Oral changes caused by tobacco free snuff

En 62-årig man remitterades för undersökning och behandling av en förändring i munslemhinnan innanför överläppen och som orsakats av påsförpackad tobaksfri snusprodukt (ONICO®, Swedish Match). Såväl den kliniska som den histopatologiska bilden var identisk med den man finner vid förändringar orsakade av tobaksbaserade påsförpackade snusprodukter. Patienten ombads att under en treveckorsperiod ändra applikation av snuset från vänster till höger sida. Efter dessa tre veckor hade förändringen helt försvunnit på vänster sida och en ny liknande den ursprungliga uppstått på höger sida

Tobaksfritt snus kan ge skador på munslemhinnan

Tobaksfritt snus kan leda till förändringar i munslemhinnan som är nästan identiska med de skador som orsakas av tobaksinnehållande snus, visar observationer vid specialisttandvårdskliniken i Halmstad

Inhibition of the Transforming Growth Factor-β/Smad Signaling Pathway in the Epithelium of Oral Lichen

The basal cells in epithelium of the erythematous form of oral lichen display hyperproliferation compared with normal oral mucosa. In this study we examined whether this is associated with disrupted production, activation, or signal transduction of the epithelial growth inhibitor transforming growth factor (TGF) β1. In situ immunostaining showed that most epithelial cells in normal oral mucosa had nuclear and cytoplasmic Smad4 and phosphorylated Smad2/3, but expressed little or no Smad7. Expression of latency-associated peptide TGF-β1, latent TGF-β binding protein 1, TGF-β type I receptor, and TGF-β type II receptor was readily seen, but only very little TGF-β1 was activated. In erythematous oral lichen, basal and lower spinous epithelial layers showed staining for latency-associated peptide TGF-β1, TGF-β type I receptor, and TGF-β type II receptor. A band with scanty staining for these molecules, but with marked staining for active TGF-β1, was seen in the upper spinous and granular layers. Numbers of epithelial cell nuclei with Smad4 and phosphorylated Smad2/3 staining were significantly reduced in erythematous oral lichen compared with normal oral mucosa. Basal and suprabasal cell layers in erythematous oral lichen showed strong cytoplasmic Smad7 protein staining, but in spinous and granular layers Smad7 was localized to the cell membrane. In situ hybridization showed strong Smad7 mRNA expression in almost all basal keratinocytes in erythematous oral lichen; by contrast, no or occasionally very weak Smad7 mRNA expression was seen in these cells in normal oral mucosa. The observations indicate that inhibition of the TGF-β/Smad pathway may account for the hyperproliferation of keratinocytes in erythematous oral lichen

Contact allergies to potential allergens in patients with oral lichen lesions.

OBJECTIVE: The aim of the present controlled study was to investigate a possible relationship between contact allergies to potential allergens and oral lichen lesions. METHODS: Eighty-three patients with oral lichen lesions (OLL) and control groups of age- and gender-matched dermatitis patients (DP, n = 83) and patch-tested dermatitis patients randomly selected from files (PSFF, n = 319) were included in the study. OLL and DP groups were patch-tested epicutaneously and examined intraorally. RESULTS: The frequencies of contact allergy to mercury and carvone were statistically higher in the OLL group than in the DP group. Surfaces of amalgam and composite restorations were statistically more frequent in the OLL group compared to the DP group. Contact allergy to nickel and colophony, the latter with a statistically significant difference, was more common in the DP group. The numerical difference found for nickel allergy was, however, not significant comparing the OLL and PSFF groups. CONCLUSION: Contact allergy to mercury was overrepresented in patients with OLL and has been reported in previous studies, but the present finding of an overrepresentation of contact allergy to carvone in patients with oral lichen lesions has not been reported previously. CLINICAL RELEVANCE: Carvone, in addition to mercury and gold, as previously suggested, can be one of the causative or maintenant factors for oral lichen lesions. Carvone-hypersensitive patients with oral lichen lesions should therefore avoid carvone-containing products for oral use

The necessity of a test reading after 1 week to detect late positive patch test reactions in patients with oral lichen lesions.

Establishing the clinical relevance of contact allergy to dental materials in patients with oral lichen lesions (OLL) may be difficult, and tests are often read only on day 3 or day 4; also, concentration of the tested allergens may vary. Several studies on dermatitis patients have shown that additional positive patch test reactions can be found after day 4. Therefore, the aim of the present study was to analyse the frequency of late positive reactions to potential allergens in patients with OLL

Contact Allergy to Gold in Patients with Oral Lichen Lesions.

The aetiology of oral lichen lesions is obscure. In this study the frequency of contact allergy to gold in 83 patients with oral lichen lesions was compared with that in two control groups, comprising 319 age- and gender-matched patients with dermatitis selected from files and 83 clinically examined dermatitis patients. All patients were tested epicutaneously with gold sodium thiosulphate. The two control groups tested were under examination for a tentative diagnosis of allergic dermatitis not related to oral problems. The frequency of contact allergy to gold was 28.9% in the patients with oral lichen lesions, 18.2% in patients selected from files, and 22.9% in the clinically examined control patients. The difference in frequency between patients with oral lichen lesions and those taken from files was statistically significant