| Objective To disscuss the relationship between meibomian gland abnormalities and obstructive sleep apnea-hypopnea syndrome and the mechanism of meibomian gland morphology changes.Methods Totally 63 patients(126 eyes) diagnosed with OSAHS from our hospital were recruited, and 44 healthy individuals(88 eyes) seeking for physical examinations served as control group. Personal information, clinical history and ocular surface disease index(OSDI) were recorded, then ocular check-up was done, including a slit lamp examination, measurement of tear break-up time, noncontact infrared meibography check-up, and meibum inspection. The prevalence of meibomian gland dropout and distortion between the two groups and in different degrees of OSAHS patients was compared.Results OSDI scores as well as BUT values between OSAHS groups and the control group were of statistical significance(all p<0.05). The prevalence of meibomian gland dropout in the OSAHS group(63/126, 60.0%) was higher than that in the control group(12/88, 13.6%)(p<0.05). The prevalence of meibomian gland dropout in different degrees of OSAHS groups(mild, moderate, and severe) was 8/18(44.4%), 14/30(46.7%), and 53/78(67.9%), respectively; the difference among those three groups was of statistical significance(p<0.05). However,there was no statistical difference in the severity of meibomian gland dropout in different degrees of OSAHS groups(mild, moderate, and severe)(F=0.731,p=0.485,p>0.05). The prevalence of meibomian gland distortion in the OSAHS group(68/126, 54.0%) was higher compared to the control group(9/88, 9.0%)(p<0.05). The prevalence of meibomian gland distortion in different degrees of OSAHS groups(mild, moderate, and severe) was 7/18(38.9%), 12/30(40.0%), and 49/78(62.8%), respectively; the difference among those three groups was of statistical significance(p<0.05). Meibomian gland orifices plugging was found in 87 eyes in the OSAHS group(87/126, 69.0%) and in32 eyes in the control group(32/88, 36.4%), and the discrepancy was significant(p<0.01). Meibum abnormality was found in 91 eyes in the OSAHS group(87/126, 69.0%) and in 32 eyes in the control group(32/88, 36.4%), and the difference between the two groups was of statistical significance(p<0.01).Conclusions OSAHS may lead to MG dropout, MG distortion, MG orifices plugging, and meibum abnormality, which in turn may cause tear film instability.Objective To explore the implications of the expression of MMP-1 and MMP-8 in the ECM of tarsal plate in mice with chronic intermittent hypoxia by immunohistochemistry.Methods Totally 46 male ICR mice(age,2 months old;body weight range,25-28g) provided by Quanzhou Medical College Experimental Animal Center were recruited. Among them, 16 mice were used to test the model of chronic intermittent hypoxia, and the remaining 30 were used for comparison. After verifying that the chronic intermittent hypoxia model was successfully established, the 30 mice were randomly separated into group A,group B and group C. The experimental process was as follows: at 9:00 am, the mice in group A were placed in a sealed box to experience hypoxia /re-oxygenation circulations till 5:00 pm every day, while the mice in group B were placed in a sealed box connected to circulating air;group C didn’t receive any disposal. After twelve weeks, all the mice were sentenced to death, and eyelids were taken from each mouse simultaneously, then the content of MMP-1 and MMP-8 in the ECM of the tarsal plate in those mice was tested by immunohistochemistry.Results Cyclical fluctuations of Sa O2 in mice was in line with changes of the oxygen concentration in the sealed box, suggesting the mouse model of chronic intermittent hypoxia was successfully established. Immunohistochemistry showed there was an upregulation of MMP-1 and MMP-8 in the extracellular matrix of the tarsal plate in mice with chronic intermittent hypoxia compared to group B as well as group C(all P<0.05), while the difference between group B and C was not significant(p>0.05).Conclusions OSAHS may lead to meibomian gland dropout and distortion. This is probably associated with the upregulation of MMP-1 and MMP-8, which participate in collagen fiber degradation in the tarsal plate. |
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