Disuse osteoporosis in hemiparetic patients often results in significant morbidity, decreased quality of life, and different clinical characteristics. The study aimed to investigate the effect of these clinical factors on bone mineral density (BMD).

This was an analytical observational study with a cross-sectional method evaluating hemiparetic patients at Cipto Mangunkusumo Hospital from 2018 to 2019. BMD (g/cm2) was assessed using dual energy X-ray absorptiometry (DXA) on the spine and both sides of the body. The relationship and correlation between BMD and delta BMD scores with clinical characteristics were analyzed. A linear regression test was used to assess the correlation between variables.

A total of 34 participants were recruited for this study. There was a difference between the healthy and paretic side of BMD of both hip and wrist (P < 0.001), strong positive correlation between the onset of hemiparesis and wrist and hip delta BMD (r = 0.779, P = 0.001 and r = 0.791, P = 0.001), and significant association between delta BMD and age and motor strength. Multivariate analysis shows that the onset of hemiparesis was a strong predictor of delta BMD (aR2 wrist = 0.486, aR2 hip = 0.614). There was a 7.36% decrease in the mean BMD score of the paretic side compared to the non-paretic side.

A low BMD score is prevalent in seven out of 10 patients with post-stroke neuromuscular deficit. Age, limb strength, the onset of hemiparesis, and rehabilitation compliance are associated with decreased BMD among patients with post-stroke neuromuscular deficit.

SARS-CoV-2 is highly transmissible and affects the respiratory system. People with COVID-19 are at higher risk of physical and mental health conditions, which could impact bone health. The aim of this review was to explore the effects of COVID-19 on BMD, BTMs, and joints. An electronic search of the PubMed, Web of Science, Scopus, and Ovid Medline databases considered studies published between 1 January 2020 and 1 November 2023. The search was limited to English, original studies in adult humans. The title and abstract of the identified papers were screened, followed by a full-text review using inclusion and exclusion criteria. The data extracted included the study and participant characteristics, BTMs, BMD, and joint abnormalities. The Newcastle-Ottawa scale quality assessment tool was used to assess the risk of bias. Five studies involving 305 out of 495 infected individuals observed a reduced BMD after COVID-19, with the most significant reduction occurring a year later. Both bone resorption and bone formation markers decreased, while regulatory markers showed higher levels in infected patients. COVID-19 may harm bone health by increasing bone regulatory markers and reducing bone formation and absorption, leading to a lower BMD. Elderly, frail, and osteopenic or osteoporotic individuals are at higher risk and should be regularly monitored for bone loss if they have long COVID.

Cardiovascular disease and osteoporotic fractures (OF) are the main diseases affecting the health of middle-aged and elderly people. With the gradual increase of population aging in China and even the world, the incidence of the two and the prevalence of high-risk groups are also showing a continuous upward trend. The relationship between the two, especially the impact of cardiovascular disease on the risk and prognosis of OF, has attracted more and more attention. Therefore, it is of great significance to fully understand the pathogenesis of cardiovascular and cerebrovascular diseases and the resulting osteoporosis and to provide targeted interventions to prevent the occurrence of diseases and fractures. This article reviews the relationship between one of the Cardiovascular disease-stroke and related therapeutic drugs and the risk of OF, and the role of oxidative stress in its pathophysiological mechanism by reviewing relevant domestic and foreign literature in recent years, in order to gain a more comprehensive understanding of the association between stroke and OF, and then provide a basis and reference for screening high-risk groups of fractures and reducing the burden on the health system caused by the disease.

The COVID-19 pandemic caused an unprecedented health crisis resulting in over 6 million deaths worldwide, a figure, which continues to grow. In addition to the excess mortality, there are individuals who recovered from the acute stages, but suffered long-term changes in their health post COVID-19, commonly referred to as long COVID. It is estimated there are currently 1.8 million long COVID sufferers by May 2022 in the UK alone. The aim of this narrative literature review is to explore the signs, symptoms and diagnosis of long COVID and the potential impact on imaging services.

Long COVID is estimated to occur in 9.5% of those with two doses of vaccination and 14.6% if those with a single dose or no vaccination. Long COVID is defined by ongoing symptoms lasting for 12 or more weeks post acute infection. Symptoms are associated with reductions in the quality of daily life and may involve multisystem manifestations or present as a single symptom.

The full impact of long COVID on imaging services is yet to be realised, but there is likely to be significant increased demand for imaging, particularly in CT for the assessment of lung disease. Educators will need to include aspects related to long COVID pathophysiology and imaging presentations in curricula, underpinned by the rapidly evolving evidence base.

Symptoms relating to long COVID are likely to become a common reason for imaging, with a particular burden on Computed Tomography services. Planning, education and updating protocols in line with a rapidly emerging evidence base is going to be essential.

Disuse osteopenia (DO) is a disorder due to reduced weight-bearing often following immobilization injuries. It is most commonly observed in the ankles and knees and is believed to be due primarily to increased bone reabsorption associated with disuse. Both traditional radiography and magnetic resonance (MR) imaging are useful in identifying abnormalities associated with DO. Specifically, linear subchondral osteopenia has been given the term "Hawkins sign" when seen in the talus, but this finding may also be seen elsewhere. When present, it not only is an indication of DO but also indicates the presence of sufficient vascular flow, and the unlikely development of avascular necrosis. We report a case of Hawkins sign of the knee demonstrated on radiography and MR and demonstrate the clinical importance of recognizing this sign, outside its usual setting, in assessing the prognosis of a healing fracture.

Microglial healing peptide 1, "MHP1", is a newly developed synthetic peptide composed of the DE and a part of the EF loop of the receptor activator of nuclear factor-кB (NFκB) ligand (RANKL). Our previous report demonstrated that MHP1 significantly inhibits Toll-like receptor (TLR) 2- and 4-induced inflammation in microglia/macrophages through RANK signaling without osteoclast activation. However, its inhibitory effects on ischemic stroke when administered intravenously have not been clarified. First, we examined whether MHP1 could penetrate the brain parenchyma. Intravenous injection of FITC-conjugated MHP1 demonstrated that MHP1 could cross the blood-brain-barrier in peri-infarct regions, but not in intact regions. Because MHP1 in the parenchyma was reduced at 60 minutes after injection, we speculated that continuous injection was necessary to achieve the therapeutic effects. To check the possible deactivation of MHP1 by continuous injection, the anti-inflammatory effects were checked in MG6 cells after incubation in 37°C for 24 hours. Although the inhibitory effects for IL6 and TNFα were reduced compared to nonincubated MHP1, its anti-inflammatory efficacy remained, indicating that continuous administration with pump was possible. The single and successive continuous administration of MHP1 starting from 4 or 6 hours after cerebral ischemia successfully reduced infarct volume and prevented the exacerbation of neurological deficits with reduced activation of microglia/macrophages and inflammatory cytokines. Different from recombinant RANKL, MHP1 did not activate osteoclasts in the paralytic arm. Although further modification of MHP1 is necessary for stabilization, the MHP1 could be a novel agent for the treatment ischemic stroke.

Evidence now suggests the role of neural effect on bone mass control. The effect of small vessel disease of the brain on osteoporosis has not been studied. The aim of this study was to investigate the association of white matter disease (WMD) of the brain with osteoporosis in the elderly.

In this retrospective cross-sectional study, 780 consecutive patient charts between 2010 and 2011 were reviewed in the Senior's Outpatient Clinic at the University of Alberta Hospital. Subjects with brain computerized tomography (CT) were included in the study. Subjects with incomplete information, intracranial hemorrhage, acute stroke, cerebral edema, and/or normal pressure hydrocephalus on the CT were excluded. WMD was quantified on CT using Wahlund's scoring protocol. Osteoporosis information was obtained from the chart, which has been diagnosed based on bone mineral density (BMD) information. Logistic regression analysis was done to determine the association of WMD severity with osteoporosis after controlling for confounding vascular risk factors.

Of the 505 subjects who were included in the study, 188 (37%) had osteoporosis and 171 (91%) of these osteoporotic subjects were females. The mean age was 79.8 ± 7.04 years. The prevalence of WMD in osteoporosis subjects was 73%. In the unadjusted logistic regression analysis, there was a significant association between WMD severity and osteoporosis (odds ratio (OR): 1.10; 95% confidence interval (CI): 1.05 - 1.14; P < 0.001) and the significance remained in the adjusted model, after correcting for age, sex and all vascular risk factors (OR: 1.11; 95% CI: 1.05 - 1.18; P < 0.001).

WMD severity of the brain was associated with osteoporosis in the elderly.

To evaluate bone marrow changes on knee magnetic resonance imaging (MRI) in patients with 3- to 6-week-long period of unloading.

MRI knee examinations were performed in 30 patients (14 men, 16 women; aged 20-53 years) at baseline and 5-10 weeks after immobilisation of the ipsilateral lower extremity; subsets of patients were examined at additional time-points. Ten volunteers (4 men, 6 women; aged 20-50 years) were studied as control cohort at two time-points. Bone marrow signal abnormalities were analysed according to: (1) severity, (2) signal alteration relative to hyaline cartilage, (3) morphology, (4) increased vascularity in the knee joint and (5) T1-signal alteration. Spearman's rank correlation test (SRC) and Kendall's tau (KT) were used to compare individual scores.

All 30 patients presented abnormal bone marrow findings after unloading, which reached a peak at 10-25 weeks (P <0.001). These findings decreased within 1 year (P < 0.001). High scores of severity were associated with confluent and patchy patterns of bone marrow (SCR = 0.923, P < 0.001 and KT = 0.877, P <0.001).

Signal abnormalities of the bone marrow related to unloading are consistent findings and most prominent 10-25 weeks following immobilisation when both confluent and patchy hyperintense patterns are present.

Disuse osteopenia is a complication of immobilisation, with reversal generally noted upon remobilisation. This case report focuses on a patient who was seen 18 years following a road traffic collision when multiple fractures were sustained. The patient had an external fixator fitted for a tibia and fibula fracture, which remained in situ for a period of 4 years. Following removal, the patient was mobilised but, still required a single crutch to aid walking. Fourteen years post removal of the fixator, the patient had a DXA scan which, demonstrated a T-score 2.5 SD lower on the affected hip. This places the patient at an increased risk of hip fracture on this side, which requires monitoring. There appear to be no current studies investigating prolonged disuse-osteopenia in patients following removal of long-term external fixators. Further research is required to quantify unilateral long-term effects to bone health and fracture risk in this population.

Stroke increases the risk of hip/femur fracture, as seen in several studies, although the time course of this increased risk remains unclear. Therefore, our purpose is to evaluate this risk and investigate the time course of any elevated risk.

We conducted a case-control study using the Dutch PHARMO Record Linkage System database. Cases (n=6763) were patients with a first hip/femur fracture; controls were matched by age, sex, and region. Odds ratio (OR) for the risk of hip/femur fracture was derived using conditional logistic regression analysis, adjusted for disease and drug history.

An increased risk of hip/femur fracture was observed in patients who experienced a stroke at any time before the index date (adjusted OR, 1.96; 95% CI, 1.65-2.33). The fracture risk was highest among patients who sustained a stroke within 3 months before the index date (adjusted OR, 3.35; 95% CI, 1.87-5.97) and among female patients (adjusted OR, 2.12; 95% CI, 1.73-2.59). The risk further increased among patients younger than 71 years (adjusted OR, 5.12; 95% CI, 3.00-8.75). Patients who had experienced a hemorrhagic stroke tended to be at a higher hip/femur fracture risk compared with those who had experienced an ischemic stroke.

Stroke is associated with a 2.0-fold increase in the risk of hip/femur fracture. The risk was highest among patients younger than 71 years, females, and those whose stroke was more recent. Fall prevention programs, bone mineral density measurements, and use of bisphosphonates may be necessary to reduce the occurrence of hip/femur fractures during and after stroke rehabilitation.

We have reported that after an acute stroke, intravenous zoledronate prevented bone loss in the hemiplegic hip. Participants from the trial also volunteered for trans-iliac bone biopsy, to assess the early effects of stroke and zoledronate on iliac bone remodelling.

Patients with acute stroke were randomly assigned to a single intravenous dose of zoledronate 4 mg or placebo within 5 weeks of stroke. Biopsies from 14 patients (3 female, 11 male, mean age 71+/-11) were suitable for analysis. These were taken at mean 10 weeks (+/-2) post-stroke, and included 5 patients who had received zoledronate. Histomorphometry was performed on undecalcified sections using light and fluorescence microscopy. Static and dynamic indices of remodelling were compared to a local reference range from healthy controls. Osteoclasts and their precursors were identified on frozen sections using tartrate resistant acid phosphatase (TRAP) staining. Dual-energy x-ray absorptiometry (DXA) of the proximal femora was performed at baseline and 6 months later.

The eroded surface in cancellous bone (ES/BS) was significantly higher in stroke patients than controls (5.7% vs. ref 1.6%, p<0.0001). Although ES/BS did not differ between zoledronate and placebo-treated groups, there were significantly fewer osteoclasts and their precursors in zoledronate-treated individuals (p=0.023). Bone formation indices (osteoid surface, OS/BS and mineralising surface, MS/BS) were significantly lower in stroke patients than controls and although OS/BS was higher in the zoledronate group than the placebo group (p=0.033), MS/BS was not different (p=0.924). There were no differences between hemiplegic and unaffected sides for any histomorphometric parameter despite asymmetric reductions in hip bone mineral density (p=0.013).

Stroke patients had higher resorption indices and lower bone forming surfaces than controls, consistent with uncoupling of bone remodelling. These findings are preliminary and a larger study is required to evaluate the contributions of gender, age and hemiplegic status to the remodelling imbalance. Zoledronate therapy was associated with a reduction in osteoclastic cell numbers consistent with its known mode of action in bone.

After stroke, many factors contribute to the loss of bone mineral density (BMD) and fracture. Pre-stroke low BMD and vertebral fracture may pose a greater risk of fractures and further contribute to additional functional loss. The purposes of this study were to assess pre-stroke BMD and vertebral fracture in patients with first stroke.

Forty-eight patients with first stroke events were included. To reflect pre-stroke BMD, the patients who underwent bone densitometry tests within 30 days from stroke onset were selected. BMD was checked at the lumbar spine and both femurs (total hip and femoral neck). Thoracic and lumbar spine X-rays were performed.

Of the 48 stroke patients, 21 (43.8%) had osteoporosis and 19 (39.6%) had osteopenia. X-ray evaluation showed that 12 (25.0%) had one or more lumbar or thoracic vertebral fractures and 8 (16.7%) had two or more vertebral fractures. Of the 12 patients who had one or more vertebral fractures, 4 (33.3%) were previously aware of the fact that they had a vertebral fracture.

Results showed a high prevalence of pre-stroke low BMD and vertebral fracture in patients experiencing first stroke. Bone loss progresses rapidly in the acute stages of stroke, and such a high prevalence of pre-stroke low BMD and vertebral fracture may pose a greater risk of fractures and further contribute to additional functional loss. Therefore, early screening and active management of osteoporosis from the acute stages of stroke is critical.

Disuse induces rapid and severe bone loss in larger mammals as a result of greatly elevated osteoclastic resorption. In this study, we tested whether risedronate (RIS), a potent inhibitor of osteoclastic activity, would effectively prevent cancellous bone loss in female beagles (5-7 years old, N = 28) subjected to single forelimb immobilization (IM) for 12 months. Age-matched, non-IM dogs served as controls (Con). Half the animals from each group received RIS 1 mg/kg p.o. daily (Con + RIS, IM + RIS). Remaining dogs received sterile water (Con, IM). Histomorphometry showed that IM caused a dramatic reduction in cancellous bone mass (-71%) of distal 2nd metacarpals, characterized by marked decreases in trabecular width (-51%) and number (-41%), and 4-fold increases in the indices of bone resorption (eroded surface, osteoclast number, and surface). Bone formation indices (calcein-labeled surface, osteoid surface, and bone formation rate) were also significantly higher in IM than in controls. Activation frequency in IM increased about 4-fold beyond control level. RIS treatment reduced, but did not abolish cancellous bone loss due to immobilization. IM animals treated with RIS lost nearly 50% of cancellous bone mass, while trabecular width and number were reduced by 31% and 25%, respectively. In both RIS-treated control and IM animals, overall bone formation parameters (mineralized bone surface fraction and bone formation rate) remained roughly at intact control levels; however, mineral apposition rate relative to intact control was reduced 40% in RIS-treated control and 86% in RIS-treated IM animals. These results indicate that high-dose RIS treatment might suppress osteoblastic function, especially under long-term disuse. Interestingly, bone resorption parameters in RIS-treated IM animals reached levels even higher than in vehicle-treated IM animals; values for eroded surface, osteoclast number, and surface were 84%, 53%, and 83% above vehicle-treated IM values, respectively. Our data indicate that risedronate treatment is partially effective in preventing cancellous bone loss during long-term disuse. Moreover, our results suggest that bisphosphonates can impair the ability of mature osteoclasts to resorb bone, but cannot overcome the strong stimulus for osteoclast recruitment caused by long-term disuse.