However, the ocular surface disease index remained essentially unchanged. Our research indicates that 3% DQS treatment provides superior safety and efficacy when compared to both artificial tears and sodium hyaluronate in addressing dry eye disease (DED) in general and following cataract surgery.
The elusive definitive treatment for dry eye disease (DED), a prevalent ocular surface condition, persists despite the development of more precise diagnostic methods and the emergence of newer therapeutic agents. Lubricating eye drops and anti-inflammatory agents remain essential in the current therapeutic paradigms for eye conditions, necessitating long-term application and being primarily palliative in their effect. Research persists not just for a curative treatment but also to elevate the potency and efficacy of current drug molecules, through upgraded formulations and delivery systems. During the last twenty years, notable advancements in preservative-free formulations, biomaterials (nanosystems and hydrogels), stem cell therapies, and the creation of a bioengineered lacrimal gland have taken place. The review meticulously summarizes current innovations in DED treatment, including biomaterials such as nanosystems, hydrogels, and contact lenses for drug delivery; cell- and tissue-based regenerative therapies for the repair of damaged lacrimal glands and ocular surfaces; and tissue engineering for the development of artificial lacrimal glands. Furthermore, this paper explores their efficacy in animal models and in vitro settings, while acknowledging any constraints. Encouraging research currently in progress requires corroborating clinical trials to evaluate safety and efficacy in humans.
Dry eye disease (DED), a chronic inflammatory condition impacting the ocular surface, can cause significant morbidity, visual impairments, and quality-of-life reductions in an estimated 5-50% of the global population. In DED, the consequences of abnormal tear secretion are tear film instability and ocular surface damage, leading to ocular surface pain, discomfort, and epithelial barrier disruption. Research indicates that autophagy regulation contributes to the development of dry eye disease, concurrent with the inflammatory reaction. Within mammalian cells, autophagy acts as a self-degradation pathway, reducing the excessive inflammation triggered by the discharge of inflammatory factors in tears. DED's management presently utilizes already-available specific autophagy modulators. Applied computing in medical science Despite existing limitations, burgeoning research into autophagy regulation within DED might incentivize the development of autophagy-altering drugs that aim to reduce the pathological consequences observed at the ocular surface. The following review discusses autophagy's influence on the etiology of dry eye disease, and also examines its potential as a therapeutic approach.
In the human body, each and every tissue and cell is affected by the endocrine system's actions. The ocular surface's constant exposure to circulating hormones necessitates the expression of their particular receptors. Dry eye disease, a multifaceted ailment, often exhibits endocrine abnormalities as a triggering component. Endocrine anomalies, including physiological factors such as fluctuations in menstrual cycles and menopause, pathological conditions like polycystic ovarian syndrome and androgen resistance, and iatrogenic interventions such as contraceptive use and antiandrogen treatments, can all lead to DED. 3-Amino-9-ethylcarbazole mouse This review examines the current state of these hormones in DED, including their mechanisms of action on ocular surface structures, and the resultant clinical implications. The investigation into the effects of androgens, estrogens, and progesterone on ocular tissues and the significance of androgen deficiency in dry eye disease (DED) is also carried out in this work. A comprehensive exploration of the physiological and pathological impacts of menopause and sex hormone replacement therapy follows. Investigating the relationship between insulin, insulin resistance, the ocular surface, and dry eye disease (DED), as well as the rising promise of topical insulin treatments for DED is the focus of this discussion. A comprehensive review of thyroid-associated ophthalmopathy, its effects on the ocular surface's structure and function, and the tissue-level impact of thyroid hormone in dry eye disease is undertaken. Furthermore, the potential influence of hormonal treatments on managing dry eye disorder (DED) has been reviewed. Considering the compelling evidence, the possibility of hormonal imbalances and their influence on DED patients should be addressed clinically.
Ophthalmic dry eye disease (DED), a prevalent and multifactorial condition, profoundly affects the quality of life. Due to alterations in our lifestyle and surroundings, this issue is now recognized as a significant public health concern. The current management of dry eye symptoms involves artificial tear solutions and anti-inflammatory treatments. Oxidative stress plays a critical role in DED, and the polyphenol class of natural compounds demonstrates promise in lessening this stress. In the skin of grapes and nuts, resveratrol is prominently featured, displaying antioxidant and anti-inflammatory properties. Clinical trials have shown improvements in glaucoma, age-related macular degeneration, retinopathy of prematurity, uveitis, and diabetic retinopathy following the use of this. Research into resveratrol's effectiveness for dry eye disease (DED) has demonstrated its potential as a therapeutic molecule. Because of its problematic delivery and low bioavailability, resveratrol has yet to see clinical application. heme d1 biosynthesis In this review, we analyze the feasibility of resveratrol in combating DED, employing various in vitro and in vivo experimental data.
Dry eye disease, a complex condition with a diverse array of causative factors and disease subtypes, commonly shows comparable clinical signs. Medications can lead to dry eye disease or symptoms of dryness by disrupting lacrimal and/or meibomian gland function and through additional mechanisms influencing ocular surface homeostasis. Eliminating the offending medication is critical to not only reversing the symptoms but also preventing further deterioration of the ocular surface inflammation, a crucial step in the management process. The review considers systemic drugs like isotretinoin and taxanes, which are known to impair meibomian gland function; immune checkpoint inhibitors, which negatively affect lacrimal glands; gliptins and antiglaucoma medications, which can lead to cicatrizing conjunctivitis; and inhibitors of epidermal growth factor receptors, fibroblast growth factor receptors, and belantamab mafodotin, that cause mucosal epitheliopathy. Clinical use of many anticancer medications, notably the newer agents, is relatively new, and consequently, the knowledge and awareness of their potential ocular side effects are still under development. To keep ophthalmologists informed, this review analyzes the link between medication use and dry eye disease, detailing symptoms and prevention. Strategies include discontinuation of the implicated drug or reducing its dose and frequency of use.
Dry eye disease (DED), an emerging health problem, impacts people across the globe. The past few years have witnessed considerable progress in the creation of new molecular entities and treatments specifically designed for DED. To evaluate and refine these therapies, dependable animal models of DED are essential for experimental research. A noteworthy strategy includes the application of benzalkonium chloride (BAC). Several DED models, induced by BAC in rabbits and mice, are detailed in the published literature. The cornea and conjunctiva, exposed to BAC, experience substantial increases in proinflammatory cytokines, alongside epithelial cell death and a decrease in mucin secretion. This cascade ultimately leads to tear film instability, closely simulating human dry eye disease. The stability profile of these models is the critical factor in deciding whether treatment should accompany the BAC instillation process or be initiated at a later time. We provide a summary of existing BAC animal models for DED, along with original data from rabbit DED models administered 0.1%, 0.15%, and 0.2% BAC twice daily over two weeks. The 02% BAC model demonstrated consistent DED signs for three weeks, whereas the 01% and 0.15% models displayed these signs for a shorter duration, lasting only one to two weeks after BAC was discontinued. The models, in their entirety, demonstrate encouraging characteristics and are frequently employed in different studies evaluating the efficacy of therapeutic drugs in treating DED.
Ocular discomfort, pain, and vision problems stem from the complex disorder of dry eye disease (DED), characterized by a loss of tear film homeostasis and an imbalance at the tear-air interface. Dry eye disorder's underlying factors, its progression, and how it is managed are all substantially affected by immune control issues. Minimizing DED symptoms and enhancing the quality of life for those impacted is the goal of DED management. The diagnosis notwithstanding, care is lacking for as many as half the patients. The limited availability of successful therapies for DED is a source of worry, and a more profound understanding of the root causes, coupled with the creation of more effective treatments, is essential for alleviating the distress of individuals affected by this condition. In consequence, the immune system's contributions to the commencement and advancement of DED have drawn considerable research attention. This paper surveys the current knowledge of the immune system's role in DED, analyzes current treatment methodologies, and explores current research into novel treatments.
The ocular surface's chronic inflammatory state, dry eye disease (DED), is a condition with multiple contributing factors. The immuno-inflammatory state of the ocular surface has a direct correlation with the severity of the disease. Impairment of the meticulously balanced functional relationship between ocular surface structural cells and resident and migratory immune cells can negatively impact the health of the ocular surface.