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In a departure from its usual format of original articles, editorials and reviews, this Special Issue of OPO features a remarkable series of six ‘Point-Counterpoint’ articles, in which leading researchers were invited to debate critical issues in myopia research. With a tight word count and reference limit, the Point-Counterpoint format offers a way for authors to provide a concise summary of a topic while conveying the excitement and intrigue that surrounds it. We asked contributors to be as provocative and outspoken in their points and counterpoints as the research literature allowed, in order to fully expose questions and uncertainties that might otherwise be familiar only to specialists, or that might be tucked away deep in the Discussion sections of rare, dusty old manuscripts. The panel of selected experts has not let us down. The six topics under discussion range from fundamental, academic research questions through to translational issues of urgent clinical relevance.

Myopia researchers have drawn heavily on studies in animal models over the years, generally employing two kinds of visual manipulations to induce myopia: form deprivation and imposed hyperopic defocus (negative lens wear). The extent to which these two experimental manipulations emulate the causal mechanisms in human myopia is a crucially important question, but one that is almost impossible to gauge at present. However, the closely related question of whether the two treatments invoke enhanced eye growth through a common mechanism has been amenable to experimental investigation. In the first Point-Counterpoint article, Ian Morgan and Regan Ashby argue the case for similarities in the mechanism(s) underlying form-deprivation myopia and lens-induced myopia, with Debora Nickla taking the opposing view that the mechanisms are different. In the second Point-Counterpoint article, Frank Schaeffel and Christine Wildsoet debate what is possibly the most intriguing question in myopia research today, ‘Can the retina alone detect the sign of defocus?’ (this topic is particularly apt for a Special Issue of OPO dedicated to Josh Wallman, as much of Josh's myopia research addressed this problem). Perceptually, blur caused by an image focused in front of, or behind, the retina is difficult to distinguish. Yet, many lines of evidence suggest the retina can accomplish the task, even when artificially ‘disconnected’ from higher brain centres. As myopic and hyperopic defocus drive eye growth in opposite directions, understanding the retina's abilities and limitations in interpreting blur thus offer an enticing route towards a myopia-prevention therapy.

Clinical trials currently underway are examining whether increasing the time spent outdoors can slow myopia progression. However, in parts of the world where the prevalence of myopia is highest, parents are often reluctant to let their children play outside for long periods. The third Point-Counterpoint article discusses the timely question of whether high light intensity, typical of that outdoors, is protective against myopia, with Ian Flitcroft and the trio of Cheryl Ngo, Seang Mei Saw and Ramamurthy Dharani taking the opposing views. If a high light level per se is crucial, then would fitting classrooms with super-bright lighting be beneficial?

Also pertinent to the theme of interventions to slow myopia progression, the fourth and fifth Point-Counterpoint articles see Neville McBrien, Brittany Carr and William Stell debate the mechanism by which atropine exerts its anti-myopia effect, and Earl Smith and the duo of Melanie Campbell and Elizabeth Irving debate whether peripheral retinal signalling underlies the anti-myopia effect of corneal reshaping therapy (CRT) and dual-focus contact lenses. There is renewed interest in the use of atropine as a treatment for myopia following promising results from clinical trials using very low dose therapy. As two of the drug's most important side-effects – mydriasis and cycloplegia – seem unrelated to atropine's anti-myopia modus operandi, and are dose-dependent, it might be possible to avoid them while preserving clinical efficacy. Clinical trials using CRT and multi-focal contact lenses have also yielded impressive outcomes in recent years. In the fifth Point-Counterpoint article, the debate surrounds the extent to which the peripheral retina can over-ride signals generated by the central retina, and indeed whether such peripheral retina-dominated effects can explain how CRT and dual-focus lenses slow myopia progression.

Looking to the future, the last in this series of Point-Counterpoint articles sees Ahmed Elsheikh and John Philips explore the potential of scleral cross-linking as a therapy for myopia. Can we expect the success achieved in treating keratoconus to be mirrored in a treatment for myopia, or are the safety issues and surgical complexities too great to overcome? To quote Friedrich Nietzsche, ‘Those who cannot understand how to put their thoughts on ice should not enter into the heat of debate’. On that note, we hope you enjoy the steely cold, scientific arguments presented in this series!