Erythrodontia due to dental plaques: A pitfall in dermatological examination

Dear Editor,

Porphyrias constitute a group of inherited or acquired metabolic disorders due to defective haem synthesis, clasically presenting as photosensitivity, skin fragility, and blistering.¹ Differentiation between the various forms of porphyria is made by clinical examination, qualitative and quantitative porphyrin estimation, fractionation in urine, blood, and stool, and plasma spectrofluorimetry. Identification of porphyria subtype is important for determining prognosis and deciding on the line of management, which may range from treatment of underlying systemic diseases such as haemochromatosis, alcohol use disorder, Hepatitis C, or HIV in acquired porphyria cutanea tarda, to bone marrow transplant in congenital erythropoietic porphyria (CEP).² In resource-limited settings like India, fractionated porphyrin estimation using High Performance Liquid Chromatography (HPLC) is often not available. Hence, clinical parameters, such as age, symptoms, and bedside qualitative porphyrin estimation using Wood’s lamp, are frequently relied upon for diagnosis.

Erythrodontia is considered a pathognomonic feature of CEP, a skin-limited but severe mutilating porphyria that manifests in infancy or early childhood with a shortened life expectancy due to significant haemolysis. The early age of presentation results in the accumulation of porphyrins in the ossifying bone and dental enamel. This feature is not seen in late onset porphyria, such as porphyria cutanea tarda (the commonest porphyria), pseudoporphyria and drug-induced porphyria.

A 25-year-old man presented with a 1-year history of blistering and increased skin fragility over sun-exposed areas, primarily the face and acral sites, along with hyperpigmentation and scarring. The patient also reported reddish discolouration of urine. His history was notable for chronic alcohol consumption, and on evaluation, the patient was detected to be Hepatitis C and HIV I/II positive with deranged liver enzymes, Serum Glutamic-Oxaloacetic Transaminase/ Serum Glutamic-Pyruvic Transaminase (SGOT/SGPT=130/133 U/L). On Wood’s lamp examination, pink-red fluorescence was noted in the urine, and interestingly, the gingival margins of the teeth including, the periodontal area, also demonstrated red fluorescence [Figure 1a]. These are unusual findings for porphyria in this age group, especially with multiple trigger factors suggesting acquired porphyria cutanea tarda. On closer inspection, we noted that the areas of red fluorescence corresponded to the dental plaques on the gingival borders of lower incisors and upper canines [Figure 1b]. The patient was diagnosed as acquired porphyria cutanea tarda and started on direct-acting antivirals (DAAs) for Hepatitis C virus, antiretroviral therapy (ART), along with lifestyle modification, resulting in good clinical improvement.

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Figure 1a:

Oral examination revealing yellowish to brown plaques on the lower incisors and upper canines (index patient).

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Figure 1b:

Wood’s lamp examination demonstrating coral-red fluorescence in the gingival margin over the dental plaques—suggestive of biofilm (index patient).

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This unusual finding, prompted the examination of other dermatology OPD patients with poor dental hygiene, and we detected red fluorescence as well under Wood’s lamp illumination, corresponding to the areas of clinically visible dental plaques [Figures 2a and 2b]. This supported our hypothesis that the red fluorescence resulted from a local factor rather than systemic porphyrin accumulation. Further, the patient underwent dental scaling, following which the fluorescence under Wood’s lamp disappeared [Figures 3a and 3b]. Moreover, we would like to highlight that classical erythrodontia (reddish-brown discolouration or fluorescence of the teeth) seen in CEP is present diffusely through the entire dental enamel, clinically seen as a brownish hue. Under Wood’s lamp examination, this appears as a diffuse, coral-red fluorescence involving the entire tooth surface, unlike localised patterns seen in other conditions.

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Figure 2a:

Yellowish plaques on the incisors in the second patient with poor dental hygiene.

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Figure 2b:

Red fluorescence of the plaques under Wood’s lamp in the second patient, indicating bacterial biofilm.

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Figure 3a:

Post-dental scaling examination showing clinical improvement (index case).

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Figure 3b:

Post-dental scaling examination showing the absence of red fluorescence under Wood’s lamp (Index case).

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On review of the literature, we found that after the initial colonisation of the tooth surface by Streptococcus mutans and other Streptococci, Porphyromonas gingivalis, a Gram-negative, anaerobic bacterium, is one of the major contributors to periodontal disease. It is commonly found in dental plaques and can proliferate under inflammatory conditions to form biofilms, utilising heme from the gingival crevicular fluid for its growth.³ Accumulation of heme metabolites like protoporphyrin IX within these biofilms can lead to red fluorescence under Wood’s lamp.⁴ In fact, autofluorescence imaging under specific light wavelengths is gaining limelight in dentistry as a rapid and effective method for detecting dental plaque bacteria.⁴

Periodontitis caused by P. gingivalis is linked to atherosclerosis, endocarditis, and increased cardiovascular risk (25% higher) in affected individuals.⁵

This case serves as a reminder to dermatologists that not all red fluorescence in the teeth under Wood’s lamp is due to systemic porphyria. Though we could not microbiologically confirm Porphyromonas, this case highlights the need to differentiate endogenous porphyrin disorders from bacterial origin fluorescence in the oral cavity, to avoid misdiagnosis and unnecessary work-up.