However, the conclusion that the extravascular pressure due to blood circulation produces a much smaller shear stress in venous stasis than those induced by normal circulation and applied mechanical loads is valid for the whole range of the parameter changes. Bone spurs may be more likely to occur if you have such conditions as osteoarthritis, spinal stenosis, spondylosis or plantar fasciitis.
This paper addresses the question of whether or not interstitial fluid flow due to the blood circulation accounts for the observed periosteal bone formation associated with comprised venous return venous stasis. Increased interstitial fluid flow induced by increased intramedullary pressure has been proposed to account for the periosteal response in venous stasis. To investigate the shear stresses acting on bone cell processes due to the blood circulation-driven interstitial fluid flow, a poroelastic model is extended to the situation in which the interstitial fluid flow in an osteon is driven by the pulsatile extravascular pressure in the osteonal canal as well as by the applied cyclic mechanical loading.
Our results show that under free download roulette system conditions, the pulsatile extravascular pressure in the osteonal canal due to cardiac contraction 10mm Hg at 2 Hz and skeletal muscle contraction 30mm Hg at 1 Hz induce peak shear stresses on the osteocyte cell processes that are two orders of magnitude lower than those induced by physiological mechanical loading microstrain at 1 Hz.
In venous stasis the induced peak shear stress is reduced further compared to the normal conditions because, although the mean intramedullary pressure is increased, the amplitude of its pulsatile component is decreased. These results suggest that the interstitial fluid flow is unlikely to cause the periosteal bone formation in venous stasis.
However, the mean interstitial fluid pressure is found to increase in venous stasis, which may pressurize the periosteum and thus play a role in periosteal bone formation. The ability of blood flow to influence bone growth, fracture healing, and remodeling has been recognized for a long time Trueta, ; Kiaer, Impaired venous circulation venous stasis has been shown to stimulate periosteal bone formation or increase bone mass in the young dog Kelly and Bronk,the young goat Welch et al.
Venous stasis was induced in the experimental animals by applying tourniquets or vein ligation that lasted from union organization and gambling days with additional 30 days recovery, Bergula et al.
There are many other studies demonstrating similar effects e. The underlying mechanism of the periosteal bone formation induced by venous stasis, however, remains unclear. Factors associated with bone vasculature such as changes of metabolites and interstitial fluid flow have been proposed to cause the periosteal bone formation found with venous stasis.
The blocked or compromised venous drainage increases bone's hydraulic resistance to the arterial supply, which may decrease the supply of nutrients and oxygen to the bone and the removal of CO 2 and other metabolites as well. Changes of oxygen tension, CO 2 tension, and local pH have been found in bone callus and bone necrosis reviewed in Kiaer, This paper does not focus on these metabolic factors, although they may be important stimuli for new bone formation in venous stasis.
Instead, we focus on the hydraulic pressure changes associated with venous stasis. Many investigators have found an increase in mean pressure and a decrease in pressure oscillation associated with the pulse pulsatile pressure inside both the venous stasis-affected veins and the marrow cavity e.
The increased intramedullary pressure has been proposed to produce increased interstitial fluid flow Kelly and Bronk, ; Hillsley and Frangos, ; Welch et al. A recent in vivo study Qin et al. However, the magnitude of fluid shear stresses due to blood circulation has never been quantitatively examined. To test the hypothesis that increased interstitial fluid flow causes the periosteal bone formation in venous stasis, an osteon model is developed to theoretically connect interstitial fluid flow with both the bone microcirculation and mechanical loading.
In this model, there are two driving forces for the interstitial fluid flow in the lacunar-canalicular porosity: Even if a fluid pressure gradient is built up in the extravascular space within the vascular canals, the pressure gradient will, in general, be very small, as evidenced in the extravascular fluid velocity that is much less than the blood flow velocity in the capillaries.
Therefore, the extravascular fluid pressure within the osteonal canals in the cortex is nearly spatially uniform and equal to the instantaneous intramedullary pressure in the marrow cavity. As a representative unit, a single osteon instead of a whole bone is modeled here. Unlike previous theoretical models that focus on tracer distribution under circulatory pressure Dillaman et al. As fluid shear stress has been proposed to be a possible stimulating signal for the osteocytes and osteoblasts that are interconnected via gap junctions in their cell processes Weinbaum et al.
However, we recognize that the mechanisms by which interstitial fluid flow stimulates bone cells are not very clear. For example, a recent study You et al. In the present study, fluid shear stress, one of most well studied secondary effects of fluid flow, is used as a useful indicator of interstitial fluid flow. The problem considered here is that of determining the bone interstitial fluid pressure field p rt in the lacunar-canalicular porosity of an osteon.
The osteon is modeled as a right circular cylinder of radius r o containing an osteonal canal that is modeled as a smaller concentric, right circular cylinder of radius best european roulette strategies i The annular region of the osteon contains the gambling treatment centre porosity Fig.
The interstitial fluid is assumed to flow through the lacunar-canalicular channels surrounding the cell processes of the osteoblasts or osteocytes as in earlier models Fig. A recent electron microscopic study has provided strong evidence of the existence of such a fiber matrix You, The mineralized matrix surrounding the lacunar-canalicular porosity has a Young's modulus Eand bone permeability at the lacunar-canalicular porosity level is theoretically determined by the detailed structures of the pericellular fiber matrix and the canalicular channels, since there are no experimental angiolytic bone of the permeability at this level Weinbaum et al.
The osteon is subjected to two types of oscillatory loading. The interstitial fluid flow due to this pulse-driven intramedullary pressure is called the blood circulation-driven fluid flow in the following text, because the driving force is the blood free roulette sniper. Due to the relative impermeability of the outer boundary cement line of the osteon, a non-leakage boundary condition is assumed as in our previous models Zeng et al.
The fluid pore pressure, radial fluid pressure gradient, and shear stress are derived in the next three sections using poroelasticity theory. To facilitate the comparison of the relative contribution of mechanical loading and blood circulation to the interstitial fluid flow, we decompose the fluid pore pressure, radial fluid gambling games instructions gradient, and shear stress into the mechanical load- and blood-induced components.
The parameters associated with the load-induced component are denoted by a subscript l and those associated with blood-induced component are denoted by a subscript b. A closely related problem was solved by Zeng et al.
The partial differential equation in cylindrical coordinates for the dimensionless bone fluid pressure P is. The boundary conditions due to the blood pressure, expressed in terms of the dimensionless pressure field Pare. The solution to Eq. In order to obtain the fluid pore pressure from the dimensionless fluid pressure, we multiply raj bansal gambling sides of Eq. The fluid pore pressure p is then given by.
Combining the sinusoidal terms with the same frequency, the fluid william hill brown halifax pressure is the summation of three terms:. The mean extravascular pressure p 0 induces a spatially uniform interstitial fluid pressure, but we will show next that it makes no contribution to the fluid pressure gradient or shear stress.
Therefore, we are going to neglect this DC component and, instead, focus on the time-varying AC component pulsatile extravascular pressure only. The amplitudes of the load and blood-induced fluid pressure components are. The dimensionless fluid pressure gradient i.
The fluid pressure gradient is obtained from the dimensionless expression as. Combining the sinusoidal terms with the same frequency, the fluid pressure gradient consists of two sinusoidal components caused by the mechanical loading and pulsatile extravascular pressure, respectively:. Previous models have shown that the shear stress, s aexperienced by a cell process of radius a in a canaliculus is directly proportional to the bone fluid pressure gradient and is also related to the detailed structure of the canalicular channel and the pericellular matrix Weinbaum et al.
Since the load- and blood-induced radial fluid pressure gradients are sinusoidal Eq. The relative compressibility between the fluid and solid phases B is taken to be 0. Except for the permeability parametric study described below, the following geometric data will be employed: The spatial distribution profiles of the pore fluid pressure, pressure gradients, and resultant fluid shear stress on the cell process membrane induced by the mechanical loading and the pulsatile extravascular pressure in the osteonal canal due to blood circulation are calculated using Eqs.
For mechanical allen christensen gambling two fundamental loading regimes are considered: For pulsatile extravascular pressure that equals the intramedullary pressure, three cases are considered: We are investigating the skeletal muscle contribution of the second case because muscle contraction has been shown to increase the intramedullary pressure, with each contraction producing a fluctuation larger than that due to the pulse pressure from the heartbeat Shim et al.
Since loading frequency has been found to roulette computer game the resultant shear stress significantly Zeng et al. The amplitude of the mechanical loading and the pulsatile extravascular pressure are assumed to remain the same, microstrain and 10 mm Hg, respectively, while their frequencies are varied from 1 to 20 Hz.
These numerical values are chosen parametrically in order to study the frequency response of the shear stress. We understand that the in vivo pulsatile extravascular pressure due to the heart beating is unlikely to have frequency components higher than 20 Hz Lawson, and the high-frequency mechanical strains usually have decreased amplitudes Fritton et al. To compare the relative magnitude of interstitial fluid flow for different loading conditions as well as for the pulsatile extravascular pressures due to blood circulation, we choose the peak shear stress as the representative parameter for the temporally and spatially varying shear stress stimulus since bone cells have been shown to respond to the magnitude of shear stress in a dose-dependent manner Reich et al.
In addition, peak shear stress has been found to occur at the canalicular openings on the osteonal canal wall in mechanically loaded bone Weinbaum et al. Since the magnitude of the peak shear stress induced by the mechanical loading and pulsatile extravascular pressure varies with the numerical values of the input parameters used in the model, a parametric study is performed to show the sensitivity of the output shear stress to the inputs of the model.
Among the many input parameters we used, bone permeability has previously been shown to have the most significant effect on the shear stress Zhang et al. Since the bone permeability is estimated from the fiber spacing of the pericellular matrix and the fluid space in the canalicular channels Weinbaum et al.
The total interstitial fluid flow is a linear summation of the load- and blood-induced components. Since both the mechanical loading and the pulsatile extravascular pressure in the osteonal canal are modeled as temporal sinusoidal signals, the fluid flow induced by the two driving forces is also sinusoidal in the time domain.
The amplitudes of the sinusoidal interstitial fluid pressure and shear stress applied on the cell membrane vary with location and depend on the frequency of the driving force Figs. The amplitude of load-induced fluid pore pressure increases radially from the canal wall to the cement line and increases with increased loading frequency Fig.
For a mechanical loading with a given magnitude, the induced fluid pressure is much higher at 20 Hz than at 1 Hz Fig. At lower loading frequencies venous angiolytic bone deposits load-induced fluid flow has enough time to relax across the osteon and thus it is difficult for the fluid pressure to build up. At higher loading frequencies the time period available for fluid relaxation is shorter and an excess fluid pressure can therefore be produced.
This result is consistent with our previous studies Weinbaum et al. On the other hand, the amplitude of blood-induced fluid gambling in dubai pressure decreases both across the osteon radius and with increasing frequency of the pulsatile extravascular pressure due to the heartbeat Fig. If the cement line had been leaky, the decrease in pore win at roulette machines pressure across the osteon would be reduced.
This model also predicts that a mean extravascular pressure in the central canal will cause a uniform pore pressure distribution across the osteon Eqs. Both the load- and blood-induced fluid flows have the same spatial distribution pattern of the fluid pressure gradients and resulting shear stress Fig.
A small but finite shear stress would be expected at this location if the cement line were leaky. Two typical mechanical loading conditions, microstrain at 1 Hz venous angiolytic bone deposits with locomotion and 10 microstrain at 20 Hz associated with posture, produce shear stress of the same approximate magnitude Fig.
If the magnitude of the cyclic mechanical loading or extravascular pressure in the osteonal canal is held constant, the peak shear stress at the canal wall surface exhibits a fold increase as the frequency increases from 1 to 20 Hz Table 1. In venous stasis 2 mm Hg at 2 Hzthe peak shear stress is 0. The peak shear stress induced by the normal pulse pressure in the osteonal canal is predicted to vary with bone permeability Table 3.
When the fiber spacing is varied from 4 to 20 nm and the fluid annulus is changed by a factor of 3, bone permeability varies over 2 orders of magnitude and the peak shear stress calculated with this model varies by a factor of The peak shear stress induced by mechanical loading has the same sensitivity to the model parameters as that induced by blood circulation shown in Table 3. To explore the interstitial fluid flow effects of venous stasis, we have expanded our poroelastic model for bone interstitial fluid flow Zeng et al.
This is the first model to provide a quantitative tool to investigate the relative contribution of blood circulation and mechanical loading to the interstitial fluid flow in terms of shear stress acting on the cell process membrane. The development of venous stasis in bone is very complicated, involving dynamic changes in the interstitial and intravascular spaces.
Although a long bone has multiple feeding and draining vessels Brookes and Revell,once one of the big veins e. More blood remains in the organ and is rerouted to the remaining functioning vessels. These vessels expand in size to accommodate the increased vascular resistance and as a consequence vascular pressure increases. This is also accompanied by an increased filtration flux across the vessel wall.
Both the vessel dilation and the fluid filtration cause the extravascular pressure to rise because bone is a relatively rigid compartment.possible pleural deposits of tumour. Liver or bone biopsy of possible deposits. cancer (SCLC, about 20% of lung can- cers) or . bleeding disorder or venous anxiolytic. Radiotherapy. • external beam. • intraluminal (brachytherapy). These results suggest that the interstitial fluid flow is unlikely to cause the periosteal bone formation in venous stasis. However, the mean interstitial fluid Missing: angiolytic deposits. Coding Tips. For collection of venous blood by venipuncture, see Collection Sedative, hypnotic or anxiolytic dependence, continuous. Sedative, hypnotic or aplastic anemia, causes bone marrow failure and myelodysplasia or .. Gaucher disease. Genetic metabolic disorder in which fat deposits may.