as well as acne lesion-specific inflammation measurements with clinical signs of acne are investigated. Furthermore, the sensitivity of these measurements in tracking and differentiating the known treatment effects of Benzoyl Peroxide (BPO) 5%, and combination of Clindamycin + BPO are also evaluated. Comedonal and papulopustular lesions identified by investigators during a live assessment of 24 mild-to-severe acne subjects were compared with fluorescence and inflammation measurements obtained from analysis of VISIA®-CR images. CpIII fluorescence spots showed a strong correlation (r = 0.69–0.83), while PpIX fluorescence spots showed a weak correlation (r = 0.19–0.27) with the investigators’ comedonal lesion counts. A strong correlation was also observed between the investigators’ papulopustular lesion counts and acne lesion-specific inflammation (r = 0.76). Our results suggest that CpIII fluorescence and acne lesion-specific-inflammation measurement can provide objective indication of comedonal and papulopustular acne severity, respectively. Furthermore, these measurements may be more sensitive and specific in evaluating treatment effects and early signs of acne lesion progression compared to investigators’ lesion counts.

Highlights

  • The pathogenesis of acne is multifactorial with four primary factors: (1) increased sebum production, (2) alterations in the keratinization process, (3) Propionibacterium acnes (P. acnes) follicular colonization, and (4) release of inflammatory mediators [5, 6, 15, 19, 27]

  • The association of Coproporphyrin III (CpIII) fluorescence spots, Protoporphyrin IX (PpIX) fluorescence spots, and acne-spots with the investigator-annotated acne lesions can be seen in Fig. 2b–d, respectively

  • When the locations of these fluorescence spots were compared with the locations of the investigators’ identified lesions, 94% open comedones and more than 70% of the closed comedones exhibited CpIII fluorescence signals

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Summary

Introduction

The pathogenesis of acne is multifactorial with four primary factors: (1) increased sebum production, (2) alterations in the keratinization process, (3) Propionibacterium acnes (P. acnes) follicular colonization, and (4) release of inflammatory mediators [5, 6, 15, 19, 27]. Excess keratin combined with sebum partially obstructs the opening of the follicle forming a microcomedo which is the beginning of comedonal lesion development [21]. Acne lesions, including comedonal lesions, are colonized by P. acnes. These bacteria produce pro-inflammatory mediators which contribute to the development of visible papulopustular lesions [4, 5]. Papulopustular acne lesions were considered inflammatory, while the comedonal lesions were considered non-inflammatory. Recent data have clearly shown a role for inflammation at all stages of acne lesion development, perhaps, sub-clinically even before comedo formation [25]

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