“RichBlend” protocol for full-face filling and collagen biostimulation

ABSTRACT The “RichBlend” protocol was designed for facial filling and collagen biostimulation, by means of a mixture of calcium hydroxyapatite (CaHA), hyaluronic acid (AH) and autologous platelet concentrates. This work reports the case of a 53-year-old patient with cutaneous photoaging, loss of facial volume, multiple rhythms in the frontal and periorbital regions, also marked skin flaccidity, especially the eyelid. The treatment was done with botulinum toxin (65 U) and the “RichBlend” protocol. Venipuncture was performed and the blood was centrifuged to obtain i-PRF (injectable platelet-rich fibrin) and plasma gel. After venipuncture and blood centrifugation, i-PRF and plasma gel were obtained. CaHA (Radiesse®) was diluted: a) in saline solution + i-PRF (hyperdilution) for biostimulationof the lower third of the face; and b) in AH (Juvederm Ultraplus XC®) + plasma gel, for hydrolifting on the forehead and dark circles, malar and temples. Plasma gel was applied to the nasogenian grooves and then the entire face was properly massaged. The “RichBlend” protocol rejuvenated the patient, as it promoted filling, volumizing, collagen formation (biostimulation), reduction of flaccidity, in addition to skin whitening. Since HA and CaHA are high-cost products, their mixture with autologous platelet concentrates, in liquid or gel form, allows the use of a greater amount of filled and biostimulator material on the face, at a more affordable cost

Anatomia cirúrgica do nervo maxilar na região zigomática

Anatomic knowledge on the zygomatic fossa is of primary importance to improve the regional anesthetic technique of the maxillary nerve. Few reports in the literature have addressed the trajectory of the maxillary nerve and its branches in this region; thus, this study aimed at presenting information about the trajectory of these nerves. Thirty human half-heads of both genders were fixed in 10% formalin and demineralized in 5% nitric acid, and the maxillary nerve was dissected since its origin on the pterygopalatine fossa until penetration into the inferior orbital fissure. It was observed that the maxillary nerve sends one to three posterior superior alveolar branches and tuberal descendent branches, which supply the soft tissue structures of the region. The posterior superior alveolar nerves are inferiorly oriented near the maxillary tuberosity, where they penetrate the alveolar canals with the posterior superior alveolar artery and send small nerve branches that continue in an extraosseous trajectory. This study found that nearly 2/3 of the trajectory of the maxillary nerve is located in the zygomatic region, with a short segment (1/3) in the pterygopalatine fossa.O conhecimento anátomo-cirúrgico da região zigomática é fundamental para o aprimoramento de técnicas anestésicas tronculares do nervo maxilar. A literatura pouco se refere à trajetória do nervo maxilar e seus ramos nessa região, portanto, o presente estudo tem como objetivo esclarecer o percurso desses nervos. Foram dissecadas ao microscópio cirúrgico MC900 (D.F.Vasconcelos), 30 hemicabeças humanas, de ambos os sexos, que foram previamente formolizadas a 10% e desmineralizadas em ácido nítrico a 5%. Observou-se que o nervo maxilar, desde sua origem na fossa pterigopalatina até penetrar na fissura orbital inferior, emite de um a três ramos alveolares superiores posteriores e ramos tuberais descendentes que vão para estruturas moles da região. Os nervos alveolares superiores posteriores, descem adjacentes à tuberosidade da maxila, na qual penetram através dos canais alveolares junto com a artéria homônima e podem emitir filetes nervosos que continuam trajeto extra-ósseo. Contrariando os achados da literatura, com este estudo observou-se que o nervo maxilar apresenta praticamente dois terços de sua trajetória na região zigomática e o restante na fossa pterigopalatina

Study of the effects of the intravascular injection of vasoconstrictors drugs present in local anesthetics on the arterial pressure of renal hypertensive and passive smoker rats

O anestésico local é o medicamento mais utilizado na Odontologia e sua associação com vasoconstrictores aumenta a duração da anestesia, diminuindo seus efeitos sistêmicos. A hipertensão e o tabagismo são freqüentes na população, sendo responsáveis por complicações sistêmicas. A felipressina, por não interferir com receptores simpáticos, poderia ser um vasoconstrictor indicado para pacientes hipertensos. O objetivo deste trabalho foi estudar a reatividade cardiovascular de animais simultaneamente hipertensos e fumantes passivos aos agentes vasoconstritores associados aos anestésicos locais, verificando também o efeito do tratamento com atenolol. Foram utilizados ratos Wistar machos, divididos em 5 grupos: 1) normotensos não fumantes; 2) normotensos fumantes passivos; 3) hipertensos não fumantes; 4) hipertensos fumantes passivos; 5) hipertensos fumantes passivos tratados com atenolol. A hipertensão renal foi induzida pela remoção do rim direito e instalação de clip de prata (abertura 0,25mm) na artéria renal esquerda, após anestesia com quetamina e xilazina. Os ratos fumantes passivos foram colocados diariamente por 10 minutos, durante 28 dias, em caixa de madeira de 30cmX25cmX15cm dividida em dois compartimentos. Em um deles, eram acesos 10 cigarros e no outro ficavam os animais. A tampa da caixa era fechada e um sistema de ventilação lançava fumaça dos cigarros para o compartimento dos ratos, num fluxo de 10l/min. Após medida indireta da pressão arterial, 14 dias após a cirurgia, o grupo tratado com atenolol foi medicado durante 14 dias seguintes (90 mg/Kg) por gavage. No 28o dia, todos receberam catéter de polietileno na artéria carótida esquerda (para medida de pressão) e outro na veia jugular direita (para injeção de drogas). Para os 5 grupos foram utilizadas: adrenalina (80, 160, 320, 640 e 1280ng) e felipressina (0,125, 0,25, 0,5, 1, 2 e 3 x 10-3UI). O catéter arterial era conectado a transdutor de pressão e o registro realizado por software específico. Foram analisadas: menor resposta hipotensora, maior resposta hipertensora e duração de resposta para cada dose. Os dados foram analisados por análise de variância de medidas repetidas, seguida do teste de Tuckey ou Holm-Sidack, com nível de significância de 5%. Os resultados mostraram que o fumo passivo reduziu significativamente a resposta vasodilatadora produzida pela adrenalina, em animais normotensos e hipertensos, potencializou suas respostas hipertensoras e aumentou a duração das respostas à adrenalina, ampliadas ainda mais pelo tratamento com atenolol. O tratamento com atenolol promoveu aumento adicional das respostas hipertensoras à adrenalina nos hipertensos-fumantes. A felipressina não apresentou ações vasodilatadoras e suas ações hipertensoras foram potencializadas pelo fumo passivo, em amplitude e duração. O atenolol não promoveu aumento adicional da amplitude das respostas à felipressina. Nos animais hipertensos, o tratamento com atenolol associado ao fumo passivo teve efeito expressivo, aumentando significativamente a duração total das respostas à felipressina. A felipressina, quando comparada à adrenalina, não apresentou efeitos hipotensores diretos, a resposta hipertensora máxima foi nitidamente inferior e a duração das respostas à felipressina foi o dobro da adrenalina. Dessa forma, a felipressina se torna uma droga interessante na hipertensão, devido a sua capacidade de promover vasoconstrição prolongada, sem potencializar a atividade simpática sistêmica.The local anesthetic is the most common drug in dentistry and the associated vasoconstrictors increase the duration of anesthesia, decreasing its systemic effects. Hypertension and smoking are problems commonly found in the general population, being responsible for systemic complications. Felypressin, a vasoconstrictor that does not interact with sympathetic receptors, could be indicated to hypertensive patients. This study investigated the cardiovascular reactivity of hypertensive and passive smoker animals under atenolol treatment to epinephrine and felypressin. Male wistar rats were divided into five groups: 1) normotensive and non-smokers, 2) normotensive and passive smokers, 3) hypertensive and non-smokers, 4) hypertensive and passive smokers; 5) hypertensive, passive smokers and treated with atenolol. Renal hypertension was induced by removal of the right kidney and installation of a silver clip (with 0.25-mm opening) in the left renal artery, after anesthesia with ketamine and xylazine. The passive smoker rats were placed, 10 minutes per day, during 28 days in a 30cmX25cmX15cm wood box divided into two compartments. Ten cigarettes were lit in one compartment, and the rats were placed in the other. The box lid was closed and a ventilation system threw the cigarette smoke to the rat compartment. After indirect measurement of blood pressure, 14 days after the surgery, the group of rats treated with atenolol was medicated during the following fourteen days (90 mg/kg) by gavage. On the 28th day, a polyethylene catheter was inserted into the left carotid artery (for direct blood pressure measurements) and into the right jugular vein (for drug injection). The groups received epinephrine (80, 160, 320, 640 and 1280ng) or felypressin (0.125, 0.25, 0.5, 1, 2 and 3 x 10-3UI). The arterial catheter was connected to a pressure transducer and recording was made by a specific computer software. The following parameters were analyzed for all groups: lower hypotensive response, higher hypertensive response and duration of response for each dose. Data were statistically analyzed by repeated measures analysis of variance, followed by Tukey test or Holm-Sidack test, at a significance level of 5%. The results showed that passive smoking significantly decreased the vasodilator response produced by epinephrine in normotensive and hypertensive animals, increasing their hypertensive responses and increased the duration of response to epinephrine, that was further increased by atenolol treatment. Atenolol treatment increased the hypertensive responses in hypertensive-smokers rats. The felypressin did not show vasodilator responses and its hypertensive responses were increased by passive smoking. The atenolol did not cause additional increase in felypressin responses. In hypertensive animals, the atenolol treatment associated with passive smoking had expressive effects, significantly increasing the total duration of response to felypressin. Felypressin, when compared with epinephrine, did not show direct hypotensive effects, the higher hypertensive responses were smaller and the duration of response to felypressin was twice the epinephrine time. Then, felypressin becomes an interesting drug to hypertensive patients, due to its capacity to promote prolonged vasoconstrictor effect without increasing the sympathetic nerve activity

Study of the effects of the intravascular injection of vasoconstrictors drugs present in local anesthetics on the arterial pressure of renal hypertensive and passive smoker rats

O anestésico local é o medicamento mais utilizado na Odontologia e sua associação com vasoconstrictores aumenta a duração da anestesia, diminuindo seus efeitos sistêmicos. A hipertensão e o tabagismo são freqüentes na população, sendo responsáveis por complicações sistêmicas. A felipressina, por não interferir com receptores simpáticos, poderia ser um vasoconstrictor indicado para pacientes hipertensos. O objetivo deste trabalho foi estudar a reatividade cardiovascular de animais simultaneamente hipertensos e fumantes passivos aos agentes vasoconstritores associados aos anestésicos locais, verificando também o efeito do tratamento com atenolol. Foram utilizados ratos Wistar machos, divididos em 5 grupos: 1) normotensos não fumantes; 2) normotensos fumantes passivos; 3) hipertensos não fumantes; 4) hipertensos fumantes passivos; 5) hipertensos fumantes passivos tratados com atenolol. A hipertensão renal foi induzida pela remoção do rim direito e instalação de clip de prata (abertura 0,25mm) na artéria renal esquerda, após anestesia com quetamina e xilazina. Os ratos fumantes passivos foram colocados diariamente por 10 minutos, durante 28 dias, em caixa de madeira de 30cmX25cmX15cm dividida em dois compartimentos. Em um deles, eram acesos 10 cigarros e no outro ficavam os animais. A tampa da caixa era fechada e um sistema de ventilação lançava fumaça dos cigarros para o compartimento dos ratos, num fluxo de 10l/min. Após medida indireta da pressão arterial, 14 dias após a cirurgia, o grupo tratado com atenolol foi medicado durante 14 dias seguintes (90 mg/Kg) por gavage. No 28o dia, todos receberam catéter de polietileno na artéria carótida esquerda (para medida de pressão) e outro na veia jugular direita (para injeção de drogas). Para os 5 grupos foram utilizadas: adrenalina (80, 160, 320, 640 e 1280ng) e felipressina (0,125, 0,25, 0,5, 1, 2 e 3 x 10-3UI). O catéter arterial era conectado a transdutor de pressão e o registro realizado por software específico. Foram analisadas: menor resposta hipotensora, maior resposta hipertensora e duração de resposta para cada dose. Os dados foram analisados por análise de variância de medidas repetidas, seguida do teste de Tuckey ou Holm-Sidack, com nível de significância de 5%. Os resultados mostraram que o fumo passivo reduziu significativamente a resposta vasodilatadora produzida pela adrenalina, em animais normotensos e hipertensos, potencializou suas respostas hipertensoras e aumentou a duração das respostas à adrenalina, ampliadas ainda mais pelo tratamento com atenolol. O tratamento com atenolol promoveu aumento adicional das respostas hipertensoras à adrenalina nos hipertensos-fumantes. A felipressina não apresentou ações vasodilatadoras e suas ações hipertensoras foram potencializadas pelo fumo passivo, em amplitude e duração. O atenolol não promoveu aumento adicional da amplitude das respostas à felipressina. Nos animais hipertensos, o tratamento com atenolol associado ao fumo passivo teve efeito expressivo, aumentando significativamente a duração total das respostas à felipressina. A felipressina, quando comparada à adrenalina, não apresentou efeitos hipotensores diretos, a resposta hipertensora máxima foi nitidamente inferior e a duração das respostas à felipressina foi o dobro da adrenalina. Dessa forma, a felipressina se torna uma droga interessante na hipertensão, devido a sua capacidade de promover vasoconstrição prolongada, sem potencializar a atividade simpática sistêmica.The local anesthetic is the most common drug in dentistry and the associated vasoconstrictors increase the duration of anesthesia, decreasing its systemic effects. Hypertension and smoking are problems commonly found in the general population, being responsible for systemic complications. Felypressin, a vasoconstrictor that does not interact with sympathetic receptors, could be indicated to hypertensive patients. This study investigated the cardiovascular reactivity of hypertensive and passive smoker animals under atenolol treatment to epinephrine and felypressin. Male wistar rats were divided into five groups: 1) normotensive and non-smokers, 2) normotensive and passive smokers, 3) hypertensive and non-smokers, 4) hypertensive and passive smokers; 5) hypertensive, passive smokers and treated with atenolol. Renal hypertension was induced by removal of the right kidney and installation of a silver clip (with 0.25-mm opening) in the left renal artery, after anesthesia with ketamine and xylazine. The passive smoker rats were placed, 10 minutes per day, during 28 days in a 30cmX25cmX15cm wood box divided into two compartments. Ten cigarettes were lit in one compartment, and the rats were placed in the other. The box lid was closed and a ventilation system threw the cigarette smoke to the rat compartment. After indirect measurement of blood pressure, 14 days after the surgery, the group of rats treated with atenolol was medicated during the following fourteen days (90 mg/kg) by gavage. On the 28th day, a polyethylene catheter was inserted into the left carotid artery (for direct blood pressure measurements) and into the right jugular vein (for drug injection). The groups received epinephrine (80, 160, 320, 640 and 1280ng) or felypressin (0.125, 0.25, 0.5, 1, 2 and 3 x 10-3UI). The arterial catheter was connected to a pressure transducer and recording was made by a specific computer software. The following parameters were analyzed for all groups: lower hypotensive response, higher hypertensive response and duration of response for each dose. Data were statistically analyzed by repeated measures analysis of variance, followed by Tukey test or Holm-Sidack test, at a significance level of 5%. The results showed that passive smoking significantly decreased the vasodilator response produced by epinephrine in normotensive and hypertensive animals, increasing their hypertensive responses and increased the duration of response to epinephrine, that was further increased by atenolol treatment. Atenolol treatment increased the hypertensive responses in hypertensive-smokers rats. The felypressin did not show vasodilator responses and its hypertensive responses were increased by passive smoking. The atenolol did not cause additional increase in felypressin responses. In hypertensive animals, the atenolol treatment associated with passive smoking had expressive effects, significantly increasing the total duration of response to felypressin. Felypressin, when compared with epinephrine, did not show direct hypotensive effects, the higher hypertensive responses were smaller and the duration of response to felypressin was twice the epinephrine time. Then, felypressin becomes an interesting drug to hypertensive patients, due to its capacity to promote prolonged vasoconstrictor effect without increasing the sympathetic nerve activity

Surgical anatomy of the maxillary nerve in the zygomatic region

Anatomic knowledge on the zygomatic fossa is of primary importance to improve the regional anesthetic technique of the maxillary nerve. Few reports in the literature have addressed the trajectory of the maxillary nerve and its branches in this region; thus, this study aimed at presenting information about the trajectory of these nerves. Thirty human half-heads of both genders were fixed in 10% formalin and demineralized in 5% nitric acid, and the maxillary nerve was dissected since its origin on the pterygopalatine fossa until penetration into the inferior orbital fissure. It was observed that the maxillary nerve sends one to three posterior superior alveolar branches and tuberal descendent branches, which supply the soft tissue structures of the region. The posterior superior alveolar nerves are inferiorly oriented near the maxillary tuberosity, where they penetrate the alveolar canals with the posterior superior alveolar artery and send small nerve branches that continue in an extraosseous trajectory. This study found that nearly 2/3 of the trajectory of the maxillary nerve is located in the zygomatic region, with a short segment (1/3) in the pterygopalatine fossa