Pulpotomie à l’oxyde de zinc eugénol des canines primaires cariées ou ayant subi un meulage dimensionnel pour raison orthodontique

Couramment réalisé au niveau de la dent primaire, la pulpotomie est devenue un traitement fort controversé depuis la mise en évidence du potentiel toxique du formaldéhyde. Afin d’évaluer, selon des critères cliniques et radiologiques, l’action de l’oxyde de zinc-eugénol non modifié, l’une des alternatives au formocrésol, 25 canines primaires cariées et 25 nécessitant un meulage dimensionnel dans le cadre de traitements interceptifs de dysharmonies dentoalvéolaires (DDM) mineures du secteur antérieur, ont subi une pulpotomie à l’aide de ce matériau. Les contrôles post-opératoires ont été réalisés à 1, 3, 6 et 12 mois, à la recherche de douleur spontanée ou provoquée, d’abcès ou de fistule, de mobilité dentaire pathologique, de résorption radiculaire interne ou externe pathologique, de destruction osseuse périapicale ou d’oblitération canalaire. La douleur n’a été relevée qu’une seule fois simultanément dans les deux groupes à 12 mois, et la présence de mobilité dentaire y a été notée de manière progressive. Les abcès sans fistules ont été le plus souvent rencontrés dans le groupe DDM que dans le groupe Carie. Les résorptions internes et pathologiques radiculaires se sont rencontrées, par contre, plus fréquemment dans le groupe Carie, où leur nombre était plus important avec le temps. Ces résorptions ont été relevées rapidement dès le troisième mois après le traitement et leur évolution a été rapide. Ces observations ont été comparées à celles relatives à la pulpotomie au formocrésol, en utilisant le test de la loi binomiale ou le test de la comparaison d’une proportion observée à une proportion de référence. Il se dégage de cette analyse que, pour les deux groupes et pour chacune des observations cliniques et radiologiques, le taux d’échec est supérieur au taux d’échec de référence. Cette étude confirme le fait que l’oxyde de zinc non modifié ne peut constituer une alternative au formocrésol dans la pulpotomie des canines primaires.Commonly performed in deciduous teeth, a pulopotomy has become a controversial treatment due to evidence of the potential toxicity of formaldehyde. In order to evaluate the performance of non-modified zinc oxide eugenol, one of the alternatives to formacresol, using clinical and radiographical evidence, 25 primary decayed canine teeth and 25 teeth requiring interproximal disking in order to reduce a minor dento-alveolar discrepancy in the anterior region were subjected to pulpotomies sing this material. Post-operative control visits were performed at 1, 3, 6 and 12 months, searching for spontaneous or provoked pain, an abscess or fistula, pathological dental mobility, pathological internal or external root resorption, periapical boney destruction or canal obliteration. Pain was only observed on one occasion simultaneously in both groups at the 12 month follow-up, and the presence of dental mobility was noted in a progressive manner. Abscesses without a fistula present were observed more frequently in teeth that were disked compared to the group of decayed teeth. On the other hand, internal and pathological root resorptions were seen more frequently in the group of decayed teeth and their numbers grew with time. These resorptions were observed as early as 3 months following treatment and they evolved rapidly. These observations were compared to pulpotomies performed with formocresol using different statistical analysis comparing observed results to control results. The analysis reveals that for both groups and for each of the clinical and radiographical observations, the rate of failure is superior to the rate of failure in the control group. This study confirms that non-modified zinc oxide eugenol cannot be used as an alternative to formocresol when performing pulpotmies in primary canine teet

Rare loss-of-function mutations of PTGIR are enriched in fibromuscular dysplasia

International audienceAbstract Aims Fibromuscular dysplasia (FMD) and spontaneous coronary artery dissection (SCAD) are related, non-atherosclerotic arterial diseases mainly affecting middle-aged women. Little is known about their physiopathological mechanisms. We aimed to identify rare genetic causes to elucidate molecular mechanisms implicated in FMD and SCAD. Methods and results We analysed 29 exomes that included familial and sporadic FMD. We identified one rare loss-of-function variant (LoF) (frequencygnomAD = 0.000075) shared by two FMD sisters in the prostaglandin I2 receptor gene (PTGIR), a key player in vascular remodelling. Follow-up was conducted by targeted or Sanger sequencing (1071 FMD and 363 SCAD patients) or lookups in exome (264 FMD) or genome sequences (480 SCAD), all independent and unrelated. It revealed four additional LoF allele carriers, in addition to several rare missense variants, among FMD patients, and two LoF allele carriers among SCAD patients, including one carrying a rare splicing mutation (c.768 + 1C>G). We used burden test to test for enrichment in patients compared to gnomAD controls, which detected a putative enrichment in FMD (PTRAPD = 8 × 10−4), but not a significant enrichment (PTRAPD = 0.12) in SCAD. The biological effects of variants on human prostaclycin receptor (hIP) signalling and protein expression were characterized using transient overexpression in human cells. We confirmed the LoFs (Q163X and P17RfsX6) and one missense (L67P), identified in one FMD and one SCAD patient, to severely impair hIP function in vitro. Conclusions Our study shows that rare genetic mutations in PTGIR are enriched among FMD patients and found in SCAD patients, suggesting a role for prostacyclin signalling in non-atherosclerotic stenosis and dissection

Rare Loss-of-function Mutations of PTGIR are enriched in Fibromuscular Dysplasia.

AimsFibromuscular dysplasia (FMD) and spontaneous coronary artery dissection (SCAD) are related, non-atherosclerotic arterial diseases mainly affecting middle-aged women. Little is known about their physiopathological mechanisms. We aimed to identify rare genetic causes to elucidate molecular mechanisms implicated in FMD and SCAD.Methods and resultsWe analysed 29 exomes that included familial and sporadic FMD. We identified one rare loss-of-function variant (LoF) (frequencygnomAD = 0.000075) shared by two FMD sisters in the prostaglandin I2 receptor gene (PTGIR), a key player in vascular remodelling. Follow-up was conducted by targeted or Sanger sequencing (1071 FMD and 363 SCAD patients) or lookups in exome (264 FMD) or genome sequences (480 SCAD), all independent and unrelated. It revealed four additional LoF allele carriers, in addition to several rare missense variants, among FMD patients, and two LoF allele carriers among SCAD patients, including one carrying a rare splicing mutation (c.768 + 1C>G). We used burden test to test for enrichment in patients compared to gnomAD controls, which detected a putative enrichment in FMD (PTRAPD = 8 × 10−4), but not a significant enrichment (PTRAPD = 0.12) in SCAD. The biological effects of variants on human prostaclycin receptor (hIP) signalling and protein expression were characterized using transient overexpression in human cells. We confirmed the LoFs (Q163X and P17RfsX6) and one missense (L67P), identified in one FMD and one SCAD patient, to severely impair hIP function in vitro.ConclusionsOur study shows that rare genetic mutations in PTGIR are enriched among FMD patients and found in SCAD patients, suggesting a role for prostacyclin signalling in non-atherosclerotic stenosis and dissection.</div