Medical Histology

Bacon, Robert L.; Niles, Nelson R.

doi:10.1007/978-1-4613-8199-0

Cited by 7 publications

(3 citation statements)

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“…The famous "Color Atlas of Cytology, Histology, and Microscopic Anatomy" for medical students by Wolfgang Kuehnel [ 91 ], which was translated into all Western languages, does not even include coronary artery morphology, leaving readers with the illusion that it is the same as in any artery of this caliber. At best, some textbooks comment briefly that the intima of elastic arteries may be thicker [ 92 , 93 ], or that the intima of coronary arteries shows the greatest age-related changes [ 94 ], still stressing the single-cell layer intimal design. Rare exceptions such as the "Histology for Pathologist"[ 95 ], chapter 33 "Blood Vessels" [ 96 ] or [ 97 ] cannot reverse this general perception because few people read them and do so too late, after this ideology has already been formed.…”

Section: Introductionmentioning

confidence: 99%

Analysis of arterial intimal hyperplasia: review and hypothesis

Субботин

2007

Theor Biol Med Model

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BackgroundDespite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology?HypothesisI argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it "benign intimal hyperplasia". However, normal or "benign" intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates early in life to form a multi-layer intimal hyperplasia and then continues to self-renew in a controlled manner throughout life, relatively rarely compromising the blood supply to the heart, causing complications requiring intervention only in a small fraction of the population, while all humans are carriers of benign hyperplasia. Unfortunately, this fundamental fact has not been widely appreciated in arteriosclerosis research and medical education, which continue to operate on the assumption that the normal arterial intima is always an "ideal" single-layer endothelium. As a result, the disease is perceived and studied as a new pathological event caused by new mechanisms. The discovery that normal coronary arteries are morphologically indistinguishable from deadly coronary arteriosclerosis continues to elicit surprise.ConclusionTwo questions should inform the priorities of our research: (1) what controls switch the single cell-layer intimal phenotype into normal hyperplasia? (2) how is normal (benign) hyperplasia maintained? We would be hard-pressed to gain practical insights without scrutinizing our premises.

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Section: Introductionmentioning

confidence: 99%

Analysis of arterial intimal hyperplasia: review and hypothesis

Субботин

2007

Theor Biol Med Model

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“…Anteriorly, they range from none (Anson, 1950;Hamilton, 1956;Kahle et al, 1978;Morris, 1966;Ferner, 1963;Quain, 1908;Rohen and Yokuchi, 1984;Snell, 1978;Truex and Kellner, 1948;Woodburne, 1973), to one (Piersol, 1907), or two (Kiss and Szentagothai, 1964;Kuntz, 1936). Others mention connecting fine strands, filaments, or trabeculae (Bacon and Niles, 1983;Clemente, 1987;Snell, 1978;Walton, 1987;Krause and Cutts, 1986;Leeson et al, 1988;Basmajian and Slonecker, 1986;Martin, 1989). The term "septum posticum" first appears in Morris (19071, who described it accurately as a "spongy collection.…”

Section: Introductionmentioning

confidence: 99%

Human spinal arachnoid septa, trabeculae, and “rogue strands”

Parkinson

1991

Am. J. Anat.

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This study was undertaken because of confusion arising from a diversity of names, descriptions, and drawings of the human spinal subarachnoid septa and trabeculae in the standard texts and dictionaries. Sixty-two complete human cords were examined under the dissecting scope. The finely "woven" adult arachnoid membrane was two-layered, and there were essentially no connecting septa or trabeculae between the cord and the arachnoid membrane anteriorly. Posteriorly, in the upper cervical region there is a scanty series of connecting fibers and fenestrated sheets 1 or 2 mm on either side of the midline; these become progressively more extensive in the lower cervical region, remain extensive to the lumbar enlargement, beyond which they progressively dwindle to end abruptly at the filum terminale origin. Throughout the cauda equina, strands are haphazardly arranged connecting the roots and supporting blood vessels. These occasionally become tangentially adherent to the arachnoid membrane. Throughout the length there are many unexplained, redundant, nonbranching, beaded, thicker "rogue strands". All of the above are of a different character from the right-angle fiber arrangement of the denticulate ligament, the two leaves of which are often separated form segmental longitudinal tunnels. The nerve rootlets (fila radicularia) for each dermatome are joined by strands and webs to each other. There was no evidence of change in number or type of connection with age.

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“…The famous "Color Atlas of Cytology, Histology, and Microscopic Anatomy" used by medical students and published by Wolfgang Kuehnel [ 94 ], which was translated into all Western languages, does not include coronary artery morphology, leaving readers with the illusion that it has the same morphology as any artery of this caliber. At best, some textbooks comment briefly that the intima of elastic arteries may be thicker [ 95 , 96 ] or that the intima of coronary arteries demonstrates the greatest age-related changes [ 97 , 98 ], still stressing the single-cell layer intimal design. An example of such misrepresentation appears in the very popular Medscape website (a part of WebMD), which advertises itself as: “Medscape from WebMD offers specialists, primary care physicians, and other health professionals the Web's most robust and integrated medical information and educational tools” [ 99 ].…”

Section: Discussionmentioning

confidence: 99%

Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis

Субботин

2012

Theor Biol Med Model

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Background An accepted hypothesis states that coronary atherosclerosis (CA) is initiated by endothelial dysfunction due to inflammation and high levels of LDL-C, followed by deposition of lipids and macrophages from the luminal blood into the arterial intima, resulting in plaque formation. The success of statins in preventing CA promised much for extended protection and effective therapeutics. However, stalled progress in pharmaceutical treatment gives a good reason to review logical properties of the hypothesis underlining our efforts, and to reconsider whether our perception of CA is consistent with facts about the normal and diseased coronary artery. Analysis To begin with, it must be noted that the normal coronary intima is not a single-layer endothelium covering a thin acellular compartment, as claimed in most publications, but always appears as a multi-layer cellular compartment, or diffuse intimal thickening (DIT), in which cells are arranged in many layers. If low density lipoprotein cholesterol (LDL-C) invades the DIT from the coronary lumen, the initial depositions ought to be most proximal to blood, i.e. in the inner DIT. The facts show that the opposite is true, and lipids are initially deposited in the outer DIT. This contradiction is resolved by observing that the normal DIT is always avascular, receiving nutrients by diffusion from the lumen, whereas in CA the outer DIT is always neovascularized from adventitial vasa vasorum . The proteoglycan biglycan, confined to the outer DIT in both normal and diseased coronary arteries, has high binding capacity for LDL-C. However, the normal DIT is avascular and biglycan-LDL-C interactions are prevented by diffusion distance and LDL-C size (20 nm), whereas in CA, biglycan in the outer DIT can extract lipoproteins by direct contact with the blood. These facts lead to the single simplest explanation of all observations: (1) lipid deposition is initially localized in the outer DIT; (2) CA often develops at high blood LDL-C levels; (3) apparent CA can develop at lowered blood LDL-C levels. This mechanism is not unique to the coronary artery: for instance, the normally avascular cornea accumulates lipoproteins after neovascularization, resulting in lipid keratopathy. Hypothesis Neovascularization of the normally avascular coronary DIT by permeable vasculature from the adventitial vasa vasorum is the cause of LDL deposition and CA. DIT enlargement, seen in early CA and aging, causes hypoxia of the outer DIT and induces neovascularization. According to this alternative proposal, coronary atherosclerosis is not related to inflammation and can occur in individuals with normal circulating levels of LDL, consistent with research findings.

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Medical Histology

Cited by 7 publications

References 0 publications

Analysis of arterial intimal hyperplasia: review and hypothesis

Analysis of arterial intimal hyperplasia: review and hypothesis

Human spinal arachnoid septa, trabeculae, and “rogue strands”

Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis

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