Bowman Break and Subbasal Nerve Plexus Changes in a Patient With Dry Eye Presenting With Chronic Ocular Pain and Vitamin D Deficiency

Shetty, Rohit; Deshpande, Kalyani; Deshmukh, Rashmi; Jayadev, Chaitra; Shroff, Rushad

doi:10.1097/ico.0000000000000785

Cited by 21 publications

(11 citation statements)

References 11 publications

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“…It was interesting that in our model the subbasal layer density remained decreased despite the quantitative recovery to baseline of nerve density in the other layers. This is consistent with other models of ocular surface injury (dry eye, vitamin D deficiency, post-refractive surgery, diabetic keratopathy) and it is thought to be related to a disruption in Bowman's layer, which serves as a scaffold for the subbasal plexus 37–39. Three-dimensional reconstitution of corneal confocal images revealed that some of the epithelial terminals arise directly from the stromal nerves bypassing the subbasal area.…”

Section: Discussionsupporting

confidence: 87%

Latent Sensitization in a Mouse Model of Ocular Neuropathic Pain

Cho

Bell

Botzet

et al. 2019

Trans. Vis. Sci. Tech.

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Purpose Chronic ocular pain is poorly understood and difficult to manage. We developed a murine model of corneal surface injury (CSI)–induced chronic ocular neuropathic pain. The study focuses on changes in corneal nerve morphology and associated short- and long-term pain-like behavior after CSI. Methods CSI was induced in mice by local application of an alkali solution (0.75 N NaOH). Corneal nerve architecture, morphology, density, and length were studied. Eye-wiping was evaluated before and after CSI in response to hypertonic saline (2 M NaCl). Naltrexone (NTX) or Naloxone-methiodide (NLX-me), opioid receptor antagonists, were given subcutaneously (s.c., 3 mg/kg) or topically (eye drop, 100 μM), and then an eye-wiping test was performed. Results CSI caused partial corneal deinnervation followed by gradual reinnervation. Regenerated nerves displayed increased tortuosity, beading, and branching. CSI enhanced hypertonic saline-induced eye-wiping behavior compared to baseline or sham-injury ( P < 0.01). This hypersensitivity peaked at 10 days and subsided 14 days after CSI. Administration of NTX, or NLX-me, a selective peripheral opioid antagonist, reinstated eye-wiping behavior in the injury group, but not in the sham groups ( P < 0.05). Conclusions This study introduces a model of chronic ocular pain and corneal neuropathy following CSI. CSI induces central and peripheral opioid receptor-dependent latent sensitization (LS) that is unmasked by systemic or topical administration of opioid antagonists. Translational Relevance This model of chronic ocular pain establishes LS as a new inhibitory mechanism in the oculotrigeminal system and may be used for potential diagnostic and therapeutic interventions for ocular neuropathy.

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Section: Discussionsupporting

confidence: 87%

Latent Sensitization in a Mouse Model of Ocular Neuropathic Pain

Cho

Bell

Botzet

et al. 2019

Trans. Vis. Sci. Tech.

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“…Deletion of VDR has also been shown to reduce β-catenin transcriptional activity and proliferation of cells at the leading edge of wound closure, and vitamin D was found to be required for a normal regenerative response of the skin to wounding 37 , 38 . Vitamin D has been found to have anti-inflammatory and immunoregulatory roles, and deficiency could result in dry eye disease 39 , 40 . The relationship of vitamin D to other ocular pathologies has also been studied, and the therapeutic potential of vitamin D has been examined 41 .…”

Section: Discussionmentioning

confidence: 99%

Effects of 1,25 and 24,25 Vitamin D on Corneal Epithelial Proliferation, Migration and Vitamin D Metabolizing and Catabolizing Enzymes

Chen

Mylarapu

et al. 2017

Sci Rep

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This study investigated the effects of 1,25(OH)2D3 and 24R,25(OH)2D3 on corneal epithelial cell proliferation, migration, and on the vitamin D activating enzyme CYP27B1 (produces 1,25(OH)2D3) and inactivating enzyme CYP24A1 (produces 24R,25(OH)2D3). The role of the vitamin D receptor (VDR) was also examined. In VDR wildtype mouse corneal epithelial cells (WT), 1,25(OH)2D3 increased CYP24A1 protein expression and decreased CYP27B1 expression. In VDR knockout mouse epithelial cells (KO), 1,25(OH)2D3 increased CYP24A1 and CYP27B1 protein expression. 1,25(OH)2D3 did not affect WT cell proliferation, but did stimulate VDR KO cell proliferation. In a human corneal epithelial cell line (HCEC), 1,25(OH)2D3 increased CYP24A1 mRNA and protein expression. 1,25(OH)2D3 increased CYP27B1 mRNA levels in HCEC, but had no effect on CYP27B1 protein levels. 1,25(OH)2D3 inhibited HCEC proliferation and stimulated cell migration in primary human epithelial cells. 24,25(OH)2D3, on the other hand, increased both CYP24A1 and CYP27B1 protein expression in WT and VDR KO cells, and stimulated cell proliferation in both WT and KO cells. In HCEC, 24,25(OH)2D3 increased CYP24A1 and CYP27B1 mRNA and protein expression, and stimulated cell migration. In human primary corneal epithelial cells, 24,25(OH)2D3 stimulated migration. We conclude that 24R,25(OH)2D3 is likely involved in corneal epithelial cell regulation independent of 1,25(OH)2D3 or VDR.

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“…Rohit Shetty found correlation between serum vitamin D and ultimately with serum calcium in evaporative dry eye disease 22 . Shetty R, Deshpande K, Deshmukh R, Jayadev C, Shroff R found that Inflammation aggravated by vitamin D deficiency and serum calcium deficiency results in an altered epithelial profile, Bowman layer damage, recruitment of dendritic cells, and altered sub-basal nerve plexus features in patients with chronic dry eye disease 23 .…”

Section: Discussionmentioning

confidence: 99%

Dry Eye and its Relationship with Status of Serum Calcium in the Body at a Tertiary Care Institute: A Case Control Study

Patil¹,

Balwir²,

Khune³

et al. 2018

MVP Journal of Medical Sciences

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Background: Dry eye is a multifactorial disease of the tears and ocular surface that results in symptoms of dryness, grittiness, redness, burning sensation or any discomfort, visual disturbance and tear film instability leading to potential damage to ocular surface. The tear film consists of three layers starting from within outwards mucus, the aqueous layer and the lipid layer. The tear film and ocular surface form a complex and stable system that can lose its equilibrium through numerous disturbing factors. Studies which also involve tests of tear functions including Schirmer's test, Tear break-up time, Fluorescein staining for determination of dry eye have found generally low prevalence rates.Hence the physiology of tear film and its binding with the eye shows that there is some involvement of serum calcium level with dry eye. The present study encourages us to assess the role of serum calcium level with patients of dry eye. Aims and Objective: To assess the role of calcium with dry eye. Material and Methods: Total 90 subjects (30 cases and 60 controls) who met the selection criteria were included in the study.

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Bowman Break and Subbasal Nerve Plexus Changes in a Patient With Dry Eye Presenting With Chronic Ocular Pain and Vitamin D Deficiency

Cited by 21 publications

References 11 publications

Latent Sensitization in a Mouse Model of Ocular Neuropathic Pain

Latent Sensitization in a Mouse Model of Ocular Neuropathic Pain

Effects of 1,25 and 24,25 Vitamin D on Corneal Epithelial Proliferation, Migration and Vitamin D Metabolizing and Catabolizing Enzymes

Dry Eye and its Relationship with Status of Serum Calcium in the Body at a Tertiary Care Institute: A Case Control Study

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