Academic literature on the topic 'Alveolar process - Growth'

Evaluation of alveolar development beyond the postnatal period of rapid septation has generally involved alveolar counting. We used an alternate approach to assess postseptation parenchymal development: measurement of the lengths of various types of alveolar septal borders. This technique directly addresses changes in the elastin fiber network that determines parenchymal complexity. Lungs from weanling and adult ferrets, inflated to 15 cmH2O, were perfusion fixed and dehydrated, and 2-μm sections were stained with Miller’s elastin stain for light microscopy. We used standard morphometric methods to measure the lengths of the various types of alveolar septal borders. Three types comprised >90% of all septal borders: 1) free septal ends (“ends”) containing an elastin cable; 2) angled meetings of two alveolar septa (“bends”), also with a cable; and 3) the near-symmetrical intersections of three septa (“junctions”) devoid of elastin. When scaled for lung volume, ends and bends were 23 and 37% greater in adults ( P < 0.001), reflecting the increase in parenchymal complexity with growth. The 17% difference in scaled junction lengths was not significant ( P = 0.10). Bends increased out of proportion to the increase in ends, and both bends and ends increased to a greater degree than any possible increase in junctions ( P < 0.001 for all comparisons). Although the interpretation of changes in the distribution of alveolar border lengths is not straightforward, an increase in bends resulting in an increase in the complexity of individual alveoli may contribute to the increase in alveolar gas-exchanging surface area with growth. Septation, the process responsible for the rapid early postnatal increase in parenchymal complexity in many species, should tend to increase the lengths of ends and junctions and decrease the lengths of bends. Therefore, these data suggest that septation is not the predominant mechanism of later postnatal parenchymal development in the ferret.

Basement membrane promotes the reassembly of isolated type II alveolar cells into alveoli-like structures, a process attributable in part to a novel cell adhesion site in the alpha 1-chain of laminin-1 (M. L. Matter and G. W. Laurie. J. Cell Biol. 124: 1083-1090, 1994). The possibility that basement membrane contains other alveolarization activities was probed by subtraction analysis and use of neutralizing antibodies. Deletion of components < 100 kDa, and subsequently < 10 kDa, reduced alveolar cross-sectional area by 70% to 22-25 x 10(3) microns2: the approximate size of alveolar-like structures formed on purified laminin-1 alone. The deleted basement membrane material was adhesive for type II alveolar cells but failed to support alveolar formation in the absence of laminin-1. Preincubation of basement membrane with neutralizing anti-epidermal growth factor (EGF), -basic fibroblast growth factor (bFGF), -insulin-like growth factor (IGF)II, or -transforming growth factor (TGF)-beta antibodies had no inhibitory effect. Because both subtracted basement membrane preparations have in common the exclusion of components < 10 kDa, these results are interpreted as pointing to a sub-10-kDa alveolarization activity(s) that plays a key accessory role in laminin-1-dependent alveolar formation.

In many mammals, including humans, removal of one lung (pneumonectomy) results in the compensatory growth of the remaining lung. Compensatory growth involves not only an increase in lung size, but also an increase in the number of alveoli in the peripheral lung; however, the process of compensatory neoalveolarization remains poorly understood. Here, we show that the expression of α-smooth muscle actin (SMA)—a cytoplasmic protein characteristic of myofibroblasts—is induced in the pleura following pneumonectomy. SMA induction appears to be dependent on pleural deformation (stretch) as induction is prevented by plombage or phrenic nerve transection ( P < 0.001). Within 3 days of pneumonectomy, the frequency of SMA+ cells in subpleural alveolar ducts was significantly increased ( P < 0.01). To determine the functional activity of these SMA+ cells, we isolated regenerating alveolar ducts by laser microdissection and analyzed individual cells using microfluidic single-cell quantitative PCR. Single cells expressing the SMA ( Acta2) gene demonstrated significantly greater transcriptional activity than endothelial cells or other discrete cell populations in the alveolar duct ( P < 0.05). The transcriptional activity of the Acta2+ cells, including expression of TGF signaling as well as repair-related genes, suggests that these myofibroblast-like cells contribute to compensatory lung growth.

Relevance. Fixing a cleft alveolar process is one of the most complicated problems in pediatric maxillofacial surgery. The difficulty lies in the fact that bone grafting of the alveolar process directly affects the growth of the upper jaw, the difficulty of performing surgery, as well as trying to form a sufficient amount of bone regenerate, while it is necessary to restore the anatomical integrity of the alveolar process for subsequent orthodontic treatment or dental implantation. Purpose: To review the literature on the use of autografts from various donor areas in patients with congenital cleft upper lip, alveolar process, hard and soft palate. Materials and methods: A literature review of the data was carried out using the electronic databases “Medline”, “Pubmed”, “Kibeleninka”. The key words in the search were: bone plastic, cleft alveolar process. The selection criteria were the articles in English and Russian containing clinical studies on the use of various types of grafts in bone grafting of the alveolar process cleft. Results: The sources of literature on the use of various autografts for bone grafting of the alveolar outgrowth in children with cleft lip and palate were analyzed. Currently, most authors are inclined to use an iliac crest autograft in surgery. Conclusion: Although more than a century has passed since the first alveolar cleft bone graft surgery was performed, the choice of bone material is still unresolved - due to the severity of complications, the impossibility of taking a sufficient amount of bone material, as well as a high percentage of material resorption, because even with the use of iliac crest bone, the volume of transplant resorption can be over 40%.

Biologically active interleukin (IL)-1β is present in the pulmonary edema fluid obtained from patients with acute lung injury and has been implicated as an important early mediator of nonpulmonary epithelial wound repair. Therefore, we tested the hypothesis that IL-1β would enhance wound repair in cultured monolayers from rat alveolar epithelial type II cells. IL-1β (20 ng/ml) increased the rate of in vitro alveolar epithelial repair by 118 ± 11% compared with that in serum-free medium control cells ( P < 0.01). IL-1β induced cell spreading and migration at the edge of the wound but not proliferation. Neutralizing antibodies to epidermal growth factor (EGF) and transforming growth factor-α or inhibition of the EGF receptor by tyrphostin AG-1478 or genistein inhibited IL-1β-induced alveolar epithelial repair, indicating that IL-1β enhances in vitro alveolar epithelial repair by an EGF- or transforming growth factor-α-dependent mechanism. Moreover, the mitogen-activated protein kinase pathway is involved in IL-1β-induced alveolar epithelial repair because inhibition of extracellular signal-regulated kinase activation by PD-98059 inhibited IL-1β-induced alveolar epithelial repair. In conclusion, IL-1β augments in vitro alveolar epithelial repair, indicating a possible novel role for IL-1β in the early repair process of the alveolar epithelium in acute lung injury.

The developing pulmonary epithelium secretes a Cl(-)-rich fluid during fetal life by a process involving active transport. To determine if alveolar cells contribute to this fluid production, we studied developing fetal rat alveolar epithelial cells (18-day gestation) in primary culture. Fetal alveolar epithelial cells aggregated to form cystic, alveolar-like structures with a fluid-filled lumen. On light and transmission electron microscopy, the cells were polarized with microvilli facing the lumen. Dexamethasone and triiodothyronine stimulated lamellar body production in many of the epithelial cells of the cyst wall. The transepithelial voltage in the cyst was -2.4 +/- 0.4 mV (lumen negative), suggesting the presence of active electrolyte transport. Bumetanide, an inhibitor of Cl- secretion in other systems, decreased the size and number of cysts. A membrane-permeant analogue of adenosine 3',5'-cyclic monophosphate (cAMP) and 3-isobutyl-1-methylxanthine increased the size of cysts, an effect that was blocked by coincubation with bumetanide. The increased size of the cysts did not result from stimulation of cell growth; in fact, [3H]thymidine incorporation was inhibited to 40% control values by cAMP, suggesting that growth was inhibited rather than stimulated. These results suggest that fetal alveolar epithelial cells secrete fluid via a cAMP-mediated Cl(-)-secretory process. Secretion of fluid by the developing alveolar epithelium may play an important role in lung development.

A reduced number of alveoli is the structural hallmark of diseases of the neonatal and adult lung, where alveoli either fail to develop (as in bronchopulmonary dysplasia), or are progressively destroyed (as in chronic obstructive pulmonary disease). To correct the loss of alveolar septa through therapeutic regeneration, the mechanisms of septa formation must first be understood. The present study characterized platelet-derived growth factor receptor-α-positive (PDGFRα+) cell populations during late lung development in mice. PDGFRα+ cells (detected using a PDGFRαGFP reporter line) were noted around the proximal airways during the pseudoglandular stage. In the canalicular stage, PDGFRα+ cells appeared in the more distal mesenchyme, and labeled α-smooth muscle actin-positive tip cells in the secondary crests and lipofibroblasts in the primary septa during alveolarization. Some PDGFRα+ cells appeared in the mesenchyme of the adult lung. Over the course of late lung development, PDGFRα+ cells consistently expressed collagen I, and transiently expressed markers of mesenchymal stem cells. With the use of both, a constitutive and a conditional PDGFRαCre line, it was observed that PDGFRα+ cells generated alveolar myofibroblasts including tip cells of the secondary crests, and lipofibroblasts. These lineages were committed before secondary septation. The present study provides new insights into the time-dependent commitment of the PDGFRα+ cell lineage to lipofibroblasts and myofibroblasts during late lung development that is needed to better understand the cellular contribution to the process of alveolarization.

We examined the effects of alveolar duct structure on particle deposition in the pulmonary acinus. The low Reynolds number velocity field of carrier gas in a geometric model of the alveolated duct was solved numerically. Particle trajectories were computed from the Langevin equation. Conditional probabilities of the trajectories were calculated with an eigenfunction expansion technique in the absence of gravity. For submicron particles, Brownian motion dominated the process; the deposition rate dramatically decreased with boundary layer growth. For fine particles, fully developed boundary layer profiles determined the deposition over most of the acinar length. The assumption of a uniform radial profile results in a substantial overestimation of the local deposition rate. The deposition rate in an alveolated duct was always smaller than that in an equivalent straight tube of the same volume. Within the alveolus the deposition pattern was markedly nonuniform, with higher deposition near the alveolar entrance ring; this finding is consistent with experimental observations in animals (e.g., see Zeltner et al. J. Appl. Physiol. 70: 1137–1145, 1991). We conclude that the structure of the alveolar duct has an important influence on aerosol particle deposition in the lung acinus.

We propose that lung morphogenesis and repair are characterized by complex cell-cell interactions of endodermal and mesodermal origin, leading to (or returning back to) an alveolar structure that can effectively exchange gases between the circulation and the alveolar space. We provide the developmental basis for cell/molecular control of lung development and disease, what is known about growth and transcription factors in normal and abnormal lung development, and how endodermal and mesodermal cell origins interact during lung development and disease. The global mechanisms that mediate mesenchymal-epithelial interactions and the plasticity of mesenchymal cells in normal lung development and remodeling provide a functional genomic model that may bring these concepts closer together. We present a synopsis followed by a vertical integration of the developmental and injury/repair mechanisms.

Chronic obstructive pulmonary disease (COPD) represents a worldwide concern with high morbidity and mortality, and is believed to be associated with accelerated ageing of the lung. Alveolar abnormalities leading to emphysema are a key characteristic of COPD. Pulmonary alveolar epithelial type 2 cells (AT2) produce surfactant and function as progenitors for type 1 cells. Increasing evidence shows elevated WNT-5A/B expression in ageing and in COPD that may contribute to the disease process. However, supportive roles for WNT-5A/B in lung regeneration were also reported in different studies. Thus, we explored the role of WNT-5A/B on alveolar epithelial progenitors (AEPs) in more detail. We established a Precision-Cut-Lung Slices (PCLS) model and a lung organoid model by co-culturing epithelial cells (EpCAM+/CD45-/CD31-) with fibroblasts in matrigel in vitro to study the impact of WNT-5A and WNT-5B. Our results show that WNT-5A and WNT-5B repress the growth of epithelial progenitors with WNT-5B preferentially restraining the growth and differentiation of alveolar epithelial progenitors. We provide evidence that both WNT-5A and WNT-5B negatively regulate the canonical WNT signaling pathway in alveolar epithelium. Taken together, these findings reveal the functional impact of WNT-5A/5B signaling on alveolar epithelial progenitors in the lung, which may contribute to defective alveolar repair in COPD.

Background. The treatment of patients born with cleft lip and palate has been gradually modified over the years as the surgical procedures have developed and improved. Multidisciplinary team care has evolved and provided improved care with enhanced results. Clefts in the alveolus can be reconstructed by alveolar bone grafting or by periosteoplasty. The main goal is to repair and close the alveolar cleft and create a continuous alveolar processes so that the teeth can erupt. Aims. This thesis has several aims: to investigate the impact of dental status and initial cleft width on the outcome of Secondary alveolar bone grafting (SABG) in patients born with unilateral cleft lip and palate (UCLP) at the 10-year follow-up (Studies I and II); to compare the outcomes of primary periosteoplasty (PPP) with those of SABG in patients born with unilateral cleft lip and alveolus (CLA) (Study III); to evaluate clinical and radiographic conditions and identify factors important for the final treatment outcomes after SABG ( Study IV); to evaluate two radiographic methods, i.e. occlusal radiographs and cone beam tomography (CBCT)) for assessing alveolar bone height ( study IV). Results. In UCLP patients, SABG achieved excellent results in terms of bone height; tended to reduce with time, correlated with dental status and dental restoration factors. Occlusal radiographs correspond well with the CBCT, for evaluating alveolar bone height in cleft area. The width of the initial cleft does not seem to affect the success of SABG. Finally, patients with CLA treated with PPP at the time of lip repair have inferior bone formation outcomes in the cleft area compared with patients treated with SABG at the time of mixed dentition. Conclusion.  Poor dental status and malpositioning negatively affect the long-term survival of bone in the alveolar cleft. The initial cleft width affects certain dental status factors. In adults with UCLP, the alveolar bone height in the cleft was correlated to the presence of gingival inflammation and restorations at 20 years follow-up. Specially designed maintenance therapy is beneficial, after complex dental restorations in the cleft area. SABG is preferred to PPP for the reconstruction of alveolar clefts.

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Recombinant Human Growth Hormone (RhGh) has been studied in cases of dental implants, TMJ pathologies and bone fractures. It is able to stimulate bone growth in a dose-dependent manner by direct stimulation of chondrocytes. It stimulates proliferation and differentiation of chondroprogenitor cells, also acts directly on osteoblasts, increasing rates of remodeling and bone formation. In this review of the literature and case report, RhGh will be used in alveolar ridge preservation procedures, with the purpose of evaluating the benefits of this technique in maintaining the postextraction bone site viable, aiming a future rehabilitation with dental implants and prostheses.

Indiana University-Purdue University Indianapolis (IUPUI)
This investigation served as a follow-up of the unilateral and bilateral cleft lip and palate patients who underwent primary alveolar bone grafting at James Whitcomb Riley Hospital of the Indiana University Medical Center. The sample consisted of 18 patients, 15 males and three females, who received primary alveolar grafts between September 7, 1983 and March 5, 1985. Thirteen had complete unilateral clefts, and five had complete bilateral clefts of the lip and palate. The mean age of the group was 8 years, and none had received orthodontic treatment. The statistical analysis of the lateral cephalometric radiographs revealed significant differences in maxillofacial growth between the Riley sample population and the non-cleft, age-matched patients in the University of Michigan Growth Study. The Riley data were, overall, statistically and proportionately smaller than the normal population. These findings are due to the smaller skeletal size of the Riley group. Arch symmetry measurements indicated that at 8 years of age there were significant differences from ideal or perfect symmetry. Due to existent dental development and scarring from the palatal procedure, these findings were expected. Ideal symmetry may not be a realistic achievement for the cleft patients. Palatal surface area values were visually analyzed through graphs. The growth patterns of the Riley population were similar to those of the normal and non-grafted cleft groups in a study from the University of Miami. The data supports the theory that primary alveolar bone grafting, as performed at James Whitcomb Riley Hospital, does not result in growth attenuation.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.

This chapter discusses the respiratory system of giraffes. The respiratory system supplies oxygen, removes of carbon dioxide and produces the airflow needed to make sounds. Giraffes do not have the velocity of airflow through the airways to vibrate vocal cords sufficiently to generate sounds able to be heard by humans but can produce sounds able to be heard by giraffes. Air reaches alveoli for gas exchange through a long trachea, which is relatively narrow (~4 cm in diameter). Dead space volume is large. A short trunk and rigid chest wall reduce the capacity of the thorax and consequently lung volume is small. Respiratory rate is low (~10 min^-1), but tidal volume is relatively big, and alveolar ventilation rate (V_A; ~60 L min^-1) delivers sufficient air despite the large dead space volume. Laryngeal muscles act to prevent food from entering the trachea a process controlled by the (short) superior and (long) inferior (recurrent) laryngeal nerves. Air that has been delivered to alveoli comes into contact with pulmonary artery blood (=cardiac output, Q; ~40 L min^-1). The V_A: Q ratio is ~1.5 (cf 0.8 in humans). Gas exchange occurs by diffusion. The surface area for diffusion is related to the number of alveoli which increase in number during growth from ~1 billion in a newborn giraffe to 11 billion in an adult. Gas carriage of oxygen and carbon dioxide is a function of erythrocytes which are small (MCV = 12 fL) but numerous (12 × 10¹² L^-1) and each liter of blood contains ~150 g of hemoglobin.

The human (and mammalian) facial skeleton is a complex response to the protection, support, and functional demands of a diversity of neurological and physiological processes that must be structurally integrated, and each places limitations on the others. The processes involve respiration (nasal and oral) and mastication (and deglutition), as well as thermoregulation through respiration. Three of the special senses (vision, smell, and taste) are housed within the facial skeleton, although only the first has a major impact on the shape and structure of the facial skeleton. The challenge in assessing the facial configura­tions of the Sunghir human remains is to partition the facial skeleton in a paleobiologically meaningful manner. Traditionally in paleoanthropology, often given differential paleontological preservation, the facial skeleton is divided initially into its two major skeletal components (cranial and mandibular). The former is then assessed in terms of structures or individual bones, with variable focus on the configurations of the orbital, nasal, and palatal regions. The latter is evaluated as a whole or divided into corporeal and ramal regions. A more meaningful approach, although still one with its limitations, is to assess the face in terms of the three major functional units of the facial anatomy: the orbital, nasal, and masticatory units. Developmentally, in simplified terms, these units are sequential in their priorities. Even though the anterior orbital margins continue to grow anteriorly with facial growth through adolescence, their internal structure is formed early, given that the ocular sphere is an extension of the brain stem and grows in concert with it. The nasal region, both the internal capsule and its skeletal aperture, forms the core of the midface, the roof of the oral cavity, the medial surfaces for the zygomatic regions, and the baseline minimum for the length of the face given that the anterior mammalian dentition cannot be posterior of the nasal aperture. The maxillary dentition with its supporting structures is hafted onto the nasal capsule through the maxillary alveolar process, and the mandible normally grows to provide proper occlusion with the forwardly displaced maxillary dentition.

Most invasive dental procedures involving removal of teeth or bone are followed by uneventful healing. However, dentists should be aware that generalized abnormalities of bone, such as osteoporosis and Paget’s dis­ease of bone, may complicate these procedures and, rarely, can lead to ongoing clinical problems. The effects of radiotherapy to the jaws and bisphosphonate treatment are well-described causes of osteonecrosis and delayed healing. Diagnosis of bone disorders often depends on integrating the results of clinical, imaging, pathological, genetic, and biochemical investigations. Although the bony skeleton is often thought of as forming just a rigid framework, it should be remembered that bone is a living, responsive tissue that plays an important role in metabolism. During development, some bones develop from a cartilaginous template and others, such as most of the craniofacial bones, form in fibrous membranes. Bone matrix is laid down by osteoblasts that are derived from the extensive meshwork of bone-lining cells that cover the bone surfaces. The bone matrix contains osteocytes that are responsive to mechanical stresses. Bone matrix is removed by osteoclasts that move over the bone sur­face, resulting in scalloped pits termed Howship’s lacunae. Bone mat­rix can be woven or lamellar in pattern. Pathologists often examine sections of bony lesions in polarized light to determine whether the pattern of the collagenous matrix is woven or lamellar, because it can be pivotal for diagnosis. It is also important for clinicians to be aware that, in order to produce a histological section of bone, the tissue must first be fixed and then demineralized to soften the matrix. When a bone biopsy is performed, the patient should be made aware that additional time will be needed to process the biopsy. Following extraction of a tooth, the socket rapidly fills with blood, which then clots. Granulation tissue, which consists of proliferating endothelial cells and fibroblasts derived from remnants of the periodontal ligament and surrounding alveolar bone, grows into the clot and organization commences. Osteoclasts begin to remodel the crestal bone and remove any small spicules of bone detached during the extraction.