José Angelo Camilli

On the incidence of the biceps brachii third head in Brazilian whites and blacks

The incidence of a third head of the biceps brachii muscle has been reported in several articles, and there is a general idea that it is a race-dependent variation. The aim of this investigation was to study the biceps brachii muscle with regard to the incidence of its third head in a mixed white and black Brazilian population. A total of 200 upper arms from adult white and black cadavers (100 whites and 100 blacks) fixed in a 10% formol solution were examined and compared. It was observed that for white subjects the incidence of the third head was 20% against 9% for the black subjects: a statistically significant difference. We suggest that other factors, in addition to racial ones, might play a part in determining the incidence of the biceps brachii third head in a population.

Repair of bone defects treated with autogenous bone graft and low-power laser.

Because bone healing at the graft site is similar to a fracture repair, the purpose of the present study was to evaluate the effects of low-power laser irradiation on the repair of rat skull defects treated with autogenous bone graft. A defect measuring 3 mm in diameter was produced in the left parietal bone and filled with an autogenous bone graft obtained from the right parietal bone. The animals were divided into 3 groups of 20 rats each: nonirradiated control, irradiated with 5.1 J/cm2, and irradiated with 10.2 J/cm2. The laser (2.4 mW, 735 nm, 3.4 × 10−2 W/cm2, 3-mm spot size) was applied three times per week for 4 weeks. Greater volume of newly formed bone was observed in the irradiated group with 10.2 J/cm2. In both irradiated groups, a greater volume of newly formed bone occurred only in the first 2 weeks. The results demonstrated that laser irradiation at the grafted site stimulated osteogenesis during the initial stages of the healing process in a skull defect of the rat and that this effect was dose dependent.

Mechanical, biochemical and morphometric alterations in the femur of mdx mice.

The bone tissue abnormalities observed in patients with Duchenne muscular dystrophy are frequently attributed to muscle weakness. In this condition, bones receive fewer mechanical stimuli, compromising the process of bone modeling. In the present study we hypothesize that other factors inherent to the disease might be associated with bone tissue impairment, irrespective of the presence of muscle impairment. Mdx mice lack dystrophin and present cycles of muscle degeneration/regeneration that become more intense in the third week of life. As observed in humans with muscular dystrophy, bone tissue abnormalities were found in mdx mice during more intense muscle degeneration due to age. Under these circumstances, muscle deficit is probably one of the factors promoting these changes. To test our hypothesis, we investigated the changes that occur in the femur of mdx mice at 21 days of age when muscle damage is still not significant. The mechanical (structural and material) and biochemical properties and morphometric characteristics of the femur of mdx and control animals were evaluated. The results demonstrated a lower strength, stiffness and energy absorption capacity in mdx femurs. Higher values for structural (load and stiffness) and material (stress, elastic modulus and toughness) properties were observed in the control group. Mdx femurs were shorter and were characterized by a smaller cortical area and thickness and a smaller area of epiphyseal trabecular bone. The hydroxyproline content was similar in the two groups, but there was a significant difference in the Ca/P ratios. Thermogravimetry showed a higher mineral matrix content in cortical bone of control animals. In conclusion, femurs of mdx mice presented impaired mechanical and biochemical properties as well as changes in collagen organization in the extracellular matrix. Thus, mdx mice developed femoral osteopenia even in the absence of significant muscle fiber degeneration. This weakness of the mdx femur is probably due to genetic factors that are directly or indirectly related to dystrophin deficiency.

Repair of cranial bone defects with calcium phosphate ceramic implant or autogenous bone graft.

Autogenous bone grafts have frequently been used in the treatment of bone defects; however, this procedure can cause clinical complications after surgery. Besides, the amount of available bone is sometimes insufficient. Therefore, synthetic biomaterials have been researched as an alternative to autogenous bone graft implants. The objective of this study was to evaluate the repair of bone defects treated with compact autogenous bone graft or porous calcium phosphate ceramics. Three defects 3 mm in diameter were produced in the skull of 21 rats. One the defects was produced in the frontal bone, which remained empty, while the others were produced in the right and left parietal bones, which were filled respectively with ceramics and autogenous bone graft. The animals were sacrificed 1, 2, 4, and 24 weeks after surgery and analyzed by light microscopy and radiography. In the twenty-fourth week, the defects filled with autogenous bone graft and ceramics had similar volumes of newly formed bone tissue. The ceramics offered favorable conditions to bone tissue growth. Thus, we concluded that the calcium phosphate ceramic implant proved to be effective in repairing defects produced in the skull of rats.

Effects of ethanol on the osteogenesis around porous hydroxyapatite implants

Alcohol consumption compromises bone tissue, and thus may either impair or stop the fixation and maintenance of osseointegrated implants. To evaluate the effects of 5% and 15% ethanol on bone neoformation around porous hydroxiapatite implants. Fifteen rats were separated into 3 groups of 5 animals each: control (CT); 5% alcohol (A); and 15% alcohol (AA). After four weeks of ethanol consumption, the rats received porous hydroxiapatite implants into surgically made cavities in the femur. After surgery, the animals continued to consume ethanol until day 90 of the experiment, when they were euthanised and their femurs removed for histological processing. Bone tissue was found around the ceramic specimens of all the animals. The largest volume of neoformed bone around ceramic specimens occurred in the CT group, and the smallest in the AA group, followed by the A group. It was concluded that ethanol consumption produced a negative effect on osteogenesis around hydroxyapatite implants. Even small doses, such as the 5% ethanol dilution can interfere with bone repair.

Bone tissue and muscle dystrophin deficiency in mdx mice

Duchenne muscular dystrophy is a neuromuscular disease caused by the lack of dystrophin that affects skeletal muscles, causing degeneration of muscle fibers and replacing them with fibrous and adipose tissue, events that gradually lead to functional loss. Patients with Duchenne muscular dystrophy have shown that bones become more fragile with age and with advancement of the disease. Muscle weakness and reduced mobility have been suggested to be the factors that promote bone deterioration. However, it seems that this does not occur in mdx mice. It has been identified in mdx mice the existence of a factor related or not to the lack of dystrophin that also participates in the impairment of bone quality. Mdx mice also exhibit muscle degeneration, but unlike human, it is compensated by muscle regeneration. In consequence, there is an increase in the muscle mass, but not necessarily of muscle contractile strength. The accommodation of this increased muscle mass promotes bone formation at specific sites, such as at tendo-osseous junctions. In addition, the inflammatory response to muscle injury may be responsible for the increase in angiogenesis and regeneration observed in mdx mice, inducing the release of cytokines and chemokines that play an important role in the recruitment of leukocytes and macrophages. Then, mdx mice may possess compensatory mechanisms in bone in response to a genetic defect.

Metabolic and structural bone disturbances induced by hyperlipidic diet in mice treated with simvastatin

Simvastatin can modulate lipid and bone metabolism. However, information related to the interaction between diet and simvastatin on bone structure and biomechanics is scarce. Thus, this study evaluated the effects of simvastatin on femoral biomechanics and cortical/trabecular bone structure in wild‐type mice nourished with a hyperlipidic diet. Three‐month‐old male wild‐type mice (C57BL6 strain) were divided into four groups: (1) group W, nourished with a standard diet; (2) group WH, fed a hyperlipidic diet; (3) group WS, nourished with a standard diet plus oral simvastatin (20 mg/kg/day); and (4) group WHS, fed a hyperlipidic diet plus oral simvastatin (20 mg/kg/day). All animals received only their specific diet and water for 60 days. Blood samples were collected for the analysis of calcium, triglycerides, total cholesterol (TC) and fraction serum levels. Diet manipulation was able to induce a dyslipidaemic status in mice, characterized by triglyceride and TC rise in WH animals. Simvastatin prevented hypercholesterolaemia and reduced TC and LDL serum levels, but did not prevent hypertriglyceridaemia and HDL serum levels in the WHS group. In the WH mice the hyperlipidaemia was associated with reduction in trabecular bone thickness, femur structural and material property alterations. Simvastatin prevented these morphological alterations and minimized femur biomechanical changes in WHS mice. Taken together, the results indicated that the hyperlipidic diet intake acts as a risk factor for bone integrity, generating bones with reduced resistance and more susceptible to fractures, an effect attenuated by simvastatin that is potentially related to the modulatory action of this drug on lipid and bone metabolism.

Morphological Characterization of Femur and Parietal Bone Mineral of Rats at Different Ages

Some microscopy studies on the mineral phase of bone have been carried out either utilizing Optical or Scanning Electron Microscopy (SEM), generally around 1000x magnification, to observe the interaction between cells and bone mineral. Other studies have been utilizing Transmission Electron Microscopy (TEM), generally around 1000000x magnification, to observe the fundamental particles that form bone mineral. The literature lacks works that utilize Scanning Electron Microscopy around 10000x magnification, particularly suitable for the study of structures composed by the aggregation of fundamental particles. The objective of this work was to study the morphologic differences between the mineral phase of femur and parietal bone of Wistar rats. Observation of the micrographs showed that the microscopic morphology of the mineral phase of femur was very similar to that of the parietal bone. It was also possible to notice that the morphology of the mineral phases varied with age, yet this variation was practically the same for the material obtained from the two types of bones.

Mechanical and morphological aspects of the calcaneal tendon of mdx mice at 21 days of age

A relationship between compromised muscles and other tissues has been demonstrated in mdx mouse, an animal model studied for understanding of Duchenne muscular dystrophy. The hypothesis is that changes in the calcaneal tendon of mdx mice occur previous to the onset of rigorous and most marked episodes of muscle degeneration, which start suddenly after 21 days of life. Thus, this study aimed to identify possible alterations in the calcaneal tendon of mdx mouse at 21 days of age. Control and mdx tendons were submitted to mechanical tensile testing, quantification of hydroxyproline, and staining with toluidine blue and picrosirius red. Hydroxyproline content was similar between mdx and control groups. The control tendon presented higher mechanical strength (load, stress, and elastic modulus) and its morphological analysis showed a larger number of round fibroblasts, nuclei with well‐decondensed chromatin, and slightly metachromatic well‐stained cytoplasmic material, different from that observed in mdx tendons. The results suggest that the absence of dystrophin in mdx mouse can provoke directly or indirectly alterations in the mechanical properties and morphology of the calcaneal tendon. Anat Rec, 296:1546–1551, 2013.

Spontaneous healing capacity of calvarial bone defects in mdx mice.

The mdx mouse is an experimental model widely used for the study of Duchenne muscular dystrophy, which is characterized by the lack of dystrophin and cycles of muscle degeneration/regeneration. Studies demonstrated elevated levels of growth factors and accelerated skin wound repair in these animals. We therefore raised the hypothesis that the bone repair process might also be altered in these animals. Thus, the objective of this study was to evaluate the spontaneous healing of calvarial defects in mdx mice by histomorphometric analysis. Animals (45 days old) were divided into mdx and control groups. A defect measuring 2 mm in diameter was produced surgically in the right parietal bone of each animal. The animals were sacrificed 15, 30, and 60 days after surgery, and the skulls were processed by routine histological procedures. No difference in the volume of new bone inside the defect was observed between the two groups at any of the three postoperative time points. There was also no difference between the different periods of healing when each group was analyzed separately. The lower quality of femoral and calvarial bone in mdx mice reported in previous studies and the similar bone regeneration rates seen in two groups suggest that the healing capacity of calvarial defects was more expressive in mdx mice than in control animals. An increase in the amount of osteogenic factors released by damaged myofibers may have favored osteogenesis during bone defect healing in mdx mice. Anat Rec, 2012.