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Cemento-ossifying fibroma (COF) is a slow-growing, well-defined unilocular benign mesenchymal odontogenic tumor, that can have sclerotic edges and mixed areas. This case report details a conservative surgical treatment approach for COF that preserved both the cortical basal bone and the tooth segment. A thirty-three-year-old female presented with an asymptomatic extensive lesion in the anterior mandible, manifesting mild facial asymmetry, with one year of evolution. Imaging revealed a mixed dense lesion with sclerotic edges, with extension to the periapex of the teeth 33-44, expanding and thinning the cortical bone. Histopathology confirmed COF, showing fibrous stroma with spherical cementoid calcifications, overlayed with intact bone tissue. Conservative surgery was performed combining enucleation and curettage, with peripheral ostectomy, maintaining the cortical basal bone from the mandibulae, and tooth by apicoectomies. Three- and ten-months postoperative imaging displayed peripheral bone neoformation at the site, indicating effectiveness in the short-term follow-up, with no evidence of residual disease or recurrence. (AU)

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Relapsing polychondritis is a rare multisystem disease involving cartilaginous and proteoglycan-rich structures. The diagnosis of this disease is mainly suggested by the presence of flares of inflammation of the cartilage, particularly in the ears, nose or respiratory tract, and more rarely, in the presence of other manifestations. The spectrum of clinical presentations may vary from intermittent episodes of painful and often disfiguring auricular and nasal chondritis to an occasional organ or even life-threatening manifestations such as lower airway collapse. There is a lack of awareness about this disease is mainly due to its rarity. In 2020, VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome, a novel autoinflammatory syndrome, was described. VEXAS syndrome is attributed to somatic mutations in methionine-41 of UBA1, the major E1 enzyme that initiates ubiquitylation. This new disease entity connects seemingly unrelated conditions: systemic inflammatory syndromes (relapsing chondritis, Sweet's syndrome, and neutrophilic dermatosis) and hematologic disorders (myelodysplastic syndrome or multiple myeloma). Therefore, this article reviews the current literature on both disease entities.

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Introduction: Congenital Generalized Lipodystrophy (CGL) is a rare autosomal recessive disease caused by mutations in genes responsible for the formation and development of adipocytes. Bone abnormalities are described. However, there is a scarcity of data. Objective: To describe bone characteristics in a large CGL1 and 2 case series. Methods: Cross-sectional study that assessed bone radiological features of CGL patients of a reference hospital in Fortaleza (CE), Brazil. Patients underwent clinical and bone mineral metabolism evaluation, radiographs of the axial and appendicular skeleton and bone mineral density (BMD) assessment by DEXA (dual energy X-ray absorptiometry). Results: Nineteen patients were included, fourteen were CGL1 and 5, CGL2. Median age was 20 years (8-42) and 58% were women. Median BMI and percentage of body fat were, respectively, 21 Kg/m² (16-24), and 10.5% (7.6-15). The median leptin concentration was 1 ng/mL (0.1-3.3). Diabetes mellitus and dyslipidemia were present in 79% and 63% of patients, respectively. Median calcium and phosphate were normal in almost all patients (95%). Median parathyroid hormone and 25-OH-vitamin D were 23 pg/mL (7-75) and 28 ng/mL (18-43). Osteolytic lesions, osteosclerosis and pseudo-osteopoikylosis, were present in 74%, 42% and 32% of patients, respectively. Lytic lesions were found predominantly in the extremities of long bones, bilaterally and symmetrically, spine was spared. Osteosclerosis was present in axial and appendicular skeleton. Pseudo-osteopoikilosis was found symmetrically in epiphyses of femur and humerus, in addition to the pelvis. BMD Z-score greater than +2.5 SD was observed in 13 patients (68.4%). BMD was higher in CGL1 compared to CGL2 in lumbar spine and total body in adults. No associations were found between high BMD and HOMA-IR (p=0.686), DM (p=0.750), osteosclerosis (p=0.127) or pseudo-osteopoikilosis (p=0.342), and, between pain and bone lesions. Fractures were found in 3 patients. Conclusion: Bone manifestations are prevalent, heterogeneous, and silent in CGL1 and CGL2. Osteolytic lesions are the most common, followed by osteosclerosis and pseudo-osteopoikilosis. Bone mass is high in most cases. There was no pain complaint related to bone lesions. Thus, systematic assessment of bone manifestations in CGL is essential. Studies are needed to better understand its pathogenesis and clinical consequences.

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Protein-encoding genes only constitute less than 2% of total human genomic sequences, and 98% of genetic information was previously referred to as "junk DNA". Meanwhile, non-coding RNAs (ncRNAs) consist of approximately 60% of the transcriptional output of human cells. Thousands of ncRNAs have been identified in recent decades, and their essential roles in the regulation of gene expression in diverse cellular pathways associated with fundamental cell processes, including proliferation, differentiation, apoptosis, and metabolism, have been extensively investigated. Furthermore, the gene regulation networks they form modulate gene expression in normal development and under pathological conditions. In this review, we integrate current information about the classification, biogenesis, and function of ncRNAs and how these ncRNAs support skeletal development through their regulation of critical genes and signaling pathways in vivo. We also summarize the updated knowledge of ncRNAs involved in common skeletal diseases and disorders, including but not limited to osteoporosis, osteoarthritis, rheumatoid arthritis, scoliosis, and intervertebral disc degeneration, by highlighting their roles established from in vivo, in vitro, and ex vivo studies.

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OBJECTIVES: Secondary hyperparathyroidism (sHPT) is an important contributor to bone disease and cardiovascular calcifications in children with chronic kidney disease (CKD). When conservative measures are ineffective, parathyroidectomy is indicated. The aim of our study was to evaluate the efficacy and safety of subtotal parathyroidectomy (sPTX) in pediatric and adolescent patients, and to provide a rationale for considering this aggressive treatment in CKD patients with uncontrolled sHPT. METHODS: We retrospectively analyzed the medical records of 19 pediatric CKD patients on dialysis with refractory sHPT who underwent sPTX at our institution between 2010 and 2020. All patients had clinical, radiological, and biochemical signs of renal osteodystrophy. RESULTS: One year after sPTX, parathyroid hormone (PTH) levels (median and interquartile range (IQR)) dropped from 2073 (1339-2484) to 164 (93-252) pg/mL (p=0.0001), alkaline phosphatase (ALP) levels from 1166 (764-2373) to 410 (126-421) IU/L (p=0.002), and the mean (±SDS) calcium-phosphate (Ca*P) product from 51±11 to 41±13 mg2/dL2 (p=0.07). Postoperatively, all patients presented with severe hungry bone syndrome (HBS) and required intravenous and oral calcium and calcitriol supplementation. None of them had other postoperative complication. Histological findings had a good correlation with preoperative parathyroid ultrasound imaging (n: 15) in 100 % and with technetium-99m (99mTc) sestamibi scintigraphy (n: 15) in 86.6 %. Clinical and radiological signs of bone disease improved in all patients. CONCLUSIONS: Pediatric sPTX is effective and safe to control sHPT and calcium-phosphate metabolism in children with CKD on dialysis and may mitigate irreversible bone deformities and progression of cardiovascular disease.

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The number of patients with functional loss of bone and cartilage tissue has shown an increasing trend. Insufficient or inappropriate conventional treatments applied for trauma, orthopedic diseases, or other bone and cartilage-related disorders can lead to bone and cartilage damage. This represents a worldwide public health issue and a significant economic burden. Advanced therapeutic medicinal products (ATMPs) proposed promising alternative therapeutic modalities by application of cell-based and tissue engineering approaches. Recently, several ATMPs have been developed to promote bone and cartilage tissue regeneration. Fifteen ATMPs, two related to bone and 13 related to cartilage, have received regulatory approval and marketing authorization. However, four ATMPs were withdrawn from the market for various reasons. However, ATMPs that are still on the market have demonstrated positive results, their broad application faced limitations. The development and standardization of methodologies will be a major challenge in the coming decades. Currently, the number of ATMPs in clinical trials using mesenchymal stromal cells or chondrocytes indicates a growing recognition that current ATMPs can be improved. Research on bone and cartilage tissue regeneration continues to expand. Cell-based therapies are likely to be clinically supported by the new ATMPs, innovative fabrication processes, and enhanced surgical approaches. In this study, we highlighted the available ATMPs that have been used in bone and cartilage defects and discussed their advantages and disadvantages in clinical applications.

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Mayaro virus (MAYV) is an emerging arbovirus member of the Togaviridae family and Alphavirus genus. MAYV infection causes an acute febrile illness accompanied by persistent polyarthralgia and myalgia. Understanding the mechanisms involved in arthritis caused by alphaviruses is necessary to develop specific therapies. In this work, we investigated the role of the CCL2/CCR2 axis in the pathogenesis of MAYV-induced disease. For this, wild-type (WT) C57BL/6J and CCR2-/- mice were infected with MAYV subcutaneously and evaluated for disease development. MAYV infection induced an acute inflammatory disease in WT mice. The immune response profile was characterized by an increase in the production of inflammatory mediators, such as IL-6, TNF, and CCL2. Higher levels of CCL2 at the local and systemic levels were followed by the significant recruitment of CCR2+ macrophages and a cellular response orchestrated by these cells. CCR2-/- mice showed an increase in CXCL-1 levels, followed by a replacement of the macrophage inflammatory infiltrate by neutrophils. Additionally, the absence of the CCR2 receptor protected mice from bone loss induced by MAYV. Accordingly, the silencing of CCL2 chemokine expression in vivo and the pharmacological blockade of CCR2 promoted a partial improvement in disease. Cell culture data support the mechanism underlying the bone pathology of MAYV, in which MAYV infection promotes a pro-osteoclastogenic microenvironment mediated by CCL2, IL-6, and TNF, which induces the migration and differentiation of osteoclast precursor cells. Overall, these data contribute to the understanding of the pathophysiology of MAYV infection and the identification future of specific therapeutic targets in MAYV-induced disease.IMPORTANCEThis work demonstrates the role of the CCL2/CCR2 axis in MAYV-induced disease. The infection of wild-type (WT) C57BL/6J and CCR2-/- mice was associated with high levels of CCL2, an important chemoattractant involved in the recruitment of macrophages, the main precursor of osteoclasts. In the absence of the CCR2 receptor, there is a mitigation of macrophage migration to the target organs of infection and protection of these mice against bone loss induced by MAYV infection. Much evidence has shown that host immune response factors contribute significantly to the tissue damage associated with alphavirus infections. Thus, this work highlights molecular and cellular targets involved in the pathogenesis of arthritis triggered by MAYV and identifies novel therapeutic possibilities directed to the host inflammatory response unleashed by MAYV.

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BACKGROUND: Mineral and bone disease in children with chronic kidney disease can cause abnormalities in calcium, phosphorus, parathyroid hormone, and vitamin D and when left untreated can result in impaired growth, bone deformities, fractures, and vascular calcification. Cinacalcet is a calcimimetic widely used as a therapy to reduce parathyroid hormone levels in the adult population, with hypocalcemia among its side effects. The analysis of safety in the pediatric population is questioned due to the scarcity of randomized clinical trials in this group. OBJECTIVE: To assess the onset of symptomatic hypocalcemia or other adverse events (serious or non-serious) with the use of cinacalcet in children and adolescents with mineral and bone disorder in chronic kidney disease. DATA SOURCES AND STUDY ELIGIBILITY CRITERIA: The bibliographic search identified 2699 references from 1927 to August/2023 (57 LILACS, 44 Web of Science, 686 PubMed, 131 Cochrane, 1246 Scopus, 535 Embase). Four references were added from the bibliography of articles found and 12 references from the gray literature (Clinical Trials). Of the 77 studies analyzed in full, 68 were excluded because they did not meet the following criteria: population, types of studies, medication, publication types and 1 article that did not present results (gray literature). PARTICIPANTS AND INTERVENTIONS: There were 149 patients aged 0-18 years old with Chronic Kidney Disease and mineral bone disorder who received cinacalcet. STUDY APPRAISAL AND SYNTHESIS METHODS: Nine eligible studies were examined for study type, size, intervention, and reported outcomes. RESULTS: There was an incidence of 0.2% of fatal adverse events and 16% of serious adverse events (p < 0.01 and I2 = 69%), in addition to 10.7% of hypocalcemia, totaling 45.7% of total adverse events. LIMITATIONS: There was a bias in demographic information and clinical characteristics of patients in about 50% of the studies and the majority of the studies were case series. CONCLUSIONS AND IMPLICATIONS OF KEY FINDINGS: If used in the pediatric population, the calcimimetic cinacalcet should be carefully monitored for serum calcium levels and attention to possible adverse events, especially in children under 50 months. SYSTEMATIC REVIEW REGISTRATION NUMBER (PROSPERO REGISTER): CRD42019132809.

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This work aimed to characterize the clinic-pathological presentation of an outbreak of auricular and laryngeal chondritis in pigs. Visits were made to pig farms, where the clinical history was obtained, and clinical and postmortem examinations were performed. In those farms, 3% to 4% of pigs presented otohematomas, which started in the nursery and extended to the finishing phase. Moreover, some finishing pigs presented with respiratory distress, initially characterized as inspiratory dyspnea, associated by an uncommon respiratory stridor and culminating in death. Grossly, nursery piglets had enlarged ears, and on the cut surface, the cartilage was fragmented and associated with blood clots. In the finishing phase, in addition to auricular lesions, the epiglottis and arytenoid cartilages were thickened and distorted, which partially occluded the lumen. Microscopically, the laryngeal and auricular cartilages were fragmented, displayed a loss of matrix basophilia, and were surrounded by lymphohistiocytic inflammatory infiltrate, with occasional multinucleated giant cells and fibrosis. The lesions exclusively affected elastic cartilages. The disease in finishing pigs led to increased mortality and was a differential diagnosis to respiratory challenges. It was not possible to determine the factor that triggered this condition; however, a nutritional association is suspected. To the authors' knowledge, this is the first report of primary auricular and laryngeal chondritis in pigs.

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Purpose: Osteoporosis is a bone disease which commonly occurred in postmenopausal women. Almost 10 percent of world population and approximately 30% of women (postmenopausal) suffer from this disease. Alternative medicine has great success in the treatment of osteoporosis disease. Bryodulcosigenin, a potent phytoconstituent, already displayed the anti-inflammatory and antioxidant effect. In this study, we made effort to analyze the antiosteoporosis effect of bryodulcosigenin against ovariectomy (OVX) induced osteoporosis in rats. Methods: Swiss albino Wistar rats were grouped into fIve groups and given an oral dose of bryodulcosigenin (10, 20 and 30 mg/kg) for eight weeks. Body weight, uterus, bone mineral density, cytokines, hormones parameters, transforming growth factor (TGF)-ß, insulin-like growth factor (IGF), osteoprotegerin (OPG), receptor activator of nuclear factor kappa-Β ligand (RANKL), and its ratio were estimated. Results: Bryodulcosigenin significantly (p < 0.001) suppressed the body weight and enhanced the uterine weight and significantly (p < 0.001) increased the bone mineral density in whole femur, caput femoris, distal femur and proximal femur. Bryodulcosigenin significantly (P < 0.001) altered the level of biochemical parameters at dose dependent manner, significantly (P < 0.001) improved the level of estrogen and suppressed the level of follicle stimulating hormone and luteinizing hormone. Bryodulcosigenin significantly (P < 0.001) improved the level of OPG and suppressed the level of RANKL. Conclusions: Bryodulcosigenin reduced the cytokines level and suppressed the TGF-ß and IGF. We concluded that bryodulcosigenin is an antiosteoporosis medication based on the findings.

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Abstract Gorham-Stout disease (GSD) is a rare bone disease characterized by an abnormal proliferation of endothelial-lined vessels and destruction of the affected bone. As it affects commonly children and young adults, it is associated with significant morbidity and mortality. To date, there is no established treatment strategy for GSD. We report through this observation a rare case of GSD in a child located in the hip and the iliac crest.

Resumo A síndrome de Gorham-Stout (SGS) é uma doença óssea rara caracterizada pela proliferação anormal de vasos endoteliais e destruição do osso acometido. Por ser comum em crianças e adultos jovens, causa morbidade e mortalidade significativas. Até o momento, não há estratégia terapêutica estabelecida para a SGS. Relatamos um caso raro de SGS no quadril e na crista ilíaca de uma criança.

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This study aimed to investigate the effects of different levels of vitamin D3 in broiler diets on performance and bone health. A total of 360 one-day old male Cobb500® broiler chicks were subjected to five treatments of different levels of vitamin D3 in diets during two rearing phases: 0 IU/kg in both phases; 625 IU/kg in starter and 500 IU/kg in grower phase (25% of commercial inclusion); 1,250 IU/kg in starter and 1,000 IU/kg in grower phase (50% of commercial inclusion); 1,875 IU/kg in starter and 1,500 IU/kg in grower phase (75% of commercial inclusion); and 2,500 IU/kg in starter and 2,000 IU/kg in grower phase (100% of commercial inclusion). The traits studied weekly were feed intake, body weight, feed conversion, and viability. At 21 and 35 days of age, tibiae and femurs were removed, dissected, and evaluated for dry matter (DM), ash (%MM), calcium (%Ca), phosphorus (%P) and breaking strength. At 35 days of age, the bones were subjected to histopathological analysis for macro- and microscopic morphological evaluation. Data were subjected to regression analysis, using α = 0.05. The variables of percentage %MM, %Ca, %P, and breaking strength experienced a positive linear effect up to the supplementation levels of approximately 25% of inclusion. The histopathological analysis found that the group that received the diet with 100% inclusion of vitamin D3 presented lesions compatible with osteopetrosis and tibial dyschondroplasia. The observed results showed that for isonutritive diets, reduced levels of vitamin D3 guaranteed performance during the evaluated period while the use of 100% of vitamin D3, as commonly used, can cause bone diseases and harm the welfare of broilers.(AU)

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BACKGROUND: There is some evidence supporting the idea that double parathyroid adenomas represent a different entity from multiglandular hyperplasia; however, the distinction among them is not straightforward. CASE PRESENTATION: We described a case of primary hyperparathyroidism (PHPT) with pronounced clinical manifestations, caused by a bilateral giant parathyroid adenoma. A 34-year-old Hispanic/Latino male was diagnosed with PHPT caused by two giant parathyroid adenomas. The preoperative tests were neck ultrasound and computed tomography scan (CT-scan), showing two masses in the territory of parathyroid glands, bilaterally distributed (right was 31 × 18 × 19 mm and the left was 38 × 15 × 14 mm); sestamibi scan was not available. Parathyroid hormone (PTH) was highly elevated. Multiple complications of PHPT were present, such as bone lytic lesions, renal and pancreatic calcifications, and cardiovascular disease, the latter of which is an overlooked complication of PHPT. Multiple endocrine neoplasia 1 and 2 (MEN 1/2) were ruled out by the absence of clinical, biochemical, and radiological findings in other endocrine glands. The patient underwent subtotal parathyroidectomy with an intraoperative histopathological study; both intraoperative and definitive histopathology results were consistent with parathyroid adenomas; afterward, adequate suppression of PTH was assured, and later on, the patient presented hungry bone syndrome (HBS). CONCLUSIONS: The diagnosis of double parathyroid adenomas is difficult. Regarding the similarities between multiglandular hyperplasia and parathyroid adenomas, this case report contributes to the further distinction between these two clinical entities. This case report also represents, in particular, the challenge of difficult diagnosis in places with limited resources, such as developing countries.

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MicroRNAs (miRNAs) are small non-coding RNA molecules that play critical roles in post-transcriptional gene regulation. They function by binding to target messenger RNA (mRNA) molecules, leading to their degradation or inhibiting their translation into proteins. In the context of skeletal diseases, such as osteoporosis, osteoarthritis, and bone metastasis, there is growing evidence osteoblastic miRNAs, are involved in the regulation of bone formation and maintenance.Osteoblasts are bone-forming cells responsible for synthesizing and depositing the extracellular matrix, which ultimately mineralizes to form bone tissue. Osteoblastic miRNAs modulate various aspects of osteoblast function, including proliferation, differentiation, mineralization, and apoptosis. Dysregulation of these miRNAs can disrupt the balance between bone formation and resorption, leading to skeletal diseases.The therapeutic implications of targeting osteoblastic miRNAs in skeletal diseases are significant. Modulating the expression levels of specific miRNAs holds promise for developing novel therapeutic strategies to enhance bone formation, prevent bone loss, and promote bone regeneration. Potential therapeutic approaches include the use of synthetic miRNA mimics to restore miRNA expression in diseases associated with miRNA downregulation or the use of anti-miRNA oligonucleotides to inhibit miRNA function in diseases associated with miRNA upregulation.miRNA-based therapies are still in the early stages of development, and further research is needed to fully understand the complexity of miRNA networks. Additionally, the delivery of miRNAs to specific target tissues and cells remains a challenge that needs to be addressed for effective clinical translation. Nonetheless, targeting osteoblastic miRNAs represents a promising avenue for future therapeutic interventions in skeletal diseases. (AU)

Los micro-ARNs (miARNss) son pequeños ARN no codificantes que desempeñan un papel fundamental en la regulación génica postranscripcional. Ejercen su función al unir-se a moléculas de ARN mensajero (ARNm), promoviendo su degradación e inhibiendo su traducción en proteínas. En el contexto de las enfermedades esqueléticas, como la osteoporosis, la osteoartritis y la metástasis ósea existe evidencia de que los miARNs osteoblásticos están involucrados en la regulación de la formación y del mantenimiento óseo. Los osteoblastos son células formadoras de hueso responsables de sintetizar y depositar la matriz extracelular, que finalmente se mineraliza para formar el hueso. Los miARNs derivados de osteoblastos modulan varios aspectos de la función de estas células, incluida la proliferación, diferenciación, mineralización y la apoptosis. La desregulación de estos miARNs puede alterar el equilibrio entre la formación y la resorción ósea, lo que lleva a enfermedades óseas. Las implicaciones terapéuticas de los miARNs osteoblásticos en enfermedades esqueléticas son significativas. La modulación de los niveles de expresión de miARNs específicos es prometedora para desarrollar nuevas estrate-gias terapéuticas a fin de mejorar la formación, prevenir la pérdida y promover la regeneración ósea. Los enfoques terapéuticos potenciales incluyen el uso de miméticos de miARNs para restaurar la expresión de miARNs o el uso de oligonucleótidos anti-miARNs para inhibir su función. Las terapias basadas en miARNs aún se encuentran en las primeras etapas de desarrollo. La administración de miARNs a las células y los tejidos específicos sigue siendo un desafío para lograr una aplicación clínica eficaz. (AU)

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We documented two stages of bone involvement due to syphilis in two adult patients infected with human immunodeficiency virus. Bony lesions of secondary versus tertiary syphilis cannot be differentiated on clinical or radiologic grounds alone. Given the rarity of this clinical presentation, there is no consensus on treatment duration and related outcomes.

Se describen dos etapas de compromiso óseo por sífilis en dos pacientes adultos infectados por el virus de la inmunodeficiencia humana. Las lesiones óseas de la sífilis secundaria y de la sífilis terciaria no se pueden diferenciar únicamente por características clínicas o radiológicas. Dada la rareza de esta presentación clínica, no hay consenso sobre la duración del tratamiento y los resultados relacionados.

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PURPOSE: Evaluate the functional health status and quality of life of patients diagnosed with Müller-Weiss disease and, secondarily, determine the influence of factors such as gender, social status, race, body mass index, and surgical and non-surgical treatment in patient outcome. METHODS: This study included 30 affected feet (18 patients) with follow-up from 2002 to 2016. Five patients were excluded from reassessment, resulting in 20 feet (13 patients). Questionnaires for functional and quality of life assessments were administered, and statistical analysis was performed. RESULTS: Patients with obesity had poor functional results and low quality of life rates. Regarding quality of life, mainly in the mental health domain, there was a significant difference (p < 0.001) that was not observed in other domains investigated, except for surgical treatment, which was superior to non-surgical treatment in terms of the physical domain (p = 0.024). Bilateral treatment was also superior to unilateral treatment in Coughlin's classification (71.4% versus 66.7%). CONCLUSIONS: Müller-Weiss disease evolved with poor functional results and low quality of life rates in patients with obesity, with no method of treatment influence on patient outcome, except for the SF-12 physical domain, where surgical treatment showed better results than conservative treatment.

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El objetivo de esta investigación fue evaluar la densidad de masa ósea (DMO), la situación nutricional, la ingesta de nutrientes y el nivel de actividad física, por medio de un estudio descriptivo, transversal, en una universidad internacional ubicada en Honduras cuyo universo es 376 empleados, con edad de 40 años y más. La muestra de 50 empleados fue estimada usando la fórmula para poblaciones finitas con una probabilidad de 90% y un error de 10%. Se tomaron medidas antropométricas con equipo SECA; densidad mineral ósea con equipo de ultrasonido en radio Sunlight MiniOmni™. Se aplicó un recordatorio de alimentos consumidos en las últimas 24 horas y el cuestionario Internacional de Actividad Física (IPAQ). Los datos se analizaron en EPI INFO v 7.2.5. El promedio de edad fue 48,9 años con 58% de mujeres participantes. El 90% tuvo sobrepeso y obesidad. Se identificaron 14 casos de DMO no normal, de éstos, uno fue osteoporosis (mujer, de 50 años y más); 93% de los casos tuvieron sobrepeso y obesidad, 43% se identificaron en personas de 40 a 49 años y 71% fueron mujeres. La actividad física fue 48% baja. El promedio de calorías consumidas/día/persona fue de 2.517; con 21% de adecuación de vitamina D, 87% de calcio, 275% de fósforo, 166,69 mg de cafeína. Se concluye que se requiere el control del sobrepeso y obesidad, así como el diagnóstico temprano de los cambios en la densidad mineral ósea, particularmente en las mujeres.

The objective of this research was to evaluate bone mass density(BMD), nutritional status, nutrient intake, and physical activity level, through a cross-sectional descriptive study, in an international university located in Honduras with a universe of 376 employees, aged 40 and over. The sample of 50 was estimated with the formula for finite population with a 90% probability and an error of 10%. Anthropometric measurements were taken with SECA equipment; bone mineral density with Sunlight MiniOmni™ radio ultrasound equipment. A 24-hour dietary recall method and the International Physical Activity Questionnaire (IPAQ) were applied. The data was analyzed in EPI INFO v 7.2.5. The average age of the people in the sample was 48,9 years with 58% of women. 90% were overweight and obese. 14 cases of non-normal BMD were identified, of these, one was osteoporosis (woman, 50 years of age and over); 93% of the cases were overweight and obese, 43% were identified in people between 40 and 49 years of age, and 71% were women. Physical activity was 48% low. The average number of calories consumed/day/person was 2.517; 21% adequacy of vitamin D, 87% of calcium, 275% of phosphorus, 166.69 mg of caffeine. It is concluded that control of overweight and obese is required, and the early diagnosis of changes in bone mass density, particularly in women.

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RESUMEN La enfermedad ósea de Paget (EOP) es un trastorno benigno, caracterizado por áreas focales de recambio óseo. Hasta el momento solo se han descrito 17 casos en Colombia. Se presenta el caso de un paciente masculino de 68 arios que consultó por otorrea e hipoacusia. Los hallazgos en la radiografía y la tomografía computarizada fueron sugestivos de malignidad craneana, se realizó una 18F-FDG PET/TC que mostró hipercaptación en el cráneo y en la columna lumbar. Se encontraron niveles altos de fosfatasa alcalina consistente con EOP. La biopsia descartó otros diagnósticos diferenciales. El paciente recibió alendronato y experimentó una mejoría sintomática y disminución en la fosfatasa alcalina.

A B S T R A C T Paget's disease of the bone (PDB) is a benign disorder characterized by focal areas of bone turnover. So far, only 17 cases have been described in Colombia. We present the case of a 68-year-old male who presented with otorrhea and deafness. The skull x-rays and computerized tomography findings were suggestive of malignancy. Consequently, an 18F-FDG PET/CT was performed and demonstrated an intense uptake in the skull and the lumbar spine. The work up showed elevated alkaline phosphatase levels consistent with PDB and the biopsy ruled out other differential diagnoses. The patient received alendronate with symptomatic improvement and decreased alkaline phosphatase levels.