Clinical Impact of Conjunctivochalasis on the Ocular Surface

Yokoi, Norihiko; Komuro, Aoi; Nishii, Masakazu; Inagaki, Kayoko; Tanioka, Hidetoshi; Kawasaki, Satoshi; Kinoshita, Shigeru

doi:10.1097/01.ico.0000178740.14212.1a

Cited by 76 publications

(45 citation statements)

References 18 publications

(24 reference statements)

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“…Several research groups have previously reported evidence of a relationship between keratoconjunctivitis sicca and conjunctivochalasis [13,14,15,16]. Additionally, we also found that patients with idiopathic SCH had severe conjunctivochalasis-induced dry eye including SPK (data not shown).…”

Section: Discussionsupporting

confidence: 65%

Location and Extent of Subconjunctival Hemorrhage

et al. 2009

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Purpose: Subconjunctival hemorrhage (SCH) is a relatively frequent disease; however, there have been no reports about its location and extent. We examined its location and extent. Methods: A total of 151 patients with SCH aged 2–94 years were studied. The conjunctiva was divided into 8 equal areas. The age, gender, medical history, ocular history and site of hemorrhage were determined for all subjects. Results: The number of areas involved by SCH showed an age-related increase. Traumatic SCH had a smaller extent compared with SCH related to hypertension, diabetes and hyperlipidemia, or idiopathic SCH. Overall, SCH was significantly more common in the inferior areas than the superior areas (55.3% vs. 25.0%, p < 0.000001). In patients with SCH secondary to trauma or diabetes, however, the temporal areas were affected more often than the nasal areas (61.5% vs. 30.8% and 73.3% vs. 20.0%, respectively). Conclusion: SCH showed an age-related increase in extent and was predominant in the inferior areas. However, traumatic SCH was usually detected as localized hemorrhage in the temporal areas.

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Section: Discussionsupporting

confidence: 65%

Location and Extent of Subconjunctival Hemorrhage

et al. 2009

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“…13,[16][17][18][19] Bulbar conjunctival folds were first described by Hughes et al 21 and named conjunctivochalasis and they have been reported in severe dry eye patients. [22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] LIPCOF might represent the first mild stages of conjunctivochalasis and thus share the same aetiology. Several causes of bulbar conjunctival folds are hypothesised: conjunctival 'looseness' as a result of inflammatory processes, 23,27,36 a decrease of elastic fibres, 27,36 aging, 25,27 or lymphatic dilation by mechanical forces between the lower lid and conjunctiva that gradually interferes with lymphatic flow.…”

Section: Introductionmentioning

confidence: 99%

The relationship between clinical signs and dry eye symptoms

Pult

Purslow

Murphy

2011

Eye

146

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Purpose To evaluate (i) the relationship between traditional and new clinical tests (lid-wiper epitheliopathy (LWE), lid-parallel conjunctival folds (LIPCOF)) and dry eye symptoms in non-contact lens wearers, and (ii) that a combination of these tests can improve predictive ability for the development of dry eye symptoms. Methods Tear meniscus height (TMH), non-invasive break-up time (NIBUT), ocular hyperaemia, LIPCOF, phenol red thread test (PRTT), corneal and conjunctival staining, and LWE grades were observed in a cohort of 47 healthy, non-lens wearers (male ¼ 17, female ¼ 30, median age ¼ 35 years, range ¼ 19-70). Symptoms were assessed using the Ocular Surface Disease Index (OSDI). Results LWE was significantly correlated to both temporal and nasal LIPCOF (0.537or o0.607, Po0.05). LIPCOF and LWE were significantly correlated to NIBUT and PRTT (r4À0.248, Po0.001). Significant correlations were found between NIBUT and TMH (r ¼ 0.461, P ¼ 0.001) and PRTT (r ¼ 0.640, Po0.001). OSDI scores were significant correlated to NIBUT, TMH, PRTT, LIPCOF, and LWE (r4|0.31|; Po0.05). Significant discriminators of OSDI þ /À were NIBUT (area under the receiver operative characteristic curve (AUC) ¼ 0.895), TMH (0.715), PRTT (0.781), LIPCOF (temporal/nasal/Sum 0.748/0.828/0.816), and LWE (0.749). Best predictive ability was achieved by combining NIBUT with nasal LIPCOF (AUC ¼ 0.944). Conclusions The individual tests NIBUT, TMH, PRTT, LIPCOF, and LWE were significantly, but moderately, related to OSDI scores. The strongest relationship appeared by combining NIBUT with nasal LIPCOF.

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“…Although initially asymptomatic, the consequence of CCh is dryness, tearing, subconjunctival hemorrhage, and incomplete lid closure. [2][3][4] The pro-inflammatory cytokines such as TNF-a and IL-1b are elevated in tears of CCh patients. [5][6][7] The coexisting ocular surface inflammation might further be aggravated by delayed tear clearance, which is frequently related to CCh.…”

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confidence: 99%

PTX3 Controls Activation of Matrix Metalloproteinase 1 and Apoptosis in Conjunctivochalasis Fibroblasts

Guo

Zhang

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Conjunctivochalasis (CCh) is an age-related inflammatory ocular surface disease manifesting redundant, loose conjunctiva folds. The pathogenic role of Pentraxin 3 (PTX3) in controlling upregulation of matrix metalloproteinase 1 (MMP-1) and MMP-3 in CCh remains undefined.METHODS. Cytolocation of PTX3 and apoptosis were compared by immunostaining and terminal deoxyribonucleotidyl transferase-mediated FITC-linked dUTP nick-end DNA labeling (TUNEL) assay between normal and CCh specimens containing the conjunctiva and the Tenon. Second to third cultures of normal and CCh fibroblasts were treated with or without Aprotinin, Batimastat, or N-isobutyl-N-(4-methoxyphenylsulfonyl)-glycylhydroxamic acid (NNGH), followed by transfection with or without PTX3 siRNA, and TNF-a or IL-1b. Cell lysates and culture media were collected to assess apoptosis measured by the Cell Death Detection ELISA and expression of PTX3, MMP-1, and MMP-3 transcripts and proteins by quantitative RT-PCR and Western blot, respectively. RESULTS. PTX3 immunostaining was negative in normal specimens, but strongly positive in the subconjunctival stroma of CCh specimens. More apoptotic cells were found in CCh samples than in normal specimens. Expression of PTX3 transcripts and protein was not constitutive in resting normal fibroblasts but was in resting CCh fibroblasts and was upregulated by IL-1b in both cell lysates and culture media of both fibroblasts. PTX3 siRNA further upregulated MMP-1 and MMP-3 transcripts in resting normal fibroblasts, but synergistically with IL-1b upregulated the expression of MMP-1 and MMP-3 transcripts only in CCh fibroblasts, with activation of MMP-1 more so than MMP-3. PTX3 siRNA knockdown also promoted cell death characterized by apoptosis and necrosis, and such cell death could be rescued by inhibitors against serine proteinase, MMP1, or MMP3.CONCLUSIONS. Perturbation of PTX3 expression might partake in apoptosis and pathogenesis of CCh by upregulating expression of MMP-1 and MMP-3, and activation of MMP-1 and MMP-3.

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Clinical Impact of Conjunctivochalasis on the Ocular Surface

Cited by 76 publications

References 18 publications

Location and Extent of Subconjunctival Hemorrhage

Location and Extent of Subconjunctival Hemorrhage

The relationship between clinical signs and dry eye symptoms

PTX3 Controls Activation of Matrix Metalloproteinase 1 and Apoptosis in Conjunctivochalasis Fibroblasts

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