【1】中提到玻璃體中IX型覆蓋在II型膠原蛋白的外面，IX型上面有硫酸軟骨素鏈。

隨著年齡增加，硫酸軟骨素和IX型膠原蛋白的丟失，導致具有粘性的II型膠原蛋白暴露在外面，聚集導致形成玻璃體混濁

【2】的文章結尾提到，硫酸軟骨素可以清除自由基，換言之，自由基具有氧化和攻擊硫酸軟骨素的的能力。

Biochemical analysis reveal that vitreous consists of a fibrillar component, comprised of collagen and glycosaminoglycans (GAGs), chiefly hyaluronan (HA) with much lower concentrations of chondroitin sulfate (CS) and heparan sulfate (HS). The core of each fibril is composed of type V/XI collagen, which is surrounded by a sheath of fibrillar type II collagen as well as a regular arrangement of type IX collagen along the outermost surface of the fibril, HA provides a swelling pressure to the collagen network and hence the vitreous gel [5–6]. Recent research has shown that the loss of CS chains from type IX collagen of the fibril surfaces together with an increased surface exposure of type II collagen can result in collagen fibrillar aggregation. Gradual and progressive aggregation of the collagen fibrils results in a redistribution of the collagen fibrils, leaving areas devoid of collagen fibrils and thereby converted into a liquid. This pathological process can progress to posterior vitreous detachment (PVD), causing blindness [7–9]. Clarifying the chemical structure of CS and other GAGs within the vitreous can improve our understanding the interaction between GAGs and collagen, important for stabilizing the vitreous fibrillar network.

（生化分析顯示，玻璃體由一種纖維組成，由膠原和糖胺聚糖（GAG）組成，主要是透明質酸（HA），其中硫酸軟骨素（CS）和硫酸乙酰肝素（HS）的濃度要低得多。每個原纖維的核心由V/XI型膠原組成，該膠原被II型膠原纖維鞘以及沿原纖維最外表面的IX型膠原的規則排列所包圍，HA向膠原網絡以及玻璃體凝膠提供膨脹壓力[5–6]。最近的研究表明，纖維表面IX型膠原中CS（硫酸軟骨素）鏈的丟失以及II型膠原表面暴露的增加可導致膠原纖維聚集。膠原纖維的逐漸聚集導致膠原纖維的重新分布，留下沒有膠原纖維的區域，從而轉化為液體-表現為液化。這種病理過程可發展為后玻璃體脫離（PVD），導致失明[7-9]。闡明玻璃體內CS和其他GAG的化學結構可以提高我們對GAG和膠原之間相互作用的理解，這對穩定玻璃纖維網絡很重要。）【3】

這段話的意思是，從內到外：

V/XI型膠原蛋白->II型膠原蛋白->IX膠原蛋白->硫酸軟骨素

Bovine vitreous CS consisted of 2S4S, 2S6S, 4S, 6S and 0S with 4S (48.8%), 0S (37.6%) and 6S (11.9%) as the main compositional disaccharides and 2S6S (1.5%) and 2S4S (0.3%) as minor ones（牛玻璃體CS由2S4S、2S6S、4S、6S和0S組成，其中4S（48.8%）、0S（37.6%）和6S（11.9%）為主要成分雙糖，2S6S（1.5%）和2S4S（0.3%）為次要成分。）【3】

Type IX collagen and versican are reportedly the major CS containing proteoglycans in the vitreous. Structural characterization of CS has relied on the isolation of vitreous proteoglycans and the subsequent analysis of the disaccharide compositions of their GAG chains. In this way, the CS GAG chains of type IX collagen in bovine vitreous was determined to be 15-60 kDa consisting predominantly of 4-sulfated (50%) and 6-sulfated (30%) with lesser amounts of unsulfated (18%) diasaccharides residues [10–11]（據報道，IX型膠原和versican是玻璃體中含有蛋白多糖的主要CS。CS的結構表征依賴于玻璃體蛋白多糖的分離及其GAG鏈雙糖成分的后續分析。通過這種方式，牛玻璃體中IX型膠原的CS-GAG鏈被確定為15-60 kDa，主要由4-硫酸酯（50%）和6-硫酸酯（30%）組成，其中含有少量未硫酸酯（18%）一糖殘基[10–11]）【3】

【4】?Filling the space between the collagen fibrils is a network of hyaluronan; this glycosaminoglycan (polysaccharide) attracts water and generates a swelling pressure that inflates the gel.（膠原纖維之間充滿了透明質酸網絡；這種糖胺聚糖（多糖）吸水并產生膨脹壓力，使凝膠膨脹。）

Vitreous structure
The vitreous is a highly hydrated gel-like structure (>98% water) that is normally acellular, apart from a few cells called hyalocytes in the vitreous cortex.7 The gel state of the vitreous is maintained by a network of long, thin collagen fibrils that are ~15?nm in diameter. The concentration of these collagen fibrils is highest in the vitreous base and decreases posteriorly, but then increases in the cortical layer of the vitreous, which is attached to the inner surface of the retina. Filling the space between the collagen fibrils is a network of hyaluronan; this glycosaminoglycan (polysaccharide) attracts water and generates a swelling pressure that inflates the gel.(玻璃體是一種高度水合的凝膠狀結構（>98%水），通常是無細胞的，除了玻璃體皮質中的一些稱為透明細胞的細胞外。7玻璃體的凝膠狀態是由一個長而薄的膠原纖維網絡維持的，其長度約為15 納米直徑。這些膠原纖維的濃度在玻璃體基底部最高，并在后部降低，但隨后在附著于視網膜內表面的玻璃體皮質層增加。膠原纖維之間充滿了透明質酸網絡；這種糖胺聚糖（多糖）吸水并產生膨脹壓力，使凝膠膨脹。)【4】

The collagen fibrils are composed of collagen types II, V/XI and IX. Collagen types II and V/XI form the core of the rope-like collagen fibrils, whereas type IX collagen molecules are regularly distributed along the fibril surfaces.7 The type IX collagen has chondroitin sulfate glycosaminoglycan chains attached to it which extend away from the fibril surfaces and space apart the collagen fibrils, thereby preventing fibril aggregation (Figure 1).8 The individual collagen fibrils are organised into small bundles, and interconnections between these bundles allow the formation of an extended network that maintains the gel state（膠原原纖維由II型、V/XI型和IX型膠原組成。II型和V/XI型膠原形成繩狀膠原原纖維的核心，而IX型膠原分子沿著原纖維表面規則分布。7.IX型膠原上附著有硫酸軟骨素-糖胺聚糖鏈，該鏈遠離原纖維表面，并與膠原原纖維隔開，從而防止原纖維聚集（圖1）。8單個膠原原纖維被組織成小束，這些束之間的相互連接允許形成一個維持凝膠狀態的擴展網絡。）【4】

a是正常玻璃體里面的膠原纖維

b是玻璃體混濁

Natural history
Many patients experience floaters, but generally the symptoms are not troublesome. The vitreous opacities are mobile and move out of the visual axis, especially after a PVD when they move anteriorly causing the symptoms to diminish.5 Serpetopoulas et al16 have mathematically shown that the shadow of a vitreous opacity on the retina is determined by the diameter of the opacity, its distance from the retina and the overall distance between the pupillary plane and the retina. As these vitreous opacities move forward, over time their conic shadow no longer reaches the retina and the patient does not perceive them or only sees them intermittently.

（自然史

許多患者都會出現漂浮物，但通常情況下癥狀并不麻煩。玻璃體混濁是可移動的，并移出視軸，尤其是在PVD后，當它們向前移動時，癥狀減輕。5 Serpetopoulas等人從數學上證明，視網膜上玻璃體混濁的陰影由混濁的直徑、其與視網膜的距離以及瞳孔平面與視網膜之間的總距離決定。隨著這些玻璃體混濁向前移動，隨著時間的推移，它們的錐形陰影不再到達視網膜，患者無法察覺或只是間歇性地看到它們。）

Alternatively Schulz-Key et al5 have suggested that because vitreoretinal surgeons are inherently reluctant to operate on patients with SVO who have excellent visual acuity（醫生不愿意為視力良好但是有飛蚊的患者進行手術）

symptomatic vitreous opacities (SVO)（癥狀性玻璃體混濁）

All these studies have suggested certain potential personality traits in patients with SVO, but at present there is no definitive evidence regarding the psychology of this cohort of patients.（所有這些研究都表明SVO患者具有某些潛在的人格特征，但目前還沒有關于這組患者心理的確切證據。）

All patients in this cohort were either pseudophakic or aphakic to avoid the progression of lenticular cataract seen in phakic patients following vitrectomy（玻切只針對假晶狀體或無晶狀體人群）

?One patient developed a post-vitrectomy RD that was successfully repaired subsequently, and one patient had progression of lenticular sclerosis. （一名患者玻切時發生視網膜后脫離，隨后修復）

Floaters-only-vitrectomy.
Recently Sebag et al39 have published a prospective study on PPV for floaters. They performed 25-gauge PPV for symptomatic floaters of at least 24 months’ duration in 76 eyes, and evaluated the efficacy in 16 patients using contrast sensitivity function and subjective visual function using NEI VFQ. In this study the authors performed Floaters-only-Vitrectomy (FOV), which is defined as vitrectomy without PVD induction if PVD is not present at the start of surgery to theoretically reduce the risk of iatrogenic retinal breaks. In addition, anterior vitreous was left in situ to protect the lens against free oxygen radicals and reduce post-PPV cataract formation. It was concluded that PPV for floaters is highly efficacious, with contrast sensitivity that was diminished by 67% in patients with floaters normalising in all cases up to 9 months post-surgery, and the visual function improving by 29.2%. This technique was found to be highly safe with no case of post-PPV retinal breaks or RD, and only 23.5% developing cataract at an average of 15 months post-operatively. The mean age of this subgroup was 60.5 years (range 53–66 years). The main risk with FOV is that not only does the absence of PVD induction intra-operatively leave the risk of vitreous detaching later and leading to post-PPV retinal breaks and RD, but also causing the recurrence of symptomatic floaters. The authors have acknowledged themselves that 1 out of 76 eyes in their cohort developed symptomatic floaters during the onset of PVD later requiring a repeat vitrectomy.（盡量減少玻璃體切除，以避免切除后氧化晶狀體）

The most serious risk of intraocular surgery is endophthalmitis, and in the context of vitrectomy for floaters, this is of utmost importance as patients invariably have excellent visual acuity before surgery. Recently there have been two reports of endophthalmitis following PPV for SVO. Henry et al41 presented a case of Staphylococcus caprae endophthalmitis following 20-G vitrectomy for vitreous floaters, which was treated with vitreous tap and intravitreal antibiotics. The patient had a pre-PPV visual acuity of 6/9, which worsened after the endophthalmitis to 6/24 at 9 months partially limited by the nuclear sclerotic cataract. Similarly, Park et al42 have published a large, prospective nation-wide study looking at endophthalmitis after PPV in UK. In their series, 28 out of a total of 48 433 eyes (1 in 1730) undergoing vitrectomy developed endophthalmitis. Two of the patients developed this complication after surgery for SVO, with one patient regaining a visual acuity of 6/9 at 6 months, whilst the other developed CMO and ended up with a visual acuity of 6/96.（玻切可能導致眼內炎）

68% of patients had floaters for >6 months with most marked symptoms generally on reading（68%的人在閱讀時漂浮物很明顯）

Mason et al,23 73% of patients described their daily severity of symptoms as ‘severe’ or ‘very severe’, 50% had problems with reading, 30% with driving, 12% with occupational tasks, and 8% with leisure activities.（73%的患者將其日常癥狀嚴重程度描述為“嚴重”或“非常嚴重”，50%的患者有閱讀問題，30%的患者有駕駛問題，12%的患者有職業任務，8%的患者有休閑活動問題。）

In series where full vitrectomy was carried out for floaters, Tan et al6 reported the incidence of cataract at 50% over a mean follow-up of 10.1 months. This is comparable to the incidence of 60% given by Schulz-Key et al5 over a mean follow-up period of 37 months. In the study by de Nie et al,21 of 50 eyes with clear lens before surgery, 19 eyes (38%) underwent cataract surgery during a period of 26.4 months. FOV with sparing of anterior vitreous is theoretically more lens friendly and the reported rate of cataract formation is lower at 23.5% (over 15 months) and 22.5% (over 18 months) in the two large studies by Sebag et al39 and Mason et al.23（定點玻切一兩年內23%會出現渾濁）

The subsequent work by Delaney et al30 was even less encouraging; the authors concluded that intravitreal Nd-YAG vitreolysis relieved symptoms in only a third of patients and the clinical improvement was only moderate in degree, subjectively being graded at no greater than 50% by 93.3% of patients.30 Moreover, in no patient was there a complete resolution of symptoms. Also laser treatment led to worsening of symptoms in 7.7% of their patients.（玻璃體腔內Nd-YAG玻璃體溶解術僅能緩解三分之一患者的癥狀，臨床改善程度僅為中度，93.3%的患者主觀評分不超過50%。30此外，沒有一名患者的癥狀完全消失。激光治療也導致7.7%的患者癥狀惡化。）

There has been a recent report of a risk of refractory open-angle glaucoma following Nd-YAG vitreolysis of vitreous floaters.52 Cowan et al52 have reported on 3 eyes of 2 patients who presented with an intraocular pressure of >40 mm Hg at varying intervals (1 week to 8 months) after this procedure. Initially all eyes were managed medically with two of them requiring selective laser trabeculoplasty and two needing glaucoma-drainage surgery with trabectome before intraocular pressure stabilised. This risk was not linked to inflammation or steroid use. The authors hypothesised that vitreous micro-debris or macrophages laden with vitreous material may have migrated anteriorly and blocked the trabecular meshwork. Intraocular pressure rise following laser vitreolysis has also been reported by Little et al,51 but it has mostly been for eyes with vitreous strands to cataract wounds and the spike of pressure has been temporary. A protracted and chronic rise in intraocular pressure presumed to be owing to decrease in outflow facility of the trabecular meshwork has not been reported by the few other studies on this subject, and this risk may need further investigation.（激光后的碎片會堵塞小梁網導致眼壓上升、開角型青光眼）

Phacoemulsification combined with deep anterior vitrectomy.
Finally phacoemulsification combined with deep anterior vitrectomy through a posterior curvilinear capsulorhexis has also been described for symptomatic floaters.4 However, there is only one paper of 10 eyes describing this technique, the major limitation being that this technique is limited to elderly individuals with advancing lens opacities and can only treat floaters in the anterior vitreous. Also cystoid macular oedema was seen post-operatively in 2 of the 10 eyes described in this paper.（聲乳化聯合深前段玻璃體切除術。

最后，對于有癥狀的漂浮物，超聲乳化聯合經后囊環形撕囊的深部前部玻璃體切除術也有報道。4然而，只有一篇10只眼的論文描述了這項技術，主要的局限性在于，這項技術僅限于患有晶狀體混濁的老年人，并且只能治療玻璃體前部的漂浮物。本文描述的10只眼中有2只眼術后出現黃斑囊樣水腫。）

?Eventually the patient should make an informed decision based on whether living with the functional consequences of a non-blinding condition outweighs the option of a highly efficacious but not risk-free procedure.（最終，患者應該根據生活在非致盲狀態下的功能性后果是否比選擇高效但非無風險的手術更重要，做出明智的決定。）

上面內容來自【4】

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Type VI collagen
Type VI collagen is a ubiquitous component of extracellular matrices and has been identified in small quantities in human and bovine vitreous.29 It is not a component of the heterotypic collagen fibrils but instead forms separate microfibrils. Type VI collagen has been shown to bind fibrillar collagens and HA,30 so it could have a role in linking together the heterotypic collagen fibrils and HA in vitreous.

（VI型膠原

VI型膠原是細胞外基質中普遍存在的成分，在人和牛的玻璃體中已被少量鑒定。29它不是異型膠原纖維的組成部分，而是形成單獨的微纖維。VI型膠原已被證明能結合原纖維膠原和透明質酸30，因此它可能在連接玻璃體中異型膠原原纖維和透明質酸方面發揮作用。）

Hyaluronan
HA is the predominant GAG in mammalian vitreous and was first isolated from bovine vitreous humour more than 70 years ago.38 It is a linear, polymeric GAG built from repeating disaccharide units (β1–4 glucuronic acid β1–3 N-acetylglucosamine)n. Chains of HA can be very long and form networks through entanglement. It is distinguished from the other GAGs in that it is not synthesised covalently, linked to a core protein, and it is never sulphated. HA is not uniformly distributed within the vitreous and is found in the highest concentration in the posterior vitreous cortex.10 In adult human vitreous, the HA concentration has been estimated to be between 65 and 400?μg/ml and the average molecular weight to be 2–4 million.

（透明質酸

HA是哺乳動物玻璃體中的主要GAG，70多年前首次從牛玻璃體中分離。38它是由重復的二糖單元（β1-4葡萄糖醛酸β1-3 N-乙酰葡萄糖胺）N構成的線性聚合物GAG。HA鏈可以很長，通過纏結形成網絡。它與其他GAG的區別在于，它不是共價合成的，與核心蛋白相連，而且從不硫酸化。透明質酸在玻璃體內分布不均勻，在玻璃體后部皮質中濃度最高。10在成人玻璃體中，HA濃度估計在65到400之間?μg/ml，平均分子量為200-400萬。）

Chondroitin sulphate proteoglycans
The repeating disaccharide unit of CS is (β1–4 glucuronic acid β1–3 N-acetylgalactosamine)n. The C-4 and/or C-6 of the N-acetylgalactosamine residues can be sulphated, modifying this repeating structure. The C-2 sulphation of the glucuronic acid occurs less frequently. The vitreous has been shown to contain two CS proteoglycans, type IX collagen (see section on collagens) and versican.15, 39 Versican is a large proteoglycan with a central domain that carries multiple CS chains. The C-terminal region contains EGF-like, lectin-like, and complement regulatory protein-like domains and the globular N-terminal region contains an HA-binding domain. The binding of versican to HA is stabilised by a glycoprotein called link protein, which has also been identified in the vitreous.39 Mutations that alter the splicing of the central CS-bearing domains of versican have been implicated in the vitreoretinopathy Wagner's syndrome.40（硫酸軟骨素蛋白多糖

CS的重復雙糖單元是（β1-4葡萄糖醛酸β1-3 N-乙酰半乳糖胺）N。N-乙酰半乳糖胺殘基的C-4和/或C-6可以被硫酸化，從而改變這種重復結構。葡萄糖醛酸的C-2硫酸化發生的頻率較低。玻璃體中含有兩種CS蛋白多糖，即IX型膠原（見膠原一節）和versican。15,39 Versican是一種大型蛋白多糖，其中心結構域攜帶多條CS鏈。C端區域包含EGF樣、凝集素樣和補體調節蛋白樣結構域，球狀N端區域包含HA結合結構域。versican與HA的結合由一種叫做link protein的糖蛋白穩定，這種糖蛋白也在玻璃體中被發現。39個突變改變了云芝can中央CS承載結構域的剪接，這些突變與玻璃體視網膜病變瓦格納綜合征有關。）

Full size image
The network of (heterotypic) collagen fibrils is essential to the gel state as removal by, for example, collagenase digestion or centrifugation converts the vitreous into a viscous liquid.45 The vitreous collagen fibrils are very long, of uniform diameter (10–20?nm depending upon species), and unbranched (Figure 3a).14 Analyses by freeze-etch rotary shadowing electron microscopy showed that the collagen fibrils are arranged in bundles within the vitreous and form an extended interconnected network by branching between these bundles.46 In the young vitreous, the collagen fibrils within these bundles appear to run closely together in parallel, but are not fused. Morphological analyses suggest that the CS chains of type IX collagen play a role in both connecting together and spacing apart the collagen fibrils within these bundles.7, 47（全尺寸圖像

由于膠原酶消化或離心等方法將玻璃體轉化為粘性液體，因此（異型）膠原纖維網絡對凝膠狀態至關重要。45玻璃體膠原纖維非常長，直徑均勻（10-20）?14冷凍蝕刻旋轉陰影電子顯微鏡分析表明，膠原原纖維在玻璃體內成束排列，并通過這些束之間的分支形成一個擴展的互連網絡。46在年輕的玻璃體中，這些束中的膠原纖維似乎緊密地平行排列，但沒有融合。形態學分析表明，IX型膠原的CS鏈在連接和分隔這些束中的膠原原纖維方面起作用。）

?It occurs in approximately 25% of the population during their lifetime（25%的人會在一生中玻璃體后脫離）

Vitreous liquefaction
The human vitreous humour undergoes an inevitable process of liquefaction (or syneresis) with ageing. Studies by Balazs and Denlinger10 showed that liquid vitreous is present after the age of 4 years with around 20% of the total vitreous volume consisting of liquid vitreous by 14–18 years of age. After the age of 40 years, there is a steady increase in liquid vitreous with a concomitant decrease in gel volume. More than half of the vitreous is liquid by the age of 80–90 years. The liquefaction process does not occur uniformly within the vitreous cavity. The pockets of liquid form in the central vitreous where they enlarge and coalesce.

（玻璃體液化

隨著年齡的增長，人類的玻璃體液不可避免地會發生液化（或脫水）。Balazs和Denlinger10的研究表明，4歲后會出現液態玻璃體，14-18歲時，液態玻璃體占玻璃體總體積的20%左右。40歲以后，液體玻璃體的數量穩步增加，同時凝膠的體積也隨之減少。超過一半的玻璃體在80-90歲時是液態的。玻璃體腔內的液化過程并不均勻。液體囊在玻璃體中央形成，并在那里擴大和合并。）

Reference：

【1】Age-related changes on the surface of vitreous collagen fibrils

【2】豬喉軟骨硫酸軟骨素的制備和自由基清除活性 - 道客巴巴

【3】Glycosaminoglycans from bovine eye vitreous humour and interaction with collagen type II - PMC

【4】Vitrectomy for primary symptomatic vitreous opacities: an evidence-based review | Eye

【5】Adult vitreous structure and postnatal changes

【6】[Histochemistry of hyaluronic acid of the bovine vitreous body by electronmicroscopy] - PubMed

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