This study evaluated the influence of type 2 diabetes mellitus on bone loss, bone repair and cytokine production in hyperglycemic rats, treated or not with metformin. The animals were distributed as follow: Non-Hyperglycemic (NH), Non Hyperglycemic with Ligature (NH-L), Treated Non Hyperglycemic (TNH), Treated Non Hyperglycemic with Ligature Treated (TNH-L), Hyperglycemic (H), Treated Hyperglycemic (TH), Hyperglycemic with Ligature (H-L), Treated Hyperglycemic with Ligature (TH-L). At 40 th day after induction of hyperglycemia, the groups NH-L, TNH-L, H-L, TH-L received a ligature to induce periodontitis. On the 69 th , the TNH, TNH-L, TH, TH-L groups received metformin until the end of the study. Bone repair was evaluated at histometric and the expression levels of Sox9, RunX2 and Osterix. Analysis of the ex-vivo expression of TNF-α, IFN-γ, IL-12, IL-4, TGF-β, IL-10, IL-6 and IL-17 were also evaluated. Metformin partially reverse induced bone loss in NH and H animals. Lower OPG/RANKL, increased OCN and TRAP expression were observed in hyperglycemic animals, and treatment with metformin partially reversed hyperglycemia on the OPG/RANKL, OPN and TRAP expression in the periodontitis. The expression of SOX9 and RunX2 were also decreased by hyperglycemia and metformin treatment. Increased ex vivo levels of TNF-α, IL-6, IL-4, IL-10 and IL-17 was observed. Hyperglycemia promoted increased IL-10 levels compared to non-hyperglycemic ones. Treatment of NH with metformin was able to mediate increased levels of TNF-α, IL-10 and IL-17, whereas for H an increase of TNF-α and IL-17 was detected in the 24- or 48-hour after stimulation with LPS. Ligature was able to induce increased levels of TNF-α and IL-17 in both NH and H. This study revealed the negative impact of hyperglycemia and/or treatment with metformin in the bone repair via inhibition of transcription factors associated with osteoblastic differentiation.
The purpose of this investigation was to evaluate the effects of lithium chloride (LiCl) on the socket healing of estrogen-deficient rats. Seventy-two rats were allocated into one of the following groups: Control, Ovariectomy and LiCl (150 mg/kg/2 every other day orally) + Ovariectomy. Animals received LiCl or water from the 14th day post-ovariectomy, until the completion of the experiment. On the 21st day after ovariectomy, the first molars were extracted. Rats were euthanized on the 10th, 20th and 30th days following extractions. Bone healing (BH), TRAP positive cells and immunohistochemical staining for OPG, RANKL, BSP, OPN and OCN were evaluated. The Ovariectomy group presented decreased BH compared to the LiCl group at 10 days, and the lowest BH at 20 days (p<0.05). At 30 days, the Ovariectomy and LiCl-groups presented lower BH than that of the Control (p<0.05). The number of TRAP-stained cells was the lowest in the LiCl group at 20 days and the highest in the Ovariectomy group at 30 days (p<0.05). At 10 days of healing, the LiCl group demonstrated stronger staining for all bone markers when compared to the other groups, while the Ovariectomy group presented higher RANKL expression than that of the Control (p<0.05). LiCl enhanced bone healing in rats with estrogen deficiency, particularly in the initial healing phases. However, as data on the effects of lithium chloride on bone tissue are still preliminary, more studies related to its toxicity and protocol of administration are necessary before its application in clinical practice.
O diabetes mellitus é uma desordem metabólica de múltipla etiologia caracterizada pela hiperglicemia crônica com distúrbios no metabolismo que podem afetar de modo negativo a cicatrização e o reparo tecidual. Diversas vias de sinalização desempenham um papel essencial na manutenção da integridade do esqueleto pela regulação positiva ou negativa das células ósseas. As semaforinas constituem uma família de proteínas ligadas a superfície celular ou secretadas que são capazes de regular a interação, morfologia e função de diferentes tipos de células. A Semaforina 3A (Sem3A) tem sido envolvida em atividades de remodelamento ósseo, e também são encontrados relatos sobre a atividade da Semaforina 4D (Sem4D) durante a reabsorção óssea realizada pelos osteoclastos. O objetivo do presente estudo foi avaliar o nível de expressão das Semaforinas 3A e 4D do tecido ósseo alveolar neoformado de ratos normo e hiperglicêmicos. Os animais foram divididos nos seguintes grupos: Não Hiperglicemicos (NH, n=10) e hiperglicêmicos (H, n=10). A hiperglicemia foi induzida nos animais pela administração de água com 10% de frutose e estreptozotocina no 14º dia após. No 76º dia após indução da hiperglicemia, todos os animais foram anestesiados e submetidos a uma exodontia para remoção dos molares inferiores. No 84º dia aconteceu à eutanásia, em seguida foi realizada uma curetagem do tecido ósseo neoformado que foi armazenado em RNA later® para extração do RNA total, tratamento com DNAse e preparo do cDNA e análise da expressão gênica de Sem3A e Sem4D. Os resultados foram submetidos a teste de normalidade e foram selecionados teste não paramétrico com nível de significância estabelecido em 5% (p <0,05). Os resultados do presente estudo sugerem que no modelo experimental utilizado, os níveis de expressão gênica de Sema 3A e 4D não estão associados ao impacto negativo da hiperglicemia sobre o reparo ósseo.
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