Canal Vessels Research Articles

Osteochondrosis in the central and third tarsal bones of young horses.

Recently, the central and third tarsal bones of 23 equine fetuses and foals were examined using micro-computed tomography. Radiological changes, including incomplete ossification and focal ossification defects interpreted as osteochondrosis, were detected in 16 of 23 cases. The geometry of the osteochondrosis defects suggested they were the result of vascular failure, but this requires histological confirmation. The study aim was to examine central and third tarsal bones from the 16 cases and to describe the tissues present, cartilage canals, and lesions, including suspected osteochondrosis lesions. Cases included 9 males and 7 females from 0 to 150 days of age, comprising 11 Icelandic horses, 2 standardbred horses, 2 warmblood riding horses, and 1 coldblooded trotting horse. Until 4 days of age, all aspects of the bones were covered by growth cartilage, but from 105 days, the dorsal and plantar aspects were covered by fibrous tissue undergoing intramembranous ossification. Cartilage canal vessels gradually decreased but were present in most cases up to 122 days and were absent in the next available case at 150 days. Radiological osteochondrosis defects were confirmed in histological sections from 3 cases and consisted of necrotic vessels surrounded by ischemic chondronecrosis (articular osteochondrosis) and areas of retained, morphologically viable hypertrophic chondrocytes (physeal osteochondrosis). The central and third tarsal bones formed by both endochondral and intramembranous ossification. The blood supply to the growth cartilage of the central and third tarsal bones regressed between 122 and 150 days of age. Radiological osteochondrosis defects represented vascular failure, with chondrocyte necrosis and retention, or a combination of articular and physeal osteochondrosis.

Utero-placental vascular remodeling during late gestation in Sprague-Dawley rats.

Remodeling of the uterine spiral arteries and blood vessels within the placenta allows delivery of nutrients to the growing utero-fetal-placental unit. While abnormal remodeling of these vessels is thought to play an important role in syndromes including intrauterine growth restriction and preeclampsia, there are a lack of studies that have quantified vascular remodeling in normal pregnant rats. Thus, the purpose of this study was to quantify time-dependent remodeling of the utero-placental vasculature during late gestation in normal pregnant rats. Timed-pregnant Sprague-Dawley rats were used. Gestational days of 14 and 19 were chosen because this when a large amount of fetal and placental growth occurs. A combined method of perfusion-casting and 3D micro-computed tomography were utilized to construct ex-vivo utero-placental vasculature images. Significant spiral artery remodeling occurred between days 14 and 19. Vessel density shifted away from a distribution of smaller to larger diameters by day 19. Total spiral artery area and average diameter were increased by day 19. Moreover, branching and tortuosity of the spiral arteries were greater by day 19. In rodents, spiral arteries feed into the central canal vessels that funnel to sites of exchange. Canal vessel area and diameter were increased by day 19. Our study supports a quantitative method to examine the placental vasculature showing that significant vascular remodeling occurs during late gestation in the utero-placental-fetal unit of the normal pregnant rat. This method may serve as a tool to investigate fundamental pathophysiological mechanisms underlying placental-related diseases in rat models.

Prilog određivanju kritične i dopuštene brzine kretanja brodova u plovnim kanalima

Prilog određivanju kritične i dopuštene brzine kretanja brodova u plovnim kanalima

Simultaneous influence of sympathetic autonomic stress on Schlemm\u2019s canal, intraocular pressure and ocular circulation

This study aimed to investigate changes in Schlemm’s canal, intraocular pressure and ocular blood circulation following the activation of the sympathetic nervous system. Twenty healthy volunteers were enrolled in this study. The cold pressor test (CPT) was adopted. Cross-sectional area of Schlemm’s canal (SCAR), superficial and deep retinal vessel densities (s-RVD;d-RVD), pupil diameter (PD), intraocular pressure (IOP), mean ocular perfusion pressure (MOPP) and heart rate variability (HRV) were measured at three time-points: baseline (T0) and 5 min (T1) and 10 min (T2) after the CPT. After cold stimulation, LF/HF index (the ratio of low frenquency and high frenquency) increased significantly. IOP decreased from 16.9 ± 1.9 mmHg at baseline to 16.4 ± 2.7 mmHg at T1 and to 15.2 ± 2.7 mmHg at T2. The nasal cross-sectional area of SCAR (SCAR-n) increased from 6283.9 ± 2696.2 µm2 at baseline to 8392.9 ± 3258.7 µm2 at T1 and to 10422.0 ± 3643.8 µm2 at T2. The temporal cross-sectional area of SCAR (SCAR-t) increased from 6414.5 ± 2218.7 µm2 at baseline to 8610.8 ± 2317.1 µm2 at T1 and to 11544.0 ± 4129.2 µm2 at T2. The expansion of Schlemm’s canal was observed after the CPT might be caused by sympathetic nerve stimulation, subsequently leading to decreased IOP.

Computed tomographic development of physeal osteochondrosis in pigs

BackgroundArticular osteochondrosis follows a dynamic development pattern. Lesions arise, in incidence peaks compatible with failure of cartilage canal vessels during incorporation into bone, and can also resolve. Lesions that resolve before examination at a single time point will constitute false-negative diagnoses. The aim of the study was to identify physeal osteochondrosis lesions in pigs and monitor their development by computed tomography (CT), to determine if they follow a similar dynamic development pattern to articular osteochondrosis.ResultsThirteen physes were evaluated bilaterally in up to eight biweekly CT scans from 18 male Landrace pigs age 70–180 days (total: 112 scans), generating 2912 scores. There were 1754 (60%) lesion-negative scores and 1158 (40%) lesion-positive scores. Positive scores comprised 138 lesions present at the start and 235 lesions that developed during the study, from 4 to 32 lesions per physis (median: 15 lesions). There were 1–2 peaks in the incidence curves for 12/13 examined physes, the exception being the proximal humerus. Positive scores also included 785 times that lesions persisted, from 1.3–4.8 examination intervals per lesion (median: 2.8 intervals). Negative scores included 190 times that lesions resolved, from 19 to 100% of lesions per physis (median: 65%). Lesions resolved by filling with bone from marginal sclerosis and reparative ossification centres. In the distal scapula and distal fibula, perichondrial new bone formation occurred that led to permanent enlargement of physeal regions. Angular limb deformity was not identified in any pig.ConclusionsPhyseal osteochondrosis followed a similar dynamic development pattern to articular osteochondrosis. There were peaks in the incidence curves, compatible with failure of vessels during incorporation into bone. In some physes, osteochondrosis led to permanent enlargement, potentially relevant for decubital ulcers. The relationship between physeal osteochondrosis and angular limb deformity must be examined further in pigs over 6 months old in future.

Rapid Development of Glaucoma Via ITV Nonselective ANGPT 1/2 Antibody: A Potential Role for ANGPT/TIE2 Signaling in Primate Aqueous Humor Outflow.

Investigate a significant, dose-related increase in IOP, leading to glaucomatous damage to the neuroretina and optic nerve following intravitreal (ITV) administration of a bispecific F(ab')2 [anti-VEGF/Angiopoietins [ANGPT]F(ab')2] molecule in adult monkeys. ITV ocular tolerability and investigation of anti-VEGF/ANGPT F(ab')2 (blocking both ANGPT1 and ANGPT2) was done in monkeys; mechanistic studies were done in neonatal mice. Following the second ITV dose of anti-VEGF/ANGPT F(ab')2, all 1.5- and 4-mg/eye treated monkeys developed elevated IOP, which eventually was associated with optic disc cupping and thinning of the neuroretinal rim. Histopathologic examination showed nonreversible axonal degeneration in the optic nerves of animals administered 1.5 mg/eye and higher that was considered secondary to high IOP. Anti-ANGPT Fab also caused elevated IOP in monkeys, but anti-VEGF Fab did not contribute to the IOP increase. In addition, an anti-ANGPT2-selective antibody did not change IOP. In mice simultaneous blockade of ANGPT1 and ANGPT2 impaired the expansion and formation of Schlemm's canal (SC) vessels, similar to genetic ablation of Angpt1/Angpt2 and their receptor TIE2. As previously reported, blocking ANGPT2 alone did not affect SC formation in mice. Dual inhibition of ANGPT1/ANGPT2, but not ANGPT2 alone, leads to increased IOP and glaucomatous damage in monkeys. This confirms a role for TIE2/ANGPT signaling in the control of IOP in adults, a finding initially identified in transgenic mice. Dual pharmacologic inhibition of ANGPT1/ANGPT2 may affect aqueous drainage and homeostasis in adult monkeys and may be useful in developing novel models of glaucoma.

The Pathogenesis of Osteochondrosis in Humans and Animals

Osteochondrosis is a disease involving failure of endochondral ossification that occurs in growing animals and children in highly specific predilection sites, resulting in the formation of a cartilaginous or osseocartilaginous flap that causes pain and locking of the joint. In veterinary medicine, the term “osteochondrosis” (OC) is used for all stages of the disease and all affected sites. In human medicine, “osteochondritis dissecans” (OCD), is the preferred term for clinical disease involving the distal femur/knee joint. In other affected sites in humans, the disease is named after the physician(s) who first recognized it at that site; the disease in humans is further subdivided into adult and juvenile forms. Until very recently, subclinical disease was not recognized in humans as the only available tissue for study was the flap removed surgically from the affected joint, which often had been present for months to years. Subclinical disease, however, is well recognized in animals due to study of predilection sites at ages prior to the age of onset of clinical disease, work that are not possible in humans. Because the appearances of the subclinical and clinical disease are completely different, and because only end‐state tissue has been available for study of the disease in humans, the pathogenesis of the disease has been poorly understood in human medicine. In pigs and horses, it has been well demonstrated that subclinical lesions of osteochondrosis involving the articular‐epiphyseal cartilage complex are composed of areas of necrotic epiphyseal cartilage that often surround necrotic cartilage canal blood vessels. The overlying articular cartilage and subjacent subchondral bone are not initially affected; however, as endochondral ossification proceeds these areas of necrotic cartilage cause a delay in the ossification front that is visible in imaging studies. Study of both naturally‐occurring and surgically‐induced disease in animals have unequivocally demonstrated that failure of cartilage canal blood supply is the cause of these lesions. Traumatic forces to the surface of the articular cartilage, even when minimal in severity, may result in collapse of the necrotic epiphyseal cartilage and cleft formation through the overlying articular cartilage, resulting in the well‐recognized clinical disease. Recent development of magnetic resonance imaging methods to identify cartilage canal vessels and areas of cartilage necrosis, as well as access to human cadaveric knee specimens, have provided strong evidence that the pathogenesis of OC/OCD in animals and humans is identical and that subclinical disease in humans occurs years before clinical disease is evident. This work provides the potential for the development of new methods of early detection of disease in humans and methods for monitoring its response to treatment.Support or Funding InformationNIH/NIAMS R01AR070020; NIH/OD K01OD021293; WM Keck FoundationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Cartilage canals in the distal intermediate ridge of the tibia of fetuses and foals are surrounded by different types of collagen.

Some epiphyseal growth cartilage canals are surrounded by a ring of hypereosinophilic matrix consisting of collagen type I. Absence of the collagen type I ring may predispose canal vessels to failure and osteochondrosis, which can lead to fragments in joints (osteochondrosis dissecans). It is not known whether the ring develops in response to programming or biomechanical force. The distribution that may reveal the function of the ring has only been described in the distal femur of a limited number of foals. It is also not known which cells are responsible for producing the collagen ring. The aims of the current study were to examine fetuses and foals to infer whether the ring forms in response to biomechanical force or programming, to describe distribution and to investigate which cell type produces the ring. The material consisted of 46 fetuses and foals from 293 days of gestation to 142 days old, of both sexes and different breeds, divided into three groups, designated the naïve group up to and including the day of birth, the adapting group from 2 days up to and including 14 days old, and the loaded group from 15 days and older. The distal tibia was sawn into parasagittal slabs and the cranial half of the central slab from the intermediate ridge was examined by light microscopy and immunohistochemical staining for collagen type I. Presence, completeness and location of the collagen ring was compared, as was the quantity of perivascular mesenchymal cells. An eosinophilic ring present on HE‐stained sections was seen in every single fetus and foal examined, which corresponded to collagen type I in immunostained sections. A higher proportion of cartilage canals were surrounded by an eosinophilic ring in the naïve and adapting groups at 73 and 76%, respectively, compared with the loaded group at 51%. When considering only patent canals, the proportion of canals with an eosinophilic ring was higher in the adapting and loaded than the naïve group of foals. The ring was present around 90 and 81% of patent canals in the deep and middle layers, respectively, compared with 58% in the superficial layer, and the ring was more often complete around deep compared with superficial canals. The ring was absent or partial around chondrifying canals. When an eosinophilic ring was present around patent canals, it was more common for the canal to contain one or more layers of perivascular mesenchymal cells rather than few to no layers. It was also more common for the collagen ring to be more complete around canals that contained many as opposed to few mesenchymal cells. In conclusion, the proportion of cartilage canals that had an eosinophilic ring was similar in all three groups of fetuses and foals, indicating that the presence of the collagen ring was mostly programmed, although some adaptation was evident. The ring was more often present around deep, compared with superficial canals, indicating a role in preparation for ossification. The collagen ring appeared to be produced by perivascular mesenchymal cells.

Discontinuities in the endothelium of epiphyseal cartilage canals and relevance to joint disease in foals.

Cartilage canals have been shown to contain discontinuous blood vessels that enable circulating bacteria to bind to cartilage matrix, leading to vascular occlusion and associated pathological changes in pigs and chickens. It is also inconsistently reported that cartilage canals are surrounded by a cellular or acellular wall that may influence whether bacterial binding can occur. It is not known whether equine cartilage canals contain discontinuous endothelium or are surrounded by a wall. This study aimed to examine whether there were discontinuities in the endothelium of cartilage canal vessels, and whether canals had a cellular or acellular wall, in the epiphyseal growth cartilage of foals. Epiphyseal growth cartilage from the proximal third of the medial trochlear ridge of the distal femur from six healthy foals that were 1, 24, 35, 47, 118 and 122 days old and of different breeds and sexes was examined by light microscopy (LM), transmission electron microscopy (TEM) and immunohistochemistry. The majority of patent cartilage canals contained blood vessels that were lined by a thin layer of continuous endothelium. Fenestrations were found in two locations in one venule in a patent cartilage canal located deep in the growth cartilage and close to the ossification front in the 118‐day‐old foal. Chondrifying cartilage canals in all TEM‐examined foals contained degenerated endothelial cells that were detached from the basement membrane, resulting in gap formation. Thirty‐three percent of all canals were surrounded by a hypercellular rim that was interpreted as contribution of chondrocytes to growth cartilage. On LM, 69% of all cartilage canals were surrounded by a ring of matrix that stained intensely eosinophilic and consisted of collagen fibres on TEM that were confirmed to be collagen type I by immunohistochemistry. In summary, two types of discontinuity were observed in the endothelium of equine epiphyseal cartilage canal vessels: fenestrations were observed in a patent cartilage canal in the 118‐day‐old foal; and gaps were observed in chondrifying cartilage canals in all TEM‐examined foals. Canals were not surrounded by any cellular wall, but a large proportion was surrounded by an acellular wall consisting of collagen type I. Bacterial binding can therefore probably occur in horses by mechanisms that are similar to those previously demonstrated in pigs and chickens.

Improved Visualization of Cartilage Canals Using Quantitative Susceptibility Mapping.

PurposeCartilage canal vessels are critical to the normal function of epiphyseal (growth) cartilage and damage to these vessels is demonstrated or suspected in several important developmental orthopaedic diseases. High-resolution, three-dimensional (3-D) visualization of cartilage canals has recently been demonstrated using susceptibility weighted imaging (SWI). In the present study, a quantitative susceptibility mapping (QSM) approach is evaluated for 3-D visualization of the cartilage canals. It is hypothesized that QSM post-processing improves visualization of the cartilage canals by resolving artifacts present in the standard SWI post-processing while retaining sensitivity to the cartilage canals.MethodsEx vivo distal femoral specimens from 3- and 8-week-old piglets and a 1-month-old human cadaver were scanned at 9.4 T with a 3-D gradient recalled echo sequence suitable for SWI and QSM post-processing. The human specimen and the stifle joint of a live, 3-week-old piglet also were scanned at 7.0 T. Datasets were processed using the standard SWI method and truncated k-space division QSM approach. To compare the post-processing methods, minimum/maximum intensity projections and 3-D reconstructions of the processed datasets were generated and evaluated.ResultsCartilage canals were successfully visualized using both SWI and QSM approaches. The artifactual splitting of the cartilage canals that occurs due to the dipolar phase, which was present in the SWI post-processed data, was eliminated by the QSM approach. Thus, orientation-independent visualization and better localization of the cartilage canals was achieved with the QSM approach. Combination of GRE with a mask based on QSM data further improved visualization.ConclusionsImproved and artifact-free 3-D visualization of the cartilage canals was demonstrated by QSM processing of the data, especially by utilizing susceptibility data as an enhancing mask. Utilizing tissue-inherent contrast, this method allows noninvasive assessment of the vasculature in the epiphyseal cartilage in the developing skeleton and potentially increases the opportunity to diagnose disease of this tissue in the preclinical stages, when treatment likely will have increased efficacy.

Histological confirmation and biological significance of cartilage canals demonstrated using high field MRI in swine at predilection sites of osteochondrosis

Cartilage canal vessels in epiphyseal cartilage have a pivotal role in the pathogenesis of osteochondrosis/osteochondritis dissecans. The present study aimed to validate high field magnetic resonance imaging (MRI) methods to visualize these vessels in young pigs. Osteochondral samples from the distal femur and distal humerus (predilection sites of osteochondrosis) of piglets were imaged post-mortem: (1) using susceptibility-weighted imaging (SWI) in an MRI scanner, followed by histological evaluation; and (2) after barium perfusion using µCT, followed by clearing techniques. In addition, both stifle joints of a 25-day-old piglet were imaged in vivo using SWI and gadolinium enhanced T1-weighted MRI, after which distal femoral samples were harvested and evaluated using µCT and histology. Histological sections were compared to corresponding MRI slices, and three-dimensional visualizations of vessels identified using MRI were compared to those obtained using µCT and to the cleared specimens. Vessels contained in cartilage canals were identified using MRI, both ex vivo and in vivo; their locations matched those observed in the histological sections, µCT images, and cleared specimens of barium-perfused tissues. The ability to visualize cartilage canal blood vessels by MRI, without using a contrast agent, will allow future longitudinal studies to evaluate their role in developmental orthopedic disease.

The Leamington Scow: the excavation of historic structures and canal vessel at Leamington Wharf, Union Canal, Edinburgh

Archaeological investigations were carried out at Leamington Wharf on the Union Canal in Fountainbridge, Edinburgh. The remains of a stone quay, wooden platforms and staging, a rope walk and a canal vessel were investigated prior to redevelopment of the site for housing. The combination of archaeological excavation and historical research has illuminated the development of this former canal basin at the terminus of the Union Canal, and provided a rare opportunity to study the remains of a canal vessel likely to date from the early to mid 19th century. A scaled model of the vessel was commissioned as part of the project and will be submitted to the local museum service as a record.

Early Lesions of Articular Osteochondrosis in the Distal Femur of Foals

Failure of the cartilage canal blood supply to epiphyseal growth cartilage has been implicated in the pathogenesis of articular osteochondrosis in horses and other animal species. In a previous study of the developmental pattern of the blood supply in the tarsus of foals, early lesions of osteochondrosis were consistently found in regions where the cartilage canal vessels traversed the chondro-osseous junction. The developmental pattern of blood vessels has also been described in the distal femoral epiphysis; however, the group of foals examined in that study did not have lesions of osteochondrosis in this location. Therefore, the relationship between the occurrence of early lesions of osteochondrosis and the developmental pattern of the blood supply to epiphyseal growth cartilage in this site in foals has not been examined. Distal femora were collected from 30 fetuses and foals (up to 11 months old) submitted for postmortem examination. Sections from the lateral trochlear ridge and medial femoral condyle of both hind limbs were examined histologically. Sixteen cartilage lesions were found in 7 of the 30 fetuses and foals. All lesions contained evidence of cartilage canal necrosis and ischemic chondronecrosis. The lesions were located in regions where cartilage canal vessels traversed the chondro-osseous junction, as previously observed in the tarsus. The location and morphology of lesions indicated that a subclinical stage of ischemic chondronecrosis existed that preceded and predisposed to the development of osteochondrosis dissecans and subchondral bone cysts.

Epiphyseal cartilage canal blood supply to the metatarsophalangeal joint of foals

It is presently unknown whether cartilage ischaemia plays any part in the pathogenesis of osteochondral fragmentation within the equine metatarsophalangeal joint, as no detailed studies on microcirculation in the area have been reported. To describe the developmental pattern of the blood supply to the epiphyseal growth cartilage in the metatarsophalangeal joint of foals. Eight Standardbred foals were sacrificed between birth and age 7 weeks to undergo a barium perfusion procedure to demonstrate vessels within growth cartilage canals of one hindlimb. The metatarso-phalangeal joint was cleared in methyl salicylate and perfused vessels studied in the intact bones. The bones were sawed into 5 mm thick slabs, decalcified and radiographed. Selected slabs were cleared in methyl salicylate for a second time and examined at low magnification. The dorsal half of the sagittal ridge of the distal third metatarsal bone and the plantar half of the proximal phalanx were examined histologically. Regions of the epiphysis with thick cartilage contained a greater number of perfused vessels than regions with thin cartilage. The cartilage canal vessels were oriented either parallel or perpendicular to the underlying ossification front. Cartilage canal vessels were incorporated into the ossification front during growth and became reliant on a subchondral arterial source. Macroscopically visible lesions were not detected in the current group of foals. On histological examination, pathological changes consisting of an area of chondronecrosis surrounded by fibrovascular granulation tissue were found in sections from the lateral proximo-plantar eminence of the proximal phalanx in the 7-week-old foal. The same anatomical feature (traversing the ossification front to enter cartilage canals) reported to render vessels vulnerable to failure in the tarsus was also present in the metatarso-phalangeal joint of foals. Osteochondrosis may occur by the same pathogenetic mechanism in the metatarso-phalangeal joint as in the tarsus of foals.

Micro-computed tomography of early lesions of osteochondrosis in the tarsus of foals

IntroductionOsteochondrosis (OC) is an important developmental orthopedic disease of human and equine patients. The disease is defined as a focal disturbance in enchondral ossification. In horses, the disturbance can occur secondary to failure of the blood supply to growth cartilage. Diagnosis of the early, subclinical stages that can clarify the etiology is currently confined to cross-sectional histological examination. The potential for micro-computed tomography (micro-CT) with angiography to detect early lesions of OC has not yet been investigated. Materials and methodsNine Standardbred foals bred from parents with OC of the tarso-crural joint were sacrificed at weekly intervals from birth to 7 weeks of age. Permanent barium angiograms were created within one hind limb post mortem, and samples collected from two predilection sites for OC within the tarso-crural joint of the perfused hind limb. The resulting 18 sample blocks were scanned with a custom-built micro-CT equipment set-up, and analyzed as 2D slices and 3D volume rendered models before sectioning for conventional histological examination. ResultsHistological examination identified eight early lesions in seven locations within six joints from the nine foals. Micro-CT with angiography was able to detect seven lesions in the same sites as histological examination. Lesions consisted of non-perfused foci within growth cartilage. No perfused vessels exited from subchondral bone deep to any lesion. Six of the seven lesions were associated with focal defects in the subchondral bone plate. Evidence of ongoing ossification was seen in three out of the seven lesions and included one separate center of ossification. ConclusionMicro-CT was a useful technique for examination of early lesions of OC. The results of micro-CT were compatible with failure of cartilage canal vessels at the point where they cross the ossification front. Resultant areas of ischemic chondronecrosis were associated with focal delay in enchondral ossification as visualized in 3D volume rendered models. Micro-CT combined with histology clarified the role of different forms of ossification in the secondary repair responses to lesions.

Epiphyseal cartilage canal blood supply to the tarsus of foals and relationship to osteochondrosis

Pathological changes in the blood supply to growth cartilage have been implicated in the pathogenesis of osteochondrosis (OC) in horses, but have not been reported using vascular perfusion techniques. To describe the developmental pattern of cartilage canal vessels in the distal tibial epiphysis and talar growth cartilage of foals. Nine foals bred from parents with OC were sacrificed between the ages of 0 and 7 weeks to undergo a barium perfusion procedure. The distal end of the tibia and the entire talus were cleared in methyl salicylate and perfused vessels studied in the intact bones. Slabs with a thickness of 4-5 mm from 3 predilection sites for OC were examined in the stereomicroscope and with light microscopy. Cartilage canals were present for a limited period of growth. Perfused vessels initially entered canals from the perichondrium. Vessels in the proximal portion of canals retained their perichondrial arterial source throughout. With time, the ossification front advanced to incorporate the mid-portion of canals; and anastomoses formed between canal vessels and subchondral vessels. A shift occurred and vessels in the distal terminus of canals came to use subchondral vessels as their arterial source. Twelve histological lesions were found in 7 foals. All contained necrotic vessels surrounded by necrotic growth cartilage and 3 caused macroscopically visible delay in endochondral ossification. Lesions were located where vessels traversed the ossification front to enter the distal terminus of canals. Cartilage canal vessels are particularly susceptible to failure at the point where they cross the ossification front, with consequences for the viability of those chondrocytes that depend on them. A better understanding of how lesions of OC arise may improve the ability to identify, monitor, prevent and treat this disorder. Involvement of cartilage canals in the pathogenesis of equine tarsal OC plausibly explains several clinical features of this disease.

Decontamination and Deactivation of the Power Burst Facility at the Idaho National Laboratory

Successful decontamination and deactivation of the Power Burst Facility located at the Idaho National Laboratory was accomplished through the use of extensive planning, job sequencing, engineering controls, continuous radiological support, and the use of a dedicated group of experienced workers. Activities included the removal and disposal of irradiated fuel, miscellaneous reactor components and debris stored in the canal, removal and disposition of a 15.6 curie Pu:Be start-up source, removal of an irradiated in-pile tube, and the removal of approximately 220,000 pounds of lead that was used as shielding primarily in Cubicle 13. The canal and reactor vessel were drained and water was transferred to an evaporation tank adjacent to the facility. The canal was decontaminated using underwater divers, and epoxy was affixed to the interior surfaces of the canal to contain loose contamination. The support structures and concrete or steel frame walls that form the confinement were left in place. The reactor core was left in place and a carbon steel shielding plate was placed over the reactor core to reduce radiation levels. All low-level waste and mixed low level waste generated as a result of the work activities was characterized and disposed.

The Cartilage Canals of the Epiphyseal Growth Cartilage and their Role in the Formation of Lesions of Osteochondrosis

Cartilage canals are temporary vascular structures within the growth cartilage. They were described as early as 1736 and the first perfusion study performed already in 1743. In its most complex form, the vascular structure consists of an arteriole, originating in the perichondrial plexus and branching out into an anastomosing network of capillaries. The capillaries circle back along the arteriole and rejoin into a venule that follows the course of the arteriole back to the plexus. The canals regress with age in a process designated as chondrification, where the content of the canals is replaced by cartilage. The process of chondrification is considered physiological; however, premature regression has been associated with the formation of lesions of osteochondrosis. The purpose of the present study was to gain further insight into the nature of chondrification and the initial steps in the pathogenesis of osteochondrosis and the relationship between these events and age, growth rate, weight and femoral shape of the individual animals. This involved studies of the distribution and pattern of regression of the cartilage canals. The articular‐epiphyseal cartilage complexes of the distal femur of 48 half‐siblings of the Norwegian Landrace pig breed were studied, combining techniques of perfusion and tissue clearing with histological and immunohistological methods. The results of this study indicate that the physiological regression of the cartilage canals is an orderly and time‐dependent process in which the endothelial cells at the termination of the vessels die by apoptosis, while perivascular cells differentiate into chondrocytes that fill in the cartilage canal with matrix. However, as the ossification front advances, the deepest portion of some of the canals form anastomoses with vessels of the subchondral bone, giving the axial portion of the growth cartilage a new source of blood supply. Lesions of osteochondrosis, typically occurring in the axial growth cartilage, are characterized by necrosis of the portion of the affected cartilage canal distal to a point of interruption, with subsequent necrosis of adjacent resting zone growth cartilage. This interruption occurs at the junction between cartilage and bone where anastomoses are formed between cartilage canal vessels and subchondral vessels.

Focal changes in blood supply during normal epiphyseal growth are central in the pathogenesis of osteochondrosis in pigs

Cartilage canals are temporary vessel-containing structures within the growth cartilage. The canals gradually regress with age in a process designated chondrification, where the content of the canals is replaced by cartilage. The process of chondrification is considered physiological; however, premature regression has been associated with the formation of lesions of osteochondrosis. The purpose of the present study was to gain further insight into the nature of and relationship between chondrification of cartilage canals and the initial steps in the pathogenesis of osteochondrosis with respect to morphology, presence of factors influencing the processes, and mode of cellular death. The articular–epiphyseal cartilage complexes of the distal femur of 48 pigs were studied, combining a technique of perfusion and tissue clearing with histological and immunohistological methods. The results provided strong evidence that the process of chondrification occurs at the terminations of the cartilage canals and is characterized by disintegration of the endothelial cells and transformation of perivascular cells into matrix-producing chondrocytes. Lesions of osteochondrosis, however, are characterized by necrosis of the portion of the affected cartilage canal distal to a point of interruption, with subsequent necrosis of adjacent resting zone growth cartilage. This interruption of the cartilage canal blood supply occurs at the junction between cartilage and bone where anastomoses are formed between cartilage canal vessels and vessels from the bone marrow. It is possible that microfractures occurring secondary to minor trauma at a vulnerable time in the development of the cartilage may be the initial event in pathogenesis of osteochondrosis.

Ossification in the human calcaneus: a model for spatial bone development and ossification

Perichondral bone, the circumferential grooves of Ranvier and cartilage canals are features of endochondral bone development. Cartilage canals containing connective tissue and blood vessels are found in the epiphysis of long bones and in cartilaginous anlagen of small and irregular bones. The pattern of cartilage canals seems to be integral to bone development and ossification. The canals may be concerned with the nourishment of large masses of cartilage, but neither their role in the formation of ossification centres nor their interaction with the circumferential grooves of Ranvier has been established. The relationships between cartilage canals, perichondral bone and the ossification centre were studied in the calcaneus of 9 to 38-wk-old human fetuses, by use of epoxy resin embedding, three-dimensional computer reconstructions and immunhistochemistry on paraffin sections. We found that cartilage canals are regularly arranged in shells surrounding the ossification centre. Whereas most of the shell canals might be involved in the nourishment of the cartilage, the inner shell is directly connected with the perichondral ossification groove of Ranvier and with large vessels from outside. In this way the inner shell canal imports extracellular matrix, cells and vessels into the cartilage. With the so-called communicating canals it is also connected to the endochondral ossification centre to which it delivers extracellular matrix, cells and vessels. The communicating canals can be considered as inverted 'internal' ossification grooves. They seem to be responsible for both build up intramembranous osteoid and for the direction of growth and thereby for orientation of the ossication centre.