Occlusal fissures in equine cheek teeth: µCT and histological findings.

Fissures on the occlusal surface of equine cheek teeth are commonly encountered during oral examination. Generally, their presence is considered abnormal but their aetiopathogenesis and clinical impact on pulp disease is still undetermined. The aims of this research were to study the extent of occlusal cheek teeth fissures using high-resolution X-ray computed tomography (µCT) imaging and their histological characteristics. Twenty-seven teeth (of 15 horses) were scanned using µCT imaging to analyse fissure extent. Histological examination of a subset of teeth (n=7) was performed. Forty-three type 1 fissures (35 type 1a, eight type 1b) were identified. The mean length of the fissure of type 1a and type 1b on the occlusal surface was 3.47+/-1.60mm and 13.64+/-7.40mm, respectively. Their mean depth was 13.22+/-10.76mm and 7.42+/-6.42mm, respectively. Potential risk factors associated with fissure depth were identified using a multivariable mixed model The location of the fissure and Triadan number were significantly associated with fissure depth. Fissures could be identified on histological sections with the presence of organic material inside the fissure, microorganisms in the continuation of the fissure extending into the dentinal tubules and the presence of reactionary dentine. This study suggests that fissures can provide a pathway for microorganisms to enter the dentinal tubules, potentially resulting in local pulpal inflammation. It appears that in healthy teeth, vital odontoblasts react by producing reactionary (tertiary) dentin, which lacks patent tubules and thus provides a proper seal.

PAFAH1B1 and the lncRNA NONHSAT073641 maintain an angiogenic phenotype in human endothelial cells.

AIM: Platelet-activating factor acetyl hydrolase 1B1 (PAFAH1B1, also known as Lis1) is a protein essentially involved in neurogenesis and mostly studied in the nervous system. As we observed a significant expression of PAFAH1B1 in the vascular system, we hypothesized that PAFAH1B1 is important during angiogenesis of endothelial cells as well as in human vascular diseases. METHOD: The functional relevance of the protein in endothelial cell angiogenic function, its downstream targets and the influence of NONHSAT073641, a long non-coding RNA (lncRNA) with 92% similarity to PAFAH1B1, were studied by knockdown and overexpression in human umbilical vein endothelial cells (HUVEC). RESULTS: Knockdown of PAFAH1B1 led to impaired tube formation of HUVEC and decreased sprouting in the spheroid assay. Accordingly, the overexpression of PAFAH1B1 increased tube number, sprout length and sprout number. LncRNA NONHSAT073641 behaved similarly. Microarray analysis after PAFAH1B1 knockdown and its overexpression indicated that the protein maintains Matrix Gla Protein (MGP) expression. Chromatin immunoprecipitation experiments revealed that PAFAH1B1 is required for active histone marks and proper binding of RNA Polymerase II to the transcriptional start site of MGP. MGP itself was required for endothelial angiogenic capacity and knockdown of both, PAFAH1B1 and MGP, reduced migration. In vascular samples of patients with chronic thromboembolic pulmonary hypertension (CTEPH), PAFAH1B1 and MGP were upregulated. The function of PAFAH1B1 required the presence of the intact protein as overexpression of NONHSAT073641, which was highly upregulated during CTEPH, did not affect PAFAH1B1 target genes. CONCLUSION: PAFAH1B1 and NONHSAT073641 are important for endothelial angiogenic function.