MATERIALS AND METHODS: 30 live Sprague-Dawley rats were used in this study. The rats' mandibular first molar tooth was extracted, and an incision wound was made on the tongue. The extraction socket and incision wound were irrigated using normal saline and different concentrations of locally processed miswak plant extracts (0.05%, 10%, and 20%) for 7 days. The rats were sacrificed for gross examination of the tooth socket and tongue healing. Both soft tissue and alveolar bone were examined microscopically.
RESULTS: Complete closure of the incision wound was observed on all rats' tongues; miswak groups showed better wound healing than control and placebo groups in the oral mucosa overlying the alveolar bones. 0.05% and 20% miswak extracts showed prominent wound healing effects in the sagittal sections of the tongue, with moderate formation of connective tissue under the wound site and notable wound contraction. The 20% miswak extract group showed the highest percentage of healed oral mucosa on the alveolar bone and higher bone deposition at the alveolar base.
CONCLUSION: A concentration of 20% miswak extract enhances the initial phase of wound healing both in oral soft and hard tissues. Miswak extract at this concentration was not toxic to the tissues and had potential therapeutic effects in oral tissue healing.
METHODS: In this study, six HCV isolates from haemodialysis (HD) patients with seronegative OCI were identified by molecular assays and phylogenetic analysis. The virus infectivity was assessed ex vivo using a primary naïve PBMC culture system. HCV isolates obtained from the PBMCs of 10 patients with chronic HCV infection (CCI) were characterised concurrently and used as positive controls in the cell culture.
RESULTS: Sequence analysis of the 5' untranslated region (UTR) and non-structural 5B (NS5B) region revealed that HCV genotype 3 was the most prevalent virus type in both the OCI and CCI groups. One of the occult HCV isolates was identified as a mixed type. The mean viral load (log10 RNA copies/106 cells) in the PBMC samples of the OCI group (M = 3.4, SD = 0.7) was lower than that of the CCI group (M = 4.6, SD = 1.7). Upon culture, de novo OCI-HCV replicates were detected in five out of six naïve PBMC cultures. Analysis of the replicates showed a single guanine addition in the domain III of 5'-UTR but the overall molecular structure was retained.
CONCLUSION: Seronegative OCI is an active form of infection that replicates at a low level in PBMCs. Seronegative OCI may share the same route of transmission as CCI. The retained viral competency may have an implication for its persistence.