Semaphorin 3A receptor inhibitor as a novel therapeutic to promote innervation of bioengineered teeth

The sensory innervation of the dental pulp is essential for tooth function and protection. It is mediated by axons originating from the trigeminal ganglia and is spatio‐temporally regulated. We have previously shown that the innervation of bioengineered teeth can be achieved only under immunosuppressive conditions. The aim of this study was to develop a model to determine the role of Semaphorin 3A (Sema3A) in the innervation of bioengineered teeth. We first analysed innervation of the dental pulp of mandibular first molars in newborn (postnatal day 0: PN0) mice deficient for Sema3A (Sema3A^?/?), a strong inhibitor of axon growth. While at PN0, axons detected by immunostaining for peripherin and NF200 were restricted to the peridental mesenchyme in Sema3A^+/+ mice, they entered the dental pulp in Sema3A^?/? mice. Then, we have implanted cultured teeth obtained from embryonic day‐14 (E14) molar germs of Sema3A^?/? mice together with trigeminal ganglia. The dental pulps of E14 cultured and implanted Sema3A^?/? teeth were innervated, whereas the axons did not enter the pulp of E14 Sema3A^+/+ cultured and implanted teeth. A “Membrane Targeting Peptide NRP1,” suppressing the inhibitory effect of Sema3A, has been previously identified. The injection of this peptide at the site of implantation allowed the innervation of the dental pulp of bioengineered teeth obtained from E14 dental dissociated mesenchymal and epithelial cells reassociations of ICR mice. In conclusion, these data show that inhibition of only one axon repellent molecule, Sema3A, allows for pulp innervation of bioengineered teeth.     

Lenabasum Reduces Porphyromonas gingivalis–Driven Inflammation

Inflammation - The aim of this study was to evaluate the potential anti-inflammatory and anti-resorptive effects of lenabasum in the context of Porphyromonas gingivalis (Pg)–induced...     

Effects of sulphasalazine in experimental arthritis

The effects of sulphasalazine and related drugs on various models of arthritis are reviewed. Dosage regimen and duration of the treatment are of importance, as is the animal species, in determining clinical, biological, or radiological responses. Considering these parameters together with differences in administration protocols, it is not surprising that various drug effects are reported in the published studies. There is some evidence that sulphasalazine displays beneficial activity in attenuating experimental synovitis, but its influence only becomes apparent after a few weeks of therapy, thus functioning as a slow-acting antirheumatic drug. In contrast, sulphasalazine does not seem to be effective on the cicatricial ossifying process. Nevertheless, the respective therapeutic and remission-inducing effects of the parent drug, sulphasalazine, and its main moieties, 5-aminosalicylic acid and sulphapyridine, remain controversial.