Elongated styloid process and atheroma in panoramic radiography and its relationship with systemic osteoporosis and osteopenia

Association between the presence of an elongated styloid process, vascular calcification (atheroma) and the potential risk factor for osteoporosis was studied. Presence of an elongated styloid process was found to be correlated with systemic osteoporosis and also between elongated styloid process and atheroma. The association between the presences of an elongated styloid process and vascular calcification (atheroma) with the potential risk factor assessment for osteoporosis was studied. Bone mineral density obtained by dual energy X-ray absorptiometry diagnosed osteopenia/osteoporosis on at least two of three sites (column, hips, and forearm) of 50 female patients. Panoramic maxillomandibular radiographs were taken and analyzed. Elongation of the styloid processes was measured and the presence of atheromas in the carotid was investigated. Eighty percent of the patients presented at least one side with elongated styloid process and the highest prevalence (87.5%) occurred in individuals between 60 and 69 years. Atheroma was found in four patients, three of which presented elongated styloid on at least one side and had diagnosed osteoporosis on at least two of the evaluated sites. Correlation was found between the elongation of the styloid process and systemic osteoporosis, and between elongated styloid process and atheroma. The method in this study might be used as part of a method for osteopenia/osteoporosis and atheroma risk assessment.

Influence of Osteopenia in Autogenous Bone Graft Healing With or Without Expanded Polytetrafluoroethylene Membranes: Histologic and Histomorphometric Study in Rats

Purpose: The aim of this study was to quantitatively evaluate and qualitatively describe autogenous bone graft healing with or without an expanded polytetrafluoroethylene (e-PTFE) membrane in ovariectornized rats. Materials and Methods: Eighty Wistar rats, weighing approximately 300 g each, were used. A graft was obtained from the parietal bone and fixed to the sidewall of each animal`s left mandibular ramus. The animals were randomly divided into four experimental groups (n = 20 in each group): group 1, sham operated and autogenous bone graft only- group 2, sham operated and autogenous bone graft covered by e-PTFE membrane; group 3, ovariectornized (OVX) and autogenous bone graft only- group 4, OVX and autogenous bone graft covered by e-PTFE membrane. The animals were sacrificed at five different time points: immediately after grafting or at 7, 21, 45, or 60 days after grafting. Histologic examination and morphometric measurement of the sections were performed, and values were submitted to statistical analyses. Results: Both groups (sham and OVX) experienced loss of the original graft volume when it was not covered by the membrane, whereas use of the membrane resulted in additional bone formation beyond the edges of the graft and under the membrane. Histologic analysis showed integration of the grafts in all animals, although a larger number of marrow spaces was found in OVX groups. Conclusions: Association of bone graft with an e-PTFE membrane resulted in maintenance of its original volume as well as formation of new bone that filled the space under the membrane. Osteopenia did not influence bone graft repair, regardless of whether or not it was associated with e-PTFE membrane, but descriptive histologic analysis showed larger numbers of marrow spaces in the bone graft and receptor bed and formation of new bone in the OVX animals. INT J ORAL MAXILLOFAC IMPLANTS 2009;24:1074-1082

Association between osteoporosis and rheumatoid arthritis in women: a cross-sectional study

CONTEXT AND OBJECTIVES: Osteoporosis has frequently been observed in patients with rheumatoid arthritis. The present study was undertaken in order to evaluate factors associated with osteoporosis among women with rheumatoid arthritis. DESIGN AND SETTING: Cross-sectional study, carried out in a public hospital in São Paulo. METHODS: The participants were 83 women with rheumatoid arthritis (53.7 ± 10.0 years old). Bone mineral density (BMD) and body composition were measured by dual energy X-ray absorptiometry. The patients were divided into three groups according to BMD: group 1, normal BMD (n = 24); group 2, osteopenia (n = 38); and group 3, osteoporosis (n = 21). Tests were performed to compare differences in means and correlations, with adjustments for age, duration of disease and cumulative corticosteroid. The relationships between clinical factors, physical activity score, dietary intake, body composition and biochemical parameters were analyzed using linear regression models. RESULTS: Mean calcium, vitamin D and omega-6 intakes were lower than the recommendations. Associations were found between BMD and age, disease duration, parathyroid hormone concentration and fat intake. The linear regression model showed that being older, with more years of disease and lower weight were negatively correlated with BMD [Total femur = 0.552 + 0.06 (weight) + 0.019 (total physical activity) - 0.05 (age) - 0.003 (disease duration); R² = 48.1; P < 0.001]. CONCLUSION: The present study indicates that nutritional factors and body composition are associated with bone mass in women with rheumatoid arthritis.

Estudo descritivo da massa óssea e fatores de risco cardiovasculares em mulheres com síndrome de Turner

A síndrome de Turner é uma das doenças genéticas mais comuns, ocorrendo em cerca de 1:2.500 recém-nascidas. Representa a forma mais freqüente de hipogonadismo hipergonadotrófico. O hipoestrogenismo é a principal causa atribuída ao aumento do risco de doenças cardiovasculares, osteopenia e osteoporose. Diante da elevada incidência dessas doenças, o objetivo deste trabalho foi analisar a densidade mineral óssea das mulheres portadoras da síndrome de Turner e verificar a presença de fatores de risco de doença cardiovascular (DCV). Foram encontrados, pelo método Dexa, 14,28 por cento das mulheres com densidade mineral óssea normal, 28,5por cento com osteopenia e 57,1por cento com osteoporose. Foi observada hipertensão em uma mulher, obesidade em outra, diabetes em duas e todas referiram ser sedentárias (sete). Ressalta-se, portanto a importância da avaliação precoce do tecido ósseo e do rastreamento dos fatores de risco de DCV, assim como o controle dos fatores modificáveis e orientações de mudança do estilo de vida com finalidade preventiva

Double disruption of alpha(2A)- and alpha(2C)-adrenoceptors results in sympathetic hyperactivity and high-bone-mass phenotype

Evidence demonstrates that sympathetic nervous system (SNS) activation causes osteopenia via beta(2)-adrenoceptor (beta(2)-AR) signaling. Here we show that female mice with chronic sympathetic hyperactivity owing to double knockout of adrenoceptors that negatively regulate norepinephrine release, alpha(2A)-AR and alpha(2C)-AR(alpha(2A)/alpha(2C)-ARKO), present an unexpected and generalized phenotype of high bone mass with decreased bone resorption and increased formation. In alpha(2A)/alpha(2C)-ARKO versus wild-type (WT) mice, micro-computed tomographic (mu CT) analysis showed increased, better connected, and more plate-shaped trabeculae in the femur and vertebra and increased cortical thickness in the vertebra, whereas biomechanical analysis showed increased tibial and femoral strength. Tibial mRNA expression of tartrate-resistant acid phosphatase (TRACP) and receptor activator of NF-kappa B (RANK), which are osteoclast-related factors, was lower in knockout (KO) mice. Plasma leptin and brain mRNA levels of cocaine amphetamine-regulated transcript (CART), which are factors that centrally affect bone turnover, and serum levels of estradiol were similar between mice strains. Tibial beta(2)-AR mRNA expression also was similar in KO and WT littermates, whereas alpha(2A)-, alpha(2B)- and alpha(2C)-AR mRNAs were detected in the tibia of WT mice and in osteoblast-like MC3T3-E1 cells. By immunohistochemistry, we detected alpha(2A)-, alpha(2B)-, alpha(2C)- and beta(2)-ARs in osteoblasts, osteoclasts, and chondrocytes of 18.5-day-old mouse fetuses and 35-day-old mice. Finally, we showed that isolated osteoclasts in culture are responsive to the selective alpha(2)-AR agonist clonidine and to the nonspecific alpha-AR antagonist phentolamine. These findings suggest that beta(2)-AR is not the single adrenoceptor involved in bone turnover regulation and show that alpha(2)-AR signaling also may mediate the SNS actions in the skeleton. (c) 2011 American Society for Bone and Mineral Research.

Mechanical vibration preserves bone structure in rats treated with glucocorticoids

Glucocorticoids are an important cause of secondary osteoporosis in humans, which decreases bone quality and leads to fractures. Mechanical stimulation in the form of low-intensity and high-frequency vibration seems to be able to prevent bone loss and to stimulate bone formation. The objective of this study was to evaluate the effects of mechanical vibration on bone structure in rats treated with glucocorticoids. Thirty 3-month-old adult male Wistar rats were randomized to three groups: control (C), glucocorticoid (G), and glucocorticoid with vibration (CV). The G and GV groups received 3.5 mg/kg/day of methylprednisolone 5 days/week for a duration of 9 weeks, and the C group received vehicle (saline solution) during the same period. The CV group was vibrated on a special platform for 30 min per day, 5 days per week during the experiment. The platform was set to provide a vertical acceleration of 1 G and a frequency of 60 Hz. Skeletal bone mass was evaluated by total body densitometry (DXA). Fracture load threshold, undecalcified bone histomorphometry, and bone volume were measured in tibias. Glucocorticoids induced a significantly lower weight gain (-9.7%) and reduced the bone mineral content (-9.2%) and trabecular number (-41.8%) and increased the trabecular spacing (+98.0%) in the G group, when compared to the control (C). Vibration (CV) was able to significantly preserve (29.2%) of the trabecular number and decrease the trabecular spacing (+ 26.6%) compared to the G group, although these parameters did not reach C group values. The fracture load threshold was not different between groups, but vibration significantly augmented the bone volume of the tibia by 21.4% in the CV group compared to the C group. Our study demonstrated that low-intensity and high-frequency mechanical vibration was able to partially inhibit the deleterious consequences of glucocorticoids on bone structure in rats. (C) 2010 Elsevier Inc. All rights reserved.

Accentuated osteoclastic response to parathyroid hormone undermines bone mass acquisition in osteonectin-null mice

Matricellular proteins play a unique role in the skeleton as regulators of bone remodeling, and the matricellular protein osteonectin (SPARC, BM-40) is the most abundant non-collagenous protein in bone In. the absence of osteonectin, mice develop progressive low turnover osteopenia, particularly affecting trabecular bone. Polymorphisms in a regulatory region of the osteonectin gene are associated with bone mass in a subset of idiopathic osteoporosis patients, and these polymorphisms likely regulate osteonectin expression. Thus it is important to determine how osteonectin gene dosage affects skeletal function. Moreover, intermittent administration of parathyroid hormone (PTH) (1-34) is the only anabolic therapy approved for the treatment of osteoporosis, and it is critical to understand how modulators of bone remodeling, such as osteonectin, affect skeletal response to anabolic agents. In this study, 10 week old female wild type, osteonectin-haploinsufficient, and osteonectin-null mice (C57Bl/6 genetic background) were given 80 mu g/kg body weight/day PTH(1-34) for 4 weeks. Osteonectin gene dosage had a profound effect on bone microarchitecture. The connectivity density of trabecular bone in osteonectin-haploinsufficient mice was substantially decreased compared with that of wild type mice, suggesting compromised mechanical properties. Whereas mice of each genotype had a similar osteoblastic response to PTH treatment, the osteoclastic response was accentuated in osteonectin-haploinsufficient and osteonectin-null mice. Eroded surface and osteoclast number were significantly higher in PTH-treated osteonectin-null mice, as was endosteal area. In vitro studies confirmed that PTH induced the formation of more osteoclast-like cells in marrow from osteonectin-null mice compared with wild type. PTH treated osteonectin-null bone marrow cells expressed more RANKL mRNA compared with wild type. However, the ratio of RANKL:OPG mRNA was somewhat lower in PTH treated osteonectin-null cultures. Increased expression of RANKL in response to PTH could contribute to the accentuated osteoclastic response in osteonectin(-/-) mice, but other mechanisms are also likely to be involved. The molecular mechanisms by which PTH elicits bone anabolic vs. bone catabolic effects remain poorly understood. Our results imply that osteonectin levels may play a role in modulating the balance of bone formation and resorption in response to PTH. (c) 2008 Elsevier Inc. All rights reserved.

Influence of estrogen deficiency and its treatment with alendronate and estrogen on bone density around osseointegrated implants: radiographic study in female rats

Objective. This study evaluated the influence of estrogen deficiency and its treatment on bone density around integrated implants. Study design. Implants were placed in female rat tibiae. The animals were assigned to 5 groups: control, sham, ovariectomy, estrogen, and alendronate. The control group was humanely killed to confirm integration of the implant. The others were submitted to ovariectomy or sham surgery. Bone density was measured by digital radiographs at 6 points on sides of the implant. Results. The analysis of radiographic bone density revealed estrogen privation had a negative impact only in the cancellous bone. The estrogen group differed significantly ( P <.05) from the ovariectomy and alendronate groups. The alendronate group presented the highest density for all evaluated regions. Conclusion. Ovariectomy caused a decrease in the radiographic bone density in the cancellous region. Estrogen replacement therapy and alendronate were effective treatments in preventing bone mass loss around integrated implants.

The Bone Histology Spectrum in Experimental Renal Failure: Adverse Effects of Phosphate and Parathyroid Hormone Disturbances

Bone disease is a common disorder of bone remodeling and mineral metabolism, which affects patients with chronic kidney disease. Minor changes in the serum level of a given mineral can trigger compensatory mechanisms, making it difficult to evaluate the role of mineral disturbances in isolation. The objective of this study was to determine the isolated effects that phosphate and parathyroid hormone (PTH) have on bone tissue in rats. Male Wistar rats were subjected to parathyroidectomy and 5/6 nephrectomy or were sham-operated. Rats were fed diets in which the phosphate content was low, normal, or high. Some rats received infusion of PTH at a physiological rate, some received infusion of PTH at a supraphysiological rate, and some received infusion of vehicle only. All nephrectomized rats developed moderate renal failure. High phosphate intake decreased bone volume, and this effect was more pronounced in animals with dietary phosphate overload that received PTH infusion at a physiological rate. Phosphate overload induced hyperphosphatemia, hypocalcemia, and changes in bone microarchitecture. PTH at a supraphysiological rate minimized the phosphate-induced osteopenia. These data indicate that the management of uremia requires proper control of dietary phosphate, together with PTH adjustment, in order to ensure adequate bone remodeling.

Chronic polyarthritis as the first manifestation of juvenile systemic lupus erythematosus patients

Objective: To evaluate the prevalence of chronic polyarthritis in juvenile systemic lupus erythematosus (JSLE) and to describe the manifestations, treatments, and outcomes in these patients. Methods: From January 1983 to July 2010, 5419 patients were followed up at the Pediatric Rheumatology Unit of the University Hospital and 271 (5%) of them had JSLE (American College of Rheumatology [ACR] criteria). `Rhupus` was classified as the overlap of juvenile idiopathic arthritis (International League of Associations for Rheumatology [ILAR] criteria) and JSLE. We evaluated demographic data, polyarthritis and other clinical manifestations, disease activity and damage, laboratory exams, radiographic findings, treatments, and outcomes. Results: The prevalence of chronic polyarthritis in this JSLE population was 2.6% (7/271). This articular involvement was the initial manifestation in all seven JSLE patients. The median duration of chronic polyarthritis was 11 months (range 2-15 months). Interestingly, rhupus with chronic polyarthritis and limitation of movement, presence of rheumatoid factor, autoantibodies, and/or radiographic abnormalities (juxtaarticular osteopenia, joint-space narrowing, or erosions) was evidenced in three patients. No patient had deformities of hands and feet associated with Jaccoud`s arthropathy or osteonecrosis. All patients were treated with nonsteroidal anti-inflammatory drugs (NSAIDs, naproxen 10-15 mg/kg/day) when polyarthritis diagnosis was established. Prednisone and antimalarials were administered at JSLE diagnosis. The three non-responsive rhupus patients were treated in conjunction with immunosuppressive drugs (methotrexate, azathioprine, and/or cyclosporine). Conclusions: Chronic polyarthritis was a rare lupus manifestation in active pediatric patients. The interesting overlap between chronic arthritis and lupus, called rhupus suggests a new entity with a different clinical profile and a poor response to treatment with NSAIDs alone. In addition, the occurrence of this association in JSLE patients could be classified as a clinical sub-group of JSLE with possible specific genetic determinants. Lupus (2011) 20, 960-964.

The association between osteoporosis and static balance in elderly women

This study aimed at answering the question: do people with high bone loss have greater postural instability? Groups were separated into group 1: women with normal bone mineral density, group 2: women with osteopenia, and group 3: women with osteoporosis. The balance was evaluated in four upright postural situations. Osteoporosis group had greater oscillation in the anteroposterior displacement in all situations compared to control group and the greatest mediolateral displacement in all situations compared to other groups. It is not known whether the presence of osteoporosis can be considered a factor aggravating the postural control. This study aimed at answering the question: do people with high bone loss have greater postural instability? This study was divided into three groups: group 1 (n = 20) consisting of women with normal bone mineral density, group 2 (n = 20) women with osteopenia, and group 3 (n = 20) women with osteoporosis. All the participants were submitted to evaluation of the balance using the Polhemus system in four upright postural situations. Osteoporosis group had greater oscillation in the anteroposterior displacement in all situations compared to control group. The osteoporosis group also showed the greatest mediolateral displacement in all situations compared to other groups. The results suggest that osteoporotic women had the worst balance, possibly due to the more pronounced body changes compared to non-osteoporotic women.

Effect of treadmill exercise on lumbar vertebrae in ovariectomized rats: anthropometrical and mechanical analyses

The purpose of this study was to examine the preventive effect of exercise on lumbar vertebrae in ovariectomized rats. Three-month-old female Wistar rats were divided into 3 groups: control group (A, n = 10); non-exercised ovariectomized group (B, n = 7) and exercised ovariectomized group (C, n = 7). The rats from group C were subjected to treadmill exercise (15 m/minute in the initial six weeks and 19 m/minute in the next six weeks, 1 hour/day, 4 days/week) for 12 weeks. At death, the fourth lumbar vertebrae were removed and an anthropometrical analysis by a paquimeter and a mechanical compression test by a universal test machine were performed. After 12 weeks, the ovariectomy decreased the superior-inferior vertebral height and the maximal braking load in group B compared to group A, while the exercise increased the vertebral mass in group C compared to both groups A and B (p < 0.01) and the stiffness compared to group B. We concluded the physical activity has an important role to prevent the osteopenia in lumbar vertebrae.

Chronic ethanol intake inhibits in vitro osteogenesis induced by osteoblasts differentiated from stem cells

The study investigated whether chronic ethanol (ETH) intake and subsequent ETH exposure of cell cultures affects osteoblast differentiation by evaluating key parameters of in vitro osteogenesis. Rats were treated with 5-20% (0.85-3.43 mM) ETH, increasing by 5% per week for a period of 4 weeks (habituation), after which the 20% level was maintained for 15 days (chronic intake). Bone-marrow stem cells from control (CONT) or ETH-treated rats were cultured in osteogenic medium which was either supplemented (ETH) or not supplemented (CONT) with 1.3 mm ethanol. Thus, four groups relating to rat treatment/culture supplementation were evaluated: (1) CONT/CONT, (2) ETH/CONT, (3) CONT/ETH and (4) ETH/ETH Cell morphology, proliferation and viability, total protein content, alkaline phosphatase (ALP) activity and bone-like nodule formation were evaluated. Chronic ethanol intake significantly reduced both food and liquid consumption and body weight gain. No difference was seen in cell morphology among treatments. Cell number was affected at 7 and 10 days as follows: CONT/CONT = CONT/ETH < ETH/CONT = ETH/ETH. Doubling time between 3 and 10 days was greater in groups of CONT animals: ETH/ETH = ETH/CONT < CONT/ETH = CONT/CONT. Cell viability and ALP activity were not affected by either animal treatment or culture exposure to ethanol. At day 21, the total protein content was affected as follows: ETH/ETH = CONT/ETH < ETH/CONT = CONT/CONT. Bone-like nodule formation was affected as follows: ETH/ETH < CONT/ETH < ETH/CONT < CONT/CONT. These results show that chronic ethanol intake, followed by the exposure of osteoblasts to ethanol, inhibited the differentiation of osteoblasts, as indicated by an increased proliferation rate and reduced bone-like nodule formation. Copyright (C) 2007 John Wiley & Sons, Ltd.

Intermittent Therapy with 1,25 Vitamin D and Calcitonin Prevents Cyclosporin-Induced Alveolar Bone Loss in Rats

Bone loss associated with cyclosporin A (CsA) therapy can result in serious morbidity to patients. Intermittent administration of 1,25 Vitamin D and calcitonin reduces osteopenia in a murine model of postmenopausal osteoporosis. The purpose of this study was to evaluate the effects of this therapeutic approach on CsA-induced alveolar bone loss in rats. Forty male Wistar rats were allocated to four experimental groups according to the treatment received during 8 weeks: (1) CsA (10 mg/kg/day, s.c.); (2) 1,25 Vitamin D (2 mu g/kg, p.o.; in weeks 1, 3, 5, and 7) plus calcitonin (2 mu g/kg, i.p.; in weeks 2, 4, 6, and 8); (3) CsA concurrently with intermittent 1,25 Vitamin D and calcitonin administration; and (4) the control treatment group (vehicle). At the end of the 8-week treatment period, serum concentrations of bone-specific alkaline phosphatase, tartrate-resistant acid phosphatase (TRAP-5b), osteocalcin, interleukin (IL)-1 beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) were measured and an analysis of bone volume, bone surface, number of osteoblasts, and osteoclasts was performed. CsA administration resulted in significant alveolar bone resorption, as assessed by a lower bone volume and an increased number of osteoclasts, and increased serum bone-specific alkaline phosphatase, TRAP-5b, IL-1 beta, IL-6, and TNF-alpha concentrations. The intermittent administration of calcitriol and calcitonin prevented the CsA-induced osteopenic changes and the increased serum concentrations of TRAP-5b and inflammatory cytokines. Intermittent calcitriol/calcitonin therapy prevents CsA-induced alveolar bone loss in rats and normalizes the production of associated inflammatory mediators.