Anthony J. Bron

Bio: Anthony J. Bron is an academic researcher from University of Oxford. The author has contributed to research in topics: Cornea & Keratoconus. The author has an hindex of 5, co-authored 8 publications receiving 1099 citations.

Wolff's Anatomy of the Eye and Orbit

Abstract: Bony orbit and paranasal sinuses Ocular appendages Orbital and cerebral vessels Extraocular muscles and ocular movements Innervation and nerves of the orbit The eyeball and its dimensions Cornea and sclera Anterior chamber and drainage angle The iris Posterior chamber and ciliary body Choroid and uveal vessels Lens and zonules The vitreous The retina Visual pathway Autonomic aminergic, peptidergic and nitrergic innervation of the eye Development of the human eye References and further reading.

Changes in collagen orientation and distribution in keratoconus corneas

Abstract: PURPOSE. To map the collagen orientation and relative distribution of collagen fibrillar mass in keratoconus corneal buttons. METHODS. Structural analysis was performed by obtaining synchrotron x-ray scattering patterns across the samples at 0.25-mm intervals. The patterns were analyzed to produce two-dimensional maps of the orientation of the lamellae and of the distribution of total and preferentially aligned lamellae. RESULTS. Compared with normal corneas, in keratoconus the gross organization of the stromal lamellae was dramatically changed, and the collagen fibrillar mass was unevenly distributed, particularly around the presumed apex of the cone. CONCLUSIONS. The development of keratoconus involves a high degree of inter- and probably intralamellar displacement and slippage that leads to thinning of the central cornea and associated changes in corneal curvature. This slippage may be promoted by a loss of cohesive forces and mechanical failure in regions where lamellae bifurcate.

The architecture of the corneal stroma.

Abstract: In recent years the evolution of modern refractive surgery has focused attention on the architecture and biological properties of the cornea In this issue of the BJO (p 437) Muller et al address the differential behaviour of the anterior and posterior stroma during corneal swelling and draw interesting conclusions about the factors maintaining corneal shape Transparency of the corneal stroma depends particularly on the degree of spatial order of its collagen fibrils which are narrow in diameter and closely packed in a regular array1-8 The collagen fibrils themselves are weak scatterers, since their fibril diameter is less than the wavelength of light, and fibril refractive index is close to that of the ground substance There is little variation in fibril diameter and separation between the anterior and posterior cornea The stromal fibrils are further organised into bundles, or lamellae, of which there are approximately 300 in the central cornea and 500 close to the limbus9 The posterior lamellae course directly across the full width of the cornea without a break, having their origins in fibres which wind around the limbus at the corneoscleral junction10-12 or, according to Radner,9 have a pseudocircular organisation at the limbus, forming the ligamentum circulare corneae On the basis of x ray diffraction studies, about 49% of the stromal lamellae are preferentially aligned orthogonally, along the vertical and horizontal meridians, while about 66% lie within a 45° sector1112 Fibrils within a lamella are in parallel array, except where branching of lamellae occurs Branching in the horizontal plane occurs throughout the stroma, whereas anteroposterior branching is found only in the anterior third13 The anterior and posterior stroma differ in specific ways In general the posterior stroma is more ordered,14 more hydrated,15 more easily swollen, and has a lower …

TFOS DEWS II pathophysiology report

Abstract: The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease. Its central mechanism is evaporative water loss leading to hyperosmolar tissue damage. Research in human disease and in animal models has shown that this, either directly or by inducing inflammation, causes a loss of both epithelial and goblet cells. The consequent decrease in surface wettability leads to early tear film breakup and amplifies hyperosmolarity via a Vicious Circle. Pain in dry eye is caused by tear hyperosmolarity, loss of lubrication, inflammatory mediators and neurosensory factors, while visual symptoms arise from tear and ocular surface irregularity. Increased friction targets damage to the lids and ocular surface, resulting in characteristic punctate epithelial keratitis, superior limbic keratoconjunctivitis, filamentary keratitis, lid parallel conjunctival folds, and lid wiper epitheliopathy. Hybrid dry eye disease, with features of both aqueous deficiency and increased evaporation, is common and efforts should be made to determine the relative contribution of each form to the total picture. To this end, practical methods are needed to measure tear evaporation in the clinic, and similarly, methods are needed to measure osmolarity at the tissue level across the ocular surface, to better determine the severity of dry eye. Areas for future research include the role of genetic mechanisms in non-Sjogren syndrome dry eye, the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation.

Stress-strain measurements of human and porcine corneas after riboflavin–ultraviolet-A-induced cross-linking

Abstract: Results: There was a significant increase in corneal rigidity after cross-linking, indicated by a rise in stress in treated porcine corneas (by 71.9%) and human corneas (by 328.9%) and in Young’s modulus by the factor 1.8 in porcine corneas and 4.5 in human corneas. The mean central corneal thickness was 850 m 70 (SD) in porcine corneas and 550 40 m in human corneas. Conclusions: RiboflavinUVA-induced collagen cross-linking led to an increase in mechanical rigidity in porcine corneas and an even greater increase in human corneas. As collagen cross-linking is maximal in the anterior 300 m of the cornea, the greater stiffening effect in human corneas can be explained by the relatively larger portion of the cornea being cross-linked in the overall thinner human cornea. J Cataract Refract Surg 2003; 29:1780 –1785 © 2003 ASCRS and ESCRS

Collagen crosslinking with riboflavin and ultraviolet-A light in keratoconus: long-term results.

Abstract: Purpose To prove the long-term dampening effect of riboflavin- and ultraviolet-A-induced collagen crosslinking on progressive keratoconus. Setting Department of Ophthalmology, C.G. Carus University Hospital, Dresden, Germany. Methods Four hundred eighty eyes of 272 patients with progressive keratoconus were included in this long-term retrospective study. The maximum follow-up was 6 years. At the first and all follow-up examinations, refraction, best corrected visual acuity (BCVA), corneal topography, corneal thickness, and intraocular pressure were recorded. Results The analysis included 241 eyes with a minimum follow-up of 6 months. The steepening decreased significantly by 2.68 diopters (D) in the first year, 2.21 D in the second year, and 4.84 D in the third year. The BCVA improved significantly (≥1 line) in 53% of 142 eyes in the first year, 57% of 66 eyes in the second year, and 58% of 33 eyes in the first year or remained stable (no lines lost) in 20%, 24%, and 29%, respectively. Two patients had continuous progression of keratoconus and had repeat crosslinking procedures. Conclusions Despite the low number of patients with a follow-up longer than 3 years, results indicate long-term stabilization and improvement after collagen crosslinking. Thus, collagen crosslinking is an effective therapeutical option for progressive keratoconus.

The International Workshop on Meibomian Gland Dysfunction: Report of the Subcommittee on Anatomy, Physiology, and Pathophysiology of the Meibomian Gland

Abstract: The tarsal glands of Meibom (glandulae tarsales) are large sebaceous glands located in the eyelids and, unlike those of the skin, are unassociated with hairs. According to Duke-Elder and Wyler,1 they were first mentioned by Galenus in 200 AD and later, in 1666, they were described in more detail by the German physician and anatomist Heinrich Meibom, after whom they are named. Lipids produced by the meibomian glands are the main component of the superficial lipid layer of the tear film that protects it against evaporation of the aqueous phase and is believed also to stabilize the tear film by lowering surface tension.2 Hence, meibomian lipids are essential for the maintenance of ocular surface health and integrity. Although they share certain principal characteristics with ordinary sebaceous glands, they have several distinct differences in anatomy, location, secretory regulation, composition of their secretory product, and function. Functional disorders of the meibomian glands, referred to today as meibomian gland dysfunction (MGD),3 are increasingly recognized as a discrete disease entity.4–8 In patients with dry eye disease, alterations in the lipid phase that point to MGD are reportedly more frequent than isolated alterations in the aqueous phase. In a study by Heiligenhaus et al.,9 a lipid deficiency occurred in 76.7% of dry eye patients compared with only 11.1% of those with isolated alterations of the aqueous phase. This result is in line with the observations by Shimazaki et al.10 of a prevalence of MGD in the absolute majority of eyes with ocular discomfort defined as dry eye symptoms. These observations noted that 64.6% of all such eyes and 74.5% of those excluding a deficiency of aqueous tear secretion were found to have obstructive MGD, or a loss of glandular tissue, or both.10 Horwath-Winter et al.11 reported MGD in 78% of dry eye patients or, if only non-Sjogren patients are considered, in 87% compared with 13% with isolated aqueous tear deficiency. It may thus be accepted that MGD is important, conceivably underestimated, and possibly the most frequent cause of dry eye disease due to increased evaporation of the aqueous tears.5,9–12 After some excellent reviews of MGD4,7,8,13,14 in the past, many new findings have been reported in recent years, and other questions remain to be identified and resolved. A sound understanding of meibomian gland structure and function and its role in the functional anatomy of the ocular surface15 is needed, to understand the contribution of the meibomian glands to dysfunction and disease. Herein, we seek to provide a comprehensive review of physiological and pathophysiological aspects of the meibomian glands.

Early eye development in vertebrates.

Abstract: This review provides a synthesis that combines data from classical experimentation and recent advances in our understanding of early eye development. Emphasis is placed on the events that underlie and direct neural retina formation and lens induction. Understanding these events represents a longstanding problem in developmental biology. Early interest can be attributed to the curiosity generated by the relatively frequent occurrence of disorders such as cyclopia and anophthalmia, in which dramatic changes in eye development are readily observed. However, it was the advent of experimental embryology at the turn of the century that transformed curiosity into active investigation. Pioneered by investigators such as Spemann and Adelmann, these embryological manipulations have left a profound legacy. Questions about early eye development first addressed using tissue manipulations remain topical as we try to understand the molecular basis of this process.