Objective?To investigate the feasibility of photochemical tissue bonding (PTB) technique in repairing limbal stem cell (LSC) deficiency and the effect on cornea wound healing.?Methods?LSCs were isolated from limbus of New Zealand rabbits by tissue block culture method, and then the LSCs of 2nd passage were cultured on de-epithelialized human amniotic membrane (HAM) for 3 weeks to prepare the HAM/LSC grafts. The LSC deficiency models of the left eyes were established by 0.5 mol/L NaOH in 24 New Zealand female rabbits, aged 3-4 months and weighing 1.5-2.0 kg. HAM/LSC grafts were used to repair the cornea wounds by sutures (suture group, n=12) or by PTB technique (PTB group, n=12). The gross was observed including the corneal transparency, erythema, and new blood vessel formation after surgery. At 3 and 28 days, the inflammatory cytokine of interleukin 1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α) were assayed by ELISA method; and the amount of new blood vessels were quantified by immunohistochemistry staining at 28 days.?Results?All animals survived to the end of the experiment. At 3 days, there was no obvious difference in the corneal transparency between 2 groups; at 28 days, the corneal transparency of PTB group was higher than that of suture group, and new blood vessels decreased. HE staining showed that mass inflammatory cells infiltrated between graft and cornea basal layer at 3 days, and no new blood vessel formed. inflammatory cells infiltration significantly decreased at 28 days in PTB group; the amount of new blood vessels was (2.0 ± 0.8)/ HP in PTB group and was (6.3 ± 1.3)/HP in suture group, showing significant difference (t=7.966, P=0.002). At 28 days, the concentrations of inflammatory cytokine of IL-1β, IL-6, and TNF-α in suture group were significantly higher than those in PTB group (P lt; 0.05); however, no significant differences were observed between 2 groups at 3 days (P gt; 0.05).?Conclusion?PTB technique can be used to fix HAM/LSC grafts, which can decrease inflammatory cell infiltration and new vessel formation, and improve the outcomes when compared with suture technique.
ObjectiveTo investigate the prevalence and risk factors of tessellation fundus (TF) among Tianjin Medical University students with different refractive statuses. MethodsA cross-sectional study. From September to December 2019, 346 students from Tianjin Medical University were randomly selected and underwent slit-lamp examination, non-cycloplegic auto-refraction, subjective refraction, best-corrected visual acuity, ocular biometric measurement, and non-dilation fundus photography. The differences in the prevalence of TF in basic characteristics and ocular biometric parameters were compared. Based on the equivalent spherical (SE), refractive status was divided into the non-myopia group (SE＞－0.50 D) and the myopia group (SE≤－0.50 D). The myopia group was further divided into mild myopia group (－3.00 D＜SE≤－0.50 D), moderate myopia group (－6.00 D＜SE≤－3.00 D), and high myopia group (SE≤－6.00 D). According to the axis length (AL), the subjects were divided into AL＜24 mm group, 24-26 mm group, and ＞26 mm group. The logistic regression was used to analyze the risk factors affecting TF. Trend tests were performed for each risk factor and TF. ResultsOf the 346 subjects, 324 (93.6%, 324/346) were myopia, of whom 73 (21.1%, 73/346), 167 (48.3%, 167/346), and 84 (24.3%, 84/346) were mild myopia, moderate myopia, and high myopia, respectively; 22 (6.4%, 22/346) were non-myopia. There were 294 (85.0%, 294/346) students with TF in the macula, including 9 (40.91%, 9/22), 58 (79.45%, 58/73), 145 (86.83%, 145/167), and 82 (97.62%, 82/84) in non-myopia, low myopia, moderate myopia, and high myopia group, respectively; 52 (15.0%, 52/346) students were without TF in the macula. There were statistically significant gender differences (χ2=4.47), SE (t=6.29), AL (t=－8.29), anterior chamber depth (Z=－2.62), lens thickness (Z=－2.23), and average corneal radius (Z=－3.58) between students with and without TF in the macula (P＜0.05). Spherical equivalent and axial length were independent risk factors for TF and its severity (P≤0.001). With an increasing degree of myopia, and increasing axial length, the risk of TF increased (P for trend＜0.001). ConclusionsThe prevalence of TF is 85.0% among Tianjin Medical University students. TF is detected in the fundus of no myopia, mild myopia, moderate myopia and high myopia. The degree of myopia is higher, the AL is longer, the possibility of TF is higher.
ObjectiveTo investigate whether the corneal shape recovered after discontinuation of long-term orthokeratology and whether orthokeratology increased the corneal astigmatism and ocular astigmatism.MethodsFrom December 2016 to April 2018, a retrospective study was conducted on 33 myopic patients who had undergone two times standard orthokeratology in the outpatient department of West China Hospital of Sichuan University, and had stopped wearing the first orthokeratology lens for one month before fitting the second orthokeratology lens. A total of 32 myopia frame glasses wearers were selected by simple random sampling as control. The changes of corneal flat meridian curvature (flat K), corneal steep meridian curvature (steep K), corneal astigmatism and ocular astigmatism before and after discontinuation of orthokeratology were analyzed.ResultsAmong the patients with baseline myopia diopter of ?0.25～?2.75 D, the average annual change of corneal flat K was (?0.03±0.21) D in the frame glasses group and (?0.24±0.14) D in the orthokeratology group, the difference was statistically significant (t=5.555, P<0.001). Among the patients with baseline myopia diopter of ?0.25～?2.75 D, the average annual change of corneal steep K was (0.20±0.42) D in the frame glasses group and (0.15±0.20) D in the orthokeratology group, the difference was not statistically significant (t=0.785, P=0.435). Among the patients with baseline myopia diopter of ?3.00～?5.75 D, the average annual change of corneal steep K was (0.29±0.39) D in the frame glasses group and (?0.01±0.20) D in the orthokeratology group, the difference was statistically significant (t=2.758, P=0.014). The average changes of corneal astigmatism were analyzed according to the difference of eyes, gender, age and baseline corneal astigmatism, the difference was not statistically significant (P>0.05), respectively. For patients with baseline astigmatism absolute value less than or equal to 0.50 D, the astigmatism annual change of the frame glasses group was 0.00 (0.50) D, and that of orthokeratology group was ?0.33 (0.48) D, the difference was statistically significant (Z=?2.301, P=0.021).ConclusionsThe flat K of the cornea becomes flatter and the steep K does not change after one month’s discontinuation of long-term orthokeratology. There was no difference in the increase of corneal astigmatism compared with those wearing frame glasses. When the baseline ocular astigmatism is less than or equal to 0.50 D, the increase of astigmatism may occur after discontinuation of orthokeratology.
Objective To investigate the influence of undercorrected orthokeratology on myopia control, and the correlation between target and central corneal epithelial damage. Methods A retrospective study was conducted on 22 undercorrected orthokeratology lens wearers (37 eyes) from January 2016 to February 2017, and 25 full corrected wearers (47 eyes) during the concurrent period were randomly selected as the control group. The changes of axial length before and after orthokeratology lens wearing and the within-6-month central corneal epithelial damage after orthokeratology lens wearing were analyzed. Results The average annual increase of axial length was (0.13±0.15) mm in the undercorrected group, and (0.14±0.16) mm in the full corrected group, the difference was not statistically significant (P>0.05). Multiple linear regression analysis showed that there was no correlation between the axial growth and the undercorrection of the target (P>0.05), but a negative correlation between the axial growth and the age (P<0.01). After using orthokeratology, the average annual growth of the axial length in children aged 7-10 years was (0.25±0.16) mm, and (0.10±0.14) mm in children aged 11-15 years, the difference was statistically significant (P<0.01). The incidence of central corneal epithelial punctate staining in the (–4.25)-(–5.00) D target group was 27.08%, and that in the (–3.00)-(–4.00) D target group was 16.67%, the difference was not statistically significant (P>0.05). Conclusions The effect of orthokeratology on myopia growth is not affected by the undercorrected target, not related to the undercorrection of target, but negatively correlated with the age. Undercorrected orthokeratology can still be used for myopia control in high myopia patients. No correlation is found between the target and central corneal staining.
Ocular neovascularization is a pathological change in various ocular diseases such as diabetic retinopathy, retinopathy of prematurity, central retinal vein occlusion and age-related macular degeneration, which seriously affects patient's vision. β receptors are expressed in conjunctiva, corneal epithelial cells, corneal endothelial cells, extraocular muscles, trabecular meshwork, ciliary muscle, lens and retina. β adrenergic receptor antagonists bind to β receptors to exert anti-angiogenic effects by inhibiting the expression of vascular endothelial growth factor (VEGF), hypoxia-inducible factor-1, interleukin-6 and other angiogenic cytokines; reducing macrophage-related inflammatory response; increasing the expression of anti-angiogenic factors. In the treatment of corneal neovascularization, choroidal neovascularization, and retinopathy of prematurity, it can significantly reduce the area of neovascularization and delay disease progression. Co-administration of anti-VEGF drugs can reduce the frequency of administration of anti-VEGF drugs. At effective therapeutic concentrations, β-adrenergic receptor antagonists are well tolerated; they have broader targets than anti-VEGF drugs, which offers new treatment strategies for ocular neovascularization such as corneal, choroidal and retinal neovascularization.
The mechanical properties of the cornea in corneal ectasia disease undergo a significant reduction, yet the alterations in mechanical properties within distinct corneal regions remain unclear. In this study, we established a rabbit corneal ectasia model by employing collagenase II to degrade the corneal matrix within a central diameter of 6 mm. Optical coherence tomography was employed for the in vivo assessment of corneal morphology (corneal thickness and corneal curvature) one month after operation. Anisotropy and viscoelastic characteristics of corneal tissue were evaluated through biaxial and uniaxial testing, respectively. The results demonstrated a marked decrease in central corneal thickness, with no significant changes observed in corneal curvature. Under different strains, the elastic modulus of the cornea exhibited no significant differences in the up-down and naso-temporal directions between the control and model groups. However, the cornea in the model group displayed a significantly lower elastic modulus compared to the control group. Specifically, the elastic modulus of the central region cornea in the model group was significantly lower than that of the entire cornea within the same group. Moreover, in comparison to the control group, the cornea in the model group exhibited a significant increase in both creep rate and overall deformation rate. The instantaneous modulus and equilibrium modulus were significantly reduced in the model cornea. No significant differences were observed between the entire cornea and the central cornea concerning these parameters. The results indicate that corneal anisotropy remains unchanged in collagenase-induced ectatic cornea. However, a significant reduction in viscoelastic properties is noticed. This study provides valuable insights for investigating changes in corneal mechanical properties within different regions of ectatic corneal disease.
Objective To observe the corneal nerve fibres damage in different stage of diabetic retinopathy (DR) with type 2 diabetes. Methods A cross-sectional study. One hundred and twenty eyes of 120 patients with type 2 diabetes served as diabetes group. According to International Clinical Diabetic Retinopathy Disease Severity Scales (2002), diabetes patients were classified into 4 subgroups: patients without diabetic retinopathy (NDR), patients with mild or moderate non-proliferative diabetic retinopathy (mNPDR), patients with severe non-proliferative diabetic retinopathy (sNPDR) and patients with proliferative diabetic retinopathy (PDR), each subgroup has 30 eyes of 30 patients. Another 30 eyes of 30 healthy participants served as control group. All eyes were scanned with HRT3 in vivo corneal confocal microscopy. Images of sub-basal nerve plexus were quantified including nerve fiber length (NFL), nerve fiber density (NFD), nerve fiber branch density (NFB), and nerve tortuosity (NT). The correlations of corneal nerve fiber with age, duration of diabetes and glycated hemoglobin (HbA1c) were analyzed using Spearman correlation analysis. Results NFL, NFD and NFB were found to be significantly lower in diabetic patients (F=147.315, 142.586, 65.898;P=0.000, 0.000, 0.000), NT was significantly greater in diabetic patients (F=39.431,P=0.000), when compared to control group. In diabetic patients, NFL, NFD and NFB were gradually reduced with DR severity, NT was gradually increased with DR severity. While the difference of NFL, NFD, NFB, NT was not statistically significant between sNPDR and PDR subgroups (P＞0.05), but was statistically significant between other subgroups (P＜0.05). Spearman correlation analysis results showed that age (r=－0.071, －0.080, 0.001, 0.100;P=0.391, 0.328, 0.991, 0.224) and HbA1c (r=－0.109, －0.115, －0.126, 0.025;P=0.238, 0.211, 0.169, 0.781) had no correlation with NFL, NFD, NFB, NT. Duration of diabetes was negatively correlated with the NFL, NFD (r=－0.212, －0.264;P= 0.020, 0.004), positive correlated with NT (r=0.261,P=0.004), and had no correlation with NFB (r=－0.119,P=0.194). Conclusions Corneal nerve fiber loss and nerve tortuosity increased were found in patients with type 2 diabetes, and even without diabetic retinopathy. The progress of corneal neuropathy was correlated with the severity of DR, but it was not change significantly between sNPDR and PDR.
Objective To review research progress of corneal tissueengineering.Methods The recent articles on corneal tissue engineering focus on source and selection of corneal cells, the effects of growth factors on culture of corneal cells in vitro. The preparation and selection of three-dimensional biomaterial scaffolds and their b and weak points were discussed. Results The corneal tissue engineering cells come from normal human corneal cells. The embryo corneal cell was excellent. Several kinds of growth factors play important roles in culture, growth and proliferation of corneal cell, and incroporated into matrix.Growth factors including basic fibroblast growth factor, keratinocyte growth factor, transforming growth factor β1 and epidermal growth factor was favor to corneal cell. Collagen, chitosan and glycosaninoglycans were chosen as biomaterial scaffolds. Conclusion Human tissue engineering cornea can be reconstructed and transplanted. It has good tissue compatibility and can be used as human corneal equivalents.
ObjectiveTo investigate the changes in the nerve fiber layer of the cornea in patients with demyelinating optic neuritis (DON) and its correlation with visual acuity. MethodsA cross-sectional study. From March 2021 to July 2022, 27 cases (39 eyes) of DON patients diagnosed in the Department of Neurology and Ophthalmology of Beijing Tongren Hospital Affiliated to Capital Medical University were enrolled in this study. According to the serological test results, the patients were divided into aquaporin 4 antibody associated optic neuritis (AQP4-ON group) and myelin oligodendrocyte glycoprotein antibody associated optic neuritis (MOG-ON group), with 15 cases (19 eyes) and 12 cases (20 eyes) respectively. According to previous history of glucocorticoid treatment, the patients were divided into glucocorticoid treated group and non-glucocorticoid treated group, with 17 cases (27 eyes) and 10 cases (12 eyes) respectively. Twenty healthy volunteers (20 eyes) with age- and gender-matched were selected as the control group. All eyes underwent best corrected visual acuity (BCVA) and in vivo confocal microscopy (IVCM) examinations. BCVA was performed using Snellen's standard logarithmic visual acuity chart, which was converted into logarithmic minimum angle resolution (logMAR) visual acuity during statistics. The corneal nerve fiber length (CNFL), corneal nerve fiber density (CNFD), corneal nerve fiber branch length (CNBL), corneal nerve fiber branch density (CNBD) and the density of corneal dendritic cells (DC) were detected by IVCM examination. Parameter comparison between groups by t-test and Kruskal-Wallis rank sum test. The correlation between logMAR BCVA and pamameters of corneal nerve fibers were analyzed using Spearman analysis. ResultsThe CNFL, CNFD, and CNBL of the DON group and the control group were (10.67±2.55) mm/mm2, (57.78±12.35) root/mm2, (3.27±1.34) mm/mm2, and (13.74±3.05) mm/mm2, (70.95±13.14) root/mm2, and (4.22±1.03) mm/mm2, respectively; the difference in CNFL, CNFD, and CNBL between the two groups were statistically significant (t=4.089, 3.795, 2.773; P＜0.05). The CNFL, CNBL, and CNBD of the affected eyes in the MOG-ON group and AQP4-ON group were (12.02±2.13) mm/mm2, (3.80±1.19) mm/mm2, (47.97±8.86) fibers/mm2, and (9.25±2.19) mm/mm2, (2.72±1.19) mm/mm2, (39.43±13.86) fibers/mm2, respectively; the differences in CNFL, CNBL, and CNBD between the two groups were statistically significant (t=－4.002, －2.706, －2.306; P＜0.05). The corneal DC density of the patients in the hormone treated group and the non-hormone treated group was (24.43±8.32) and (41.22±9.86) cells/mm2, respectively. The difference in corneal DC density between the two subgroups was statistically significant (P＜0.001). Correlation analysis showed that there was a significant negative correlation between logMAR BCVA and CNBL and CNFL in patients with DON (r=－0.422, －0.456; P＜0.05). ConclusionsThere are different degrees of corneal nerve fiber damage in patients with different types of DON. There was a negative correlation between BCVA and the length of corneal nerve fibers.
Objective
To investigate the clinical manifestations and gene mutation of a pedigree with retinal lattice degeneration and granular corneal dystrophy (GCD) type 2.
Methods
Ten members in 3 generations of a pedigree with retinal lattice degeneration and GCD2 were included in the study, including 6 patients (3 males and 3 females) and 4 healthy family members. All members underwent visual acuity, slit lamp microscope, three-mirror lens, fundus color photography, optical coherence tomography, and corneal endothelial cells counting. Genomic DNA was extracted from peripheral venous blood (2 ml) from all the subjects and their spouses, who had no related inherited diseases. The next generation sequencing method was used to detect the mutation sites of transforming growth factor β (TGFBI), and all results underwent Sanger verification.
Results
Among the 12 eyes of 6 patients, the visual acuity was FC/20 cm-1.0. In the superficial central corneal stroma, snowflake-like deposits were observed in three cases (6 eyes), and a small amount of granular deposits were observed in three cases (6 eyes). Corneal endothelial cell counts were normal. Retinal lattice degeneration were observed in 3 cases, 6 eyes (including 3 cases of rhegmatogenous retinal detachment in 4 eyes); retinal thinning without obvious lattice degeneration in 4 eyes of 2 patients. Nystagmus in 1 patient and fundus examination showed no significant abnormalities. DNA sequencing results showed that the proband and 4 patients had missense mutation of TGFBI gene in exon 4 c.371G＞ A, the mutation site corresponding to the amino acid change encoded by TGFBI gene No. 124 Amino acids, from arginine to histidine (p.R124H). Patients with this mutation have varying degrees of clinical phenotype.
Conclusions
The mutation of c.701G＞ A (p.R124H) in TGFBI gene is the causative gene of GCD in this pedigree. The patients with this mutation have different clinical phenotypes.
