Abstract: Uveitis can cause significant visual morbidity and often affects younger adults of working age. Anterior uveitis, or inflammation limited to the anterior chamber (AC), iris, and/or ciliary body comprises the majority of uveitis cases. Current clinical biomarkers and conventional grading scales for intraocular inflammation are mostly subjective and have only a moderate degree of interobserver reliability, and as such they have significant limitations when used in either clinical practice or research related to uveitis. In recent years, novel imaging techniques and applications have emerged that can supplement exam findings to detect subclinical disease, monitor quantitative biomarkers of disease progression or treatment effect, and provide overall a more nuanced understanding of disease entities. The first part of this review discusses automated algorithms for optical coherence tomography (OCT) image processing and analysis as a means to assess and describe intraocular inflammation with higher resolution than that afforded by conventional AC and vitreous cell ordinal grading scales. The second half of the review focuses on anterior segment OCT and OCT angiography (OCTA) in scleritis and iritis, especially with regards to their ability to directly image and characterize the pathologic structures and vasculature underlying these diseases. Finally, we briefly review experimental animal research with promising but more distant human clinical applications, including in vivo molecular microscopy of inflammatory markers and investigation of gold nanoparticles as a potential contrast agent in OCT imaging. Imaging modalities are discussed in the broader context of trends within the field of uveitis towards greater objectivity and quantifiable outcome measures and biomarkers.
Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.
Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.
Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.
Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.
Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.
Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.
