Maria Siponen

Association of oral lichen planus with thyroid disease in a Finnish population: a retrospective case-control study

OBJECTIVE The objective of this study was to estimate the association between the history of thyroid disease and the prevalence of oral lichen planus (OLP)/oral lichenoid lesions (OLL). STUDY DESIGN This was a retrospective case-control study using data from the medical records of 222 OLP/OLL patients and 222 age- and sex-matched controls who had visited the Institute of Dentistry, University of Oulu or the Oral and Maxillofacial Department, Oulu University Hospital, from 1992 to 2001. Clinical characteristics of OLP/OLL lesions, other oral mucosal diseases, presence of cutaneous LP, history of allergies, medical history, and the use of regular medications were recorded. The relative odds of OLP, OLL, and OLP/OLL associated with selected patient characteristics were estimated by logistic regression. RESULTS History of any thyroid gland pathosis was found in 15% (n=22) of the 152 cases with OLP, in 13% (n=9) of the 70 cases with OLL, and in 8% (n=18) of the control subjects; the estimated odds ratios (with 95% confidence intervals) being 2.12 (1.06 to 4.21) for OLP and 1.57 (0.62 to 3.73) for OLL. When confined to hypothyroidism only, this disease was found in 10% (n=15) of the OLP cases, 9% (n=6) of the OLL cases, and 5% (n=11) of the controls; the estimated odds ratios being 2.39 (1.05 to 5.61) for OLP and 1.73 (0.56 to 4.90) for OLL. CONCLUSION The association of OLP/OLL and thyroid disease, especially between hypothyroidism and OLP, calls for further investigations in other populations and into the possible mechanisms behind this association.

TLR4 and TLR9 are induced in oral lichen planus

BACKGROUND The role of Toll-like receptors (TLRs) has been elucidated in many human infectious, autoimmune and neoplastic diseases. Previously, TLR2 and TLR4 expression in oral lichen planus (OLP) was described. The aim of our study was to examine expression patterns of TLR4 and TLR9 in normal oral mucosa and OLP and describe the effect of topical tacrolimus treatment on the expression of TLR4 and TLR9 in OLP. METHODS Toll-like receptor 4 and TLR9 expression was analysed by immunohistochemistry in five samples of normal oral mucosa and 50 samples of OLP (31 representing clinically white and 19 clinically erythematous/erosive lesions). We evaluated also the effect of topical tacrolimus on TLR4 and TLR9 expression in a patient with OLP. RESULTS Toll-like receptor 4 and TLR9 expression was increased in OLP epithelium compared with normal epithelium (P < 0.001); no significant difference between the two clinical types of OLP was observed. TLR9 expression was strongest in the superficial layer of the epithelium (P < 0.001), while the expression of TLR4 was strongest in the basal layer (P < 0.001). Treatment of OLP lesions with topical tacrolimus resulted in clinical improvement but had no effect on TLR expression levels. CONCLUSIONS Toll-like receptor 4 and TLR9 are induced in OLP; our finding confirms the results of a previous study. TLR4 and TLR9 may play a part in the pathogenesis of OLP. Further studies are needed to dissect the definitive role of TLRs in OLP pathogenesis and progression and to determine the effect of tacrolimus on the function of TLRs.

Idiopathic lenticular mucocutaneous pigmentation (Laugier-Hunziker syndrome): A report of a case

Laugier-Hunziker syndrome (LHS) is an acquired, benign, macular hyperpigmentation of the lips and oral mucosa, often associated with pigmentation of the nails. It is a rare disorder thought to be more common than the number of reported cases would suggest. It is important to include this condition in the differential diagnosis of diffuse oral pigmentation. Here we report the first case of the Laugier-Hunziker syndrome in Scandinavia. Other conditions causing diffuse or multifocal pigmented oral lesions are discussed.

Healing of extraction sockets in collagenase‐2 (matrix metalloproteinase‐8)‐deficient mice

Matrix metalloproteinase-8 (MMP-8) participates in skin wound healing and inflammation. We hypothesized that MMP-8 plays a role in wound healing after tooth extraction and in periapical inflammation. Bone formation, collagen metabolism, and inflammation in tooth extraction socket and in periapical lesions were analyzed in wild-type mice and in MMP-8-deficient (MMP-8(-/-)) mice. New trabecular bone area in the extraction sockets and in periapical lesions were similar in both groups. In extraction sockets significantly more type III procollagen was synthesized, and the neutrophil and MMP-9 levels were lower in MMP-8(-/-) mice. The amount of Fas ligand, identified as a substrate for MMP-8, was lower in alveolar mucosa but higher in alveolar bone of MMP-8(-/-) mice. These results indicate that MMP-8 can modulate inflammation and collagen metabolism of alveolar bone and mucosa.

Multifocal lateral periodontal cysts: a report of 4 cases and review of the literature

Lateral periodontal cyst (LPC) is a developmental jaw cyst of odontogenic origin. It has characteristic histopathologic features that are identical to those seen in the peripherally occurring gingival cyst of adults (GCA). The polycystic variant of LPC is termed the botryoid odontogenic cyst (BOC). The histogenetic origin of LPC is probably the rests of dental lamina in the alveolar bone. In the case of BOC, it might be that several adjacent epithelial rests simultaneously undergo cystic change and eventually form a polycystic lesion. Few previous examples of multifocal occurrence of LPC can be found in the literature. We report an additional 4 patients with this rare presentation of multiple, separate LPCs, and review the literature on this topic.

Widening of the inferior alveolar canal: a case report with atypical lymphocytic infiltration of the nerve

Widening of the inferior alveolar (mandibular) canal is a rare radiological finding. It is most often associated with neurofibromatosis. Rarely, a malignant process such as lymphoma may cause ill-defined enlargement of the mandibular canal. We present a unique case of a 33-year-old male who gradually developed sensory loss of his left lower lip and cheek and a well-defined tube-like widening of his left mandibular canal. The histopathological findings of the lesion were unusual in that they indicated atypical lymphocytic infiltration of the nerve tissue. The differential diagnoses regarding the clinical, radiological, and histopathological findings are discussed.

Histamine H4 receptor signalling in tongue cancer and its potential role in oral carcinogenesis - a short report

PurposeRecent reports indicate that histamine and its novel, high-affinity histamine H4 receptor (H4R) play a role in carcinogenesis, and thus H4R signalling has become a focus of increasing interest in the pathogenesis of many cancers. The roles of H4R in oral epithelial dysplasia (OED) and oral tongue squamous cell carcinoma (OTSCC) are unknown. The purpose of this study was to assess H4R expression in OTSCC patients and in OTSCC-derived cell lines.MethodsBiopsies taken from OED, OTSCC and healthy oral mucosa were studied by immunostaining. Primary human oral keratinocytes (HOKs) and two OTSCC-derived cell lines (HSC-3 and SCC-25) were used for the in vitro studies. Quantitative real-time PCR was used to measure oncogene expression in the stimulated HOKs.ResultsWe found that H4R-immunoreactivity was significantly reduced in the OED and OTSCC samples, especially in the samples with higher histopathological grades and noticeably increased mast cell counts. The presence of H4R in HSC-3 cells had clearly waned, in contrast to the HOKs. Gene expression data indicated that histamine-relevant inflammatory and environmental elements may participate in the regulation of oncogenes.ConclusionsOur results suggest an association between H4R and oral carcinogenesis. Furthermore, our findings raise a potential implication of histamine-mediated factors in the regulation of oncogenes, possibly via mast cells, as crucial components of the tumor microenvironment. The identification of new elements that govern oral cancer development is highly relevant for the development of novel therapeutic approaches in OTSCC.

Cathepsin K expression is increased in oral lichen planus

BACKGROUND Oral lichen planus (OLP) is an idiopathic T-cell-mediated mucosal inflammatory disease. Cathepsin K (Cat K) is one of the lysosomal cysteine proteases. It is involved in many pathological conditions, including osteoporosis and cancer. The expression and role of Cat K in OLP are unknown. METHODS Twenty-five oral mucosal specimens diagnosed histopathologically as OLP and fourteen healthy controls (HC) were used to study the immunohistochemical (IHC) expression of Cat K. Colocalization of Cat K with CD1a, Melan-A, CD68, CD45, mast cell tryptase (MCT), and Toll-like receptors (TLRs) 4 and 9 were studied using double IHC and/or immunofluorescence (IF) staining. Expression of Cat K was also evaluated in OLP tissue samples before and after topical tacrolimus treatment. RESULTS Cat K was expressed in a higher percentage of cells in the epithelial zone, and the staining intensity was stronger in the stroma in OLP compared to controls (P < 0.001). In OLP, Cat K was present mostly in melanocytes and macrophages and sporadically in basal keratinocytes, endothelial cells, and extracellularly. Cat K was found also in some fibroblasts in HC and OLP samples. Coexpression of Cat K and TLRs 4 and 9 was seen in some dendritic cells (presumably melanocytes) and macrophages. In OLP, tacrolimus treatment reduced the expression of Cat K in the epithelium but increased it in the stroma. CONCLUSIONS These results suggest that Cat K is involved in the pathogenesis of OLP. Cat K possibly takes part in the modulation of matrix molecules and cellular receptors.

Altered expression of hyaluronan, HAS1‐2, and HYAL1‐2 in oral lichen planus

BACKGROUND Oral lichen planus (OLP) is an immune-mediated mucosal disease of unclear etiology and of unresolved pathogenesis. Hyaluronan (HA) is an extracellular matrix glycosaminoglycan involved in inflammation and tumor progression. However, its presence in OLP has not been reported. We therefore aimed to study the immunohistochemical expression of HA, its receptor CD44, hyaluronan synthases (HAS1-3), and hyaluronidases (HYAL1-2) in OLP. METHODS The presence of HA, CD44, HAS1-3, and HYAL1-2 was studied by immunohistochemical methods in 55 OLP and 23 control oral mucosal specimens (CTR). The localization, intensity, and differences of the epithelial expression between OLP and CTRs were analyzed. RESULTS HA and CD44 were found on cell membranes in the epithelial basal and intermediate layers in CTR and OLP specimens. The HA staining intensity was stronger in the basal layer of the epithelium in OLP than in CTRs (P < 0.001). HAS1 (P = 0.001) and HAS2 (P < 0.001) showed stronger staining in the basal and weaker staining in the superficial (P < 0.001) epithelial layers in OLP than in CTRs. The immunostaining of HAS3 was low in both OLP and CTRs. Positive HYAL1 and HYAL2 staining were mainly found in the basal and intermediate epithelial layers, and their intensities were significantly increased in OLP, except HYAL 2 in the intermediate epithelial layer. CONCLUSIONS HA, HAS1-2, and HYAL1-2 have altered expression in OLP compared to CTRs and may therefore have a role in OLP pathogenesis.