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Development of vitreous humor

Development of vitreous humor


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I have tried reading about development of vitreous humor but it is all very confusing. When does it first developed ? Does it renew itself ? Please provide reliable sources…


Look at this scheme -

As I stated before, vitreous is 99% water and is not an organ itself, thus the "replacement of vitreous" is actually = 99% water re-production and the only organ inside the eye which can perform this - ciliary body.

Consequently, if the vitreous was removed and replaced by gas or saline it will be replaced by aqueous which produced by ciliary body - this process takes 8 weeks to completely replace foreign substance as a gas by aqueous.


Structure of Human Eye (With Diagram) | Human Body

The eye is a hollow, spherical structure measuring about 2.5 cm in diameter.

Its wall is composed of three coats:

1. The outer fibrous coat— sclera, cornea.

2. The middle vascular coat— choroid, ciliary body, iris.

3. The inner nervous coat— retina.

It is divided into the sclera and the cornea.

It covers most of the eye ball. The sclera or white of the eye contains many collagen fibres. It protects and maintains shape of the eye ball.

It is a transparent portion that forms the anterior one- sixth of the eyeball. The cornea admits and helps to focus light waves as they enter the eye. The cornea is avascular (i.e., gets no blood supply). This part of eye absorbs oxygen from the air. The cornea was one of the first organs to be successfully transplanted because it lacks blood vessels.

At the junction of the sclera and cornea there is a structure called the canal of Schlemm. From the anterior chamber the aqueous humour, which is continuously produced, is drained off into the canal of Schlemm and then into the blood.

It comprises the choroid, the ciliary body and the iris.

The choroid lies adjacent to the sclera and contains numerous blood vessels that supply nutrients and oxygen to the other tissues especially of retina. It also contains pigmented cells that absorb light and prevent it from being reflected within the eyeball.

The ciliary body extends towards the inside of the eye from the choroid coat. It is composed of the ciliary muscles and the ciliary processes. The ciliary pro­cesses secrete aqueous humour.

The ciliary muscles are smooth muscles and are of two types: circular and meridional. Attached to the ciliary body are the suspensory ligaments, which are in turn attached to the cap­sule that surrounds the lens of the eye. The capsule and ligaments, to­gether with the ciliary body, hold the lens in place.

The iris is a circular muscular diaphragm containing the pigment giving eye its colour. It sepa­rates the aqueous humour region into anterior and posterior chambers. It extends from the cili­ary body across the eyeball in front of the lens. It has an opening in the centre called the pupil. It contains two types of smooth muscles, circular muscles (sphincters) and radial muscles (dilators), of ectodermal origin.

The iris controls the amount of light entering the eye by the radial muscles contracting in dim light and the circular muscles contracting in bright light.

Both of these sets of muscles are under the control of the autonomic nervous system. Sympathetic stimulation causes the radial muscles to contract and the pupil to dilate, or get larger. Parasympathetic stimulation causes the circular muscles to contract and the pupil to constrict.

3. Neural Coat— The Retina:

The retina is the neural and sensory layer of the eye ball. Its external surface is in contact with the choroid and its internal surface with the vitreous humour. A small oval, yellowish area of the retina lying exactly opposite the centre of the cornea is named the macula lutea or yellow spot which has at its middle a shallow depression, the fovea centralis. The fovea centralis has cone cells only.

It is devoid of rods and blood vessels. The fovea centralis is the place of most distinct vision. Here the nerve fibres from the light-sensitive cells leave the eyeball to form the optic nerve.

An artery and a vein also pass through the optic disc. This area is called the blind spot because it is devoid of receptor cells. Ora serrata (= ora terminalis) is a special structure which demarcates the sensitive part of retina from its non-sensory part.

Beginning from the external surface (choroid side), the retina consists of the following layers:

This layer lies close to the choroid. It consists of a single layer of cells containing pigment. These pigment cells appear to be rectangular in vertical section, their width being greater than their height. The cells give rise to pigmented pro­cesses (projections), extending into the next layer.

(ii) Layer of Rods and Cones:

The rods are processes of rod cells and cones are processes of cone cells. The total number of rods in the human retina has been estimated at 110 to 125 million and cones at 6.3 to 6.8 million (Osterberg 1935).

The rods contain a photosensitive pigment called the rhodopsin (= visual purple). Rhodopsin is composed of opsin and retinene. The opsin is a protein and is called scotopsin in rhodopsin. The retinene is an aldehyde of vitamin A and is also called retinal.

The rods mainly enable the animal to see in the darkness, therefore, rods are present in large number in nocturnal animals. The photosensitive pigment in the cones is of three types namely: porpyrosin, iodopsin and cyanopsin which give response to red, green and blue light respectively.

The sensations of different colours are produced by various combinations of these three types of cones and their photo-pigments. When the three types of cones are stimulated equally, a sensation of white light is produced. The protein in cone pigment is called photopsin, which is different from scotopsin of rhodopsin.

(iii) External Nuclear Layer:

This layer contains the cell bodies and nuclei of rod and cone cells.

(iv) External Plexiform Layer (= Outer Synaptic zone):

This layer consists only of nerve fibres that form a plexus (network). The axons of rods and cones synapse here with dendrites of bipolar neurons. Processes of horizontal cells also take part in the formation of these synapses.

(v) Internal Nuclear Layer:

This layer contains the cell bodies and nuclei of three types of neurons:

(vi) Internal Plexiform Layer. (= Inner Synaptic Zone):

This layer consists of synapsing nerve fibres of bipolar neurons, ganglion cells and amacrine cells. This layer also contains some horizontally placed internal plexiform cells and also a few ganglion cells.

(vii) Layer of Ganglion Cells:

This layer contains the cell bodies of ganglion cells. Axon of each ganglion cell gives rise to a fibre of the optic nerve.

(viii) Layer of Optic Nerve Fibres:

This layer is made up of axons of ganglion cells that form the optic nerve. The optic nerves are connected with the brain. The nerve fibres from all parts of the retina converge to leave through a blind spot (= Optic disc) which contains no rods and cones and, therefore, no image is formed at this spot.

Retinal Gliocytes (= Cells of Muller):

In addition to bipolar, horizontal neurons and amacrine cells, the internal nuclear layer also contains the cell bodies of the retinal gliocytes (= cells of Muller). These cells form numerous protoplasmic processes that extend through almost the whole thickness of the retina and form external and internal limiting mem­branes.

The internal limiting membrane separates the retina from the vitreous humour. Retinal gliocytes support the neurons of the retina and may en-sheath them. They also have nutritive function. Some astrocytes (other glial cells) are also present in between the retinal neurons.

Contents of the Eye Ball:

It is a transparent, biconvex, elastic structure that bends light waves as they pass through its surfaces. The lens separates the aqueous and vitreous humours. It is composed of epithelial cells that have large amounts of clear cytoplasm in the form of fibres.

Its capsule is composed of layers of intercellular protein. The lens can change shape from moment to moment and, by doing so, focuses light waves into the retina from objects at different distances from the eye. The lens can also change shape from year to year, thereby accounting for changes in vision.

The space between the cornea and the lens is called the aqueous chamber which contains a thin watery fluid called aqueous humour. The epithelium of the ciliary process continuously secretes a watery fluid, the aqueous humour.

The aqueous humour helps to maintain the shape of the front part of the eye and provides nutrients to the lens and cornea. As stated earlier, the aqueous humour is continuously drained off into the canal of Schlemm and then into the blood. The pressure in the eye, called intraocular pressure is produced mainly by the aqueous humour.

The space between the lens and retina is called the vitreous chamber which is filled with a transparent gel called the vitreous humour.

It helps to maintain the shape of the eyeball and also contributes to intraocular pressure (pressure inside the eyeball). Unlike the aqueous humour, the vitreous humour cannot be replaced in any significant quantity. Therefore, in puncture wounds of the eye it is important to prevent the escape of vitreous humour.

Extrinsic Eye Muscles and their Nerve Supply:

There are six extrinsic muscles attached to the eyeball. Four of these muscles are straight and two are oblique. These muscles are median rectus, lateral rectus, superior rectus, inferior rectus, superior oblique and inferior oblique.

The oculomotor (3rd cranial nerve) innervates the median rectus, superior rectus, inferior rectus and inferior oblique. The trochlear (4th cranial nerve) supplies the superior oblique. The abducens (6th cranial nerve) innervates the lateral rectus.

The Accessory Structures of the Eye:

These include the eyebrows, the eyelids and eyelashes, the conjunctiva and the lacrimal apparatus.

These are two arched eminences of skin surmounting the supra­orbital margins of the frontal bone. Numerous hairs project obliquely from the surface of the skin. The function of the eyebrows is to protect the anterior aspect of the eyeball from sweat, dust and other foreign bodies.

2. The Eyelids (Palpebrae) and Eyelashes:

The eyelids are two movable folds situated above and below front of the eye. On their free edges, there are outgrowths of hairs— the eyelashes. The third eyelid is vestigial and is called plica semilunaris (nictitating mem­brane). The inner surface of each eyelid and parts of the eyeball are covered with mucous membrane, called the conjunctiva.

Glands of Zeis are modified sebaceous glands which are associated with the follicles of eye lashes. They open into the follicles of eye lashes. Meibomian or tarsal glands are also modified sebaceous glands (oil glands) which are present along the edges of the eyelids.

They produce an oily secretion which serves to lubricate the corneal surface and hold a thin layer of tears over the comea. Glands of Moll are modified sweat glands at the edge of the eye lid.

It is a transparent mucous membrane, which covers the internal palpe­bral surfaces, and folds on to the anterior sclera and comea where it is continuous with the comeal epithelium. The conjunctiva helps to protect the eye ball and keeps it moist. It is this membrane that becomes inflamed in conjunctivitis or “pink eye”.

4. The Lacrimal Apparatus:

The lacrimal apparatus of each eye consists of a lacri­mal gland and its numerous ducts, the superior and inferior canaliculi, a lacrimal sac and a nasolacrimal duct. The lacrimal gland is situated in the orbit on the superior, lateral surface of the eyeball.

The lacrimal gland secretes tears which are composed of water, salts and bactericidal protein called lysozyme. The tears flow into the superior and inferior canaliculi, then to the lacrimal sac and through the nasolacrimal duct into the nasal cavity.

The function of tears is to bathe the front of the eye, washing away any dust, grit and microorganisms. Lysozyme destroys microorganisms present on the front of the eyeball. In emotional states the secre­tion of tears may be increased and if the nasolacrimal duct cannot carry them all into the nasal cavity, they overflow. Gland cells in the conjunctiva also secrete a mucous substance that is a component of tears.

A layer of adipose tissue surrounds the eyeball in the orbit. It serves as a soft, shockproof pad.

The light rays pass through comea, aqueous humour, lens and vitreous humour and focus on retina where they generate potentials (impulses) in rods and cones. As we know, human eyes have remarkable power of accommodation by changing the convexity of the lens.

By the action of iris muscles the size of pupil can be increased or decreased. In bright light the pupil is constricted. In dim light it is dilated. Due to the action of the muscles of the ciliary body and the suspensory ligament, the focal length of the lens can be changed. Then the objects can be focused in different intensity of light from varying distances.

The photosensitive compounds (photo pigments) in the human eyes are composed of opsin (a protein) and retinal (an aldehyde of vitamin A). Light induces dissociation of retinal from opsin which changes the structure of the opsin. Thus potential differences are generated in the photoreceptor cells.

This causes action potentials in the ganglion cells through the bipolar cells. These action potentials (impulses) are transmitted by the optic nerves to the visual cortex area in the occipital lobe of the cerebral hemisphere of the brain where the neural impulses are analysed and erect image is recognised.

In the darkness, rhodopsin is resynthesized from opsin and retenene to restore the dark vision. It is called dark adaptation. It is considered that there are three different kinds of cones, each of which contains a different light-sensitive pigment,

(a) Cones that contain erythrolable are most sensitive to red light,

(b) Cones that contain chlorolable are most sensitive to green light,

(c) Cones that contain cyanolable are most sensitive to blue light.

Combinations of these three colours of light produce all the colours human can see. This is in accordance with the trichromacy theory.

When both the eyes can be focused simultaneously on a common object, as in human eyes, it is called binocular vision. It is just reverse to the monocular vision, as in many animals like rabbit, in which each eye focuses its own object and both the eyes cannot focus on one object.


Apart from the degeneration of age, there are other causes that can cause, favor or anticipate the onset of a DPV.

Symptoms of DPV

When the vitreous is detached, in case of symptoms, the most frequent are the appearance of &ldquomyodesopsia or flying flies&rdquo that are seen suddenly when looking at clear areas and move with the movement of the eyes explained by Kang Zhang. This may be due to the fact that the vitreous is attached through the hyaloid to the retina and when it detaches it can cause small vitreous bleeding or because the junction between the hyaloid and the optic nerve (weiss ring) becomes visible as an opacity .

What possible consequences does it have?

We must say that the posterior vitreous detachment is not in itself pathology but is a physiological process resulting from the natural development of the eye. This process usually takes place without incident, but exceptionally, when the hyalloid separates from the retina, it can pull it and produce a small bleeding (vitreous hemorrhage) and even a retinal detachment whose main symptom is the appearance of a «curtain »In the visual field.

Vitreous detachment is a physiological process resulting from the natural development of the eye.

Given the circumstances, it is very important to go to periodic ophthalmological examinations and in case the vitreous humor separation process is detected, a specialist will check that it is carried out normally and without causing damage to the retina. In addition, in those patients who have suffered retinal tears or hemorrhages during the vitreous detachment of one of their eyes, they must remain attentive to the appearance of symptoms in the other because it increases the risk of suffering from these problems.

Weiss ring

Some vitreous detachments make the Weiss ring visible, which is the area where the hialoid adheres to the optic nerve.

IMPORTANT: If a person notices a sudden increase in the size and quantity of floating spots (myodesopsia) accompanied or not by the appearance of light flashes (photopsies), it should be evaluated by an ophthalmologist who assesses and discards lesions such as a retinal detachment or other similar injuries result from vitreous traction during detachment.

Should I follow any treatment?

Despite the annoyance of vitreous opacities (flying flies or floating bodies) that may appear as a result of detachment, this circumstance is generally harmless and does not require treatment . The most frequent is that, after a while, we stop visualizing these opacities. Otherwise, the possibility of applying laser vitreolysis to dissolve vitreous floats that impede correct vision could be assessed.

Ophthalmological treatment is required in cases where the movement of the vitreous gel and its separation cause holes or tears that damage the retina. In these cases, an Argon laser treatment is applied that generates a barrier around the affected area of ​​the retina and strengthens it.

Generally the vitreous detachment does not require treatment, but it does check the ophthalmologist to verify that everything happens normally.

Frequently asked questions (FAQ)

If I have had DPV, can I have cataract surgery?

Without a doubt, YES. Having suffered a posterior vitreous detachment does not contraindicate cataract surgery. So much so, that it is estimated that more than 50% of people over 65 who are operated on cataracts have in turn the vitreous detached.

For added safety, the ophthalmologist scans the fundus for possible retinal lesions before surgery.

Can it be cured or corrected?

No, but it doesn’t require it either. A detachment of vitreous humor that is carried out correctly and in a controlled manner is completely harmless and does not alter vision so it does not have a treatment. The treatment for its possible consequences in case they originate.

How do I know if I have vitreous detachment?

There are no unambiguous symptoms and those that do not always manifest themselves. The sudden appearance of floating bodies is an indication. It is usually diagnosed in an ophthalmologic office and most of the time in routine eye exams.


Contents

Floaters are from objects in pockets of liquid within the vitreous humour, the thick fluid or gel that fills the eye, [7] or between the vitreous and the retina. The vitreous humour, or vitreous body, is a jelly-like, transparent substance that fills the majority of the eye. It lies within the vitreous chamber behind the lens, and is one of the four optical components of the eye. [8] Thus, floaters follow the rapid motions of the eye, while drifting slowly within the pocket of liquid. When they are first noticed, the natural reaction is to attempt to look directly at them. However, attempting to shift one's gaze toward them can be difficult because floaters follow the motion of the eye, remaining to the side of the direction of gaze. Floaters are, in fact, visible only because they do not remain perfectly fixed within the eye. Although the blood vessels of the eye also obstruct light, they are invisible under normal circumstances because they are fixed in location relative to the retina, and the brain "tunes out" stabilized images through neural adaptation. [3]

Floaters are particularly noticeable when looking at a blank surface or an open monochromatic space, such as blue sky. Despite the name "floaters", many of these specks have a tendency to sink toward the bottom of the eyeball, in whichever way the eyeball is oriented the supine position (looking up or lying back) tends to concentrate them near the fovea, which is the center of gaze, while the textureless and evenly lit sky forms an ideal background against which to view them. [7] The brightness of the daytime sky also causes the eyes' pupils to contract, reducing the aperture, which makes floaters less blurry and easier to see.

Floaters present at birth usually remain lifelong, while those that appear later may disappear within weeks or months. [9] They are not uncommon, and do not cause serious problems for most persons they represent one of the most common presentations to hospital eye services. A survey of optometrists in 2002 suggested that an average of 14 patients per month per optometrist presented with symptoms of floaters in the UK. [10] However, floaters are more than a nuisance and a distraction to those with severe cases, especially if the spots seem constantly to drift through the field of vision. The shapes are shadows projected onto the retina by tiny structures of protein or other cell debris discarded over the years and trapped in the vitreous humour or between the vitreous and retina. Floaters can even be seen when the eyes are closed on especially bright days, when sufficient light penetrates the eyelids to cast the shadows. [ citation needed ] It is not, however, only elderly persons who are troubled by floaters they can also become a problem to younger people, especially if they are myopic. They are also common after cataract operations or after trauma.

Floaters are able to catch and refract light in ways that somewhat blur vision temporarily until the floater moves to a different area. Often they trick persons who are troubled by floaters into thinking they see something out of the corner of their eye that really is not there. Most persons come to terms with the problem, after a time, and learn to ignore their floaters. For persons with severe floaters it is nearly impossible to ignore completely the large masses that constantly stay within almost direct view.

There are various causes for the appearance of floaters, of which the most common are described here.

Floaters can occur when eyes age in rare cases, floaters may be a sign of retinal detachment or a retinal tear. [11]

Vitreous syneresis Edit

The cause of a vitreous floater is due to vitreous syneresis (liquefaction) and contraction with age. Additionally, trauma or injury to the globe can cause vitreous floaters. [12]

Vitreous detachments and retinal detachments Edit

In time, the liquefied vitreous body loses support and its framework contracts. This leads to posterior vitreous detachment, in which the vitreous membrane is released from the sensory retina. During this detachment, the shrinking vitreous can stimulate the retina mechanically, causing the patient to see random flashes across the visual field, sometimes referred to as "flashers", a symptom more formally referred to as photopsia. The ultimate release of the vitreous around the optic nerve head sometimes makes a large floater appear, usually in the shape of a ring ("Weiss ring"). [13] As a complication, part of the retina might be torn off by the departing vitreous membrane, in a process known as retinal detachment. This will often leak blood into the vitreous, which is seen by the patient as a sudden appearance of numerous small dots, moving across the whole field of vision. Retinal detachment requires immediate medical attention, as it can easily cause blindness. Consequently, both the appearance of flashes and the sudden onset of numerous small floaters should be rapidly investigated by an eye care provider. [14]

Posterior vitreous detachment is more common in people who:

  • are nearsighted
  • have undergone cataract surgery
  • have had Nd:YAG laser surgery of the eye
  • have had inflammation inside the eye. [15]

Regression of the hyaloid artery Edit

The hyaloid artery, an artery running through the vitreous humour during the fetal stage of development, regresses in the third trimester of pregnancy. Its disintegration can sometimes leave cell matter. [16]

Other common causes Edit

Patients with retinal tears may experience floaters if red blood cells are released from leaky blood vessels, and those with uveitis or vitritis, as in toxoplasmosis, may experience multiple floaters and decreased vision due to the accumulation of white blood cells in the vitreous humour. [17]

Other causes for floaters include cystoid macular edema and asteroid hyalosis. The latter is an anomaly of the vitreous humour, whereby calcium clumps attach themselves to the collagen network. The bodies that are formed in this way move slightly with eye movement, but then return to their fixed position. [ citation needed ]

Floaters are often readily observed by an ophthalmologist or an optometrist with the use of an ophthalmoscope or slit lamp. However, if the floater is near the retina, it may not be visible to the observer even if it appears large to the patient.

Increasing background illumination or using a pinhole to effectively decrease pupil diameter may allow a person to obtain a better view of his or her own floaters. The head may be tilted in such a way that one of the floaters drifts towards the central axis of the eye. In the sharpened image the fibrous elements are more conspicuous. [18]

The presence of retinal tears with new onset of floaters was surprisingly high (14% 95% confidence interval, 12–16%) as reported in a meta-analysis published as part of the Rational Clinical Examination Series in the Journal of the American Medical Association. [19] Patients with new onset flashes and/or floaters, especially when associated with visual loss or restriction in the visual field, should seek more urgent ophthalmologic evaluation.

While surgeries do exist to correct for severe cases of floaters, there are no medications (including eye drops) that can correct for this vitreous deterioration. Floaters are often caused by the normal aging process and will usually become less bothersome as a person learns to ignore them. Looking up/down and left/right will cause the floaters to leave the direct field of vision as the vitreous humour swirls around due to the sudden movement. [20] If floaters significantly increase in numbers and/or severely affect vision, then one of the below treatments may be necessary.

As of 2017 [update] , insufficient evidence is available to compare the safety and efficacy of surgical vitrectomy with laser vitreolysis for the treatment of floaters. A 2017 Cochrane Review did not find any relevant studies that compared the two treatments. [21]

Aggressive marketing campaigns have promoted the use of laser vitreolysis for the treatment of floaters. [22] [23] No strong evidence currently exists for the treatment of floaters with laser vitreolysis. The strongest available evidence comparing these two treatment modalities are retrospective case series. [24]

Surgery Edit

Vitrectomy may be successful in treating more severe cases. [25] [26] The technique usually involves making three openings through the part of the sclera known as the pars plana. Of these small gauge instruments, one is an infusion port to resupply a saline solution and maintain the pressure of the eye, the second is a fiber optic light source, and the third is a vitrector. The vitrector has a reciprocating cutting tip attached to a suction device. This design reduces traction on the retina via the vitreous material. A variant sutureless, self-sealing technique is sometimes used.

Like most invasive surgical procedures, however, vitrectomy carries a risk of complications, [27] including: retinal detachment, anterior vitreous detachment and macular edema – which can threaten vision or worsen existing floaters (in the case of retinal detachment).

Laser Edit

Laser vitreolysis is a possible treatment option for the removal of vitreous strands and opacities (floaters). In this procedure an ophthalmic laser (usually a yttrium aluminium garnet (YAG) laser) applies a series of nanosecond pulses of low-energy laser light to evaporate the vitreous opacities and to sever the vitreous strands. When performed with a YAG laser designed specifically for vitreolysis, reported side effects and complications associated with vitreolysis are rare. However, YAG lasers have traditionally been designed for use in the anterior portion of the eye, i.e. posterior capsulotomy and iridotomy treatments. As a result, they often provide a limited view of the vitreous, which can make it difficult to identify the targeted floaters and membranes. They also carry a high risk of damage to surrounding ocular tissue. Accordingly, vitreolysis is not widely practised, being performed by very few specialists. One of them, John Karickhoff, has performed the procedure more than 1,400 times and claims a 90 percent success rate. [28] However, the MedicineNet web site states that "there is no evidence that this [laser treatment] is effective. The use of a laser also poses significant risks to the vision in what is otherwise a healthy eye." [29]

Medication Edit

Enzymatic vitreolysis has been trialed to treat vitreomacular adhesion (VMA) and anomalous posterior vitreous detachment. Although the mechanism of action may have an effect on clinically significant floaters, as of March 2015 [update] there are no clinical trials being undertaken to determine whether this may be a therapeutic alternative to either conservative management, or vitrectomy. [30]

A vitreous detachment typically affects patients older than the age of 50 and increases in prevalence by age 80. Individuals who are myopic or nearsighted have an increased risk of vitreous floaters. Additionally, eyes with an inflammatory disease after direct trauma to the globe or have recently undergone eye surgery have an increased chance of developing a vitreous floater. Men and women appear to be affected equally. [12]


What are the symptoms of vitreous detachment?

The most common symptom of vitreous detachment is a sudden increase in floaters (small dark spots or squiggly lines that float across your vision). When your vitreous detaches, strands of the vitreous often cast new shadows on your retina — and those shadows appear as floaters.

You may also notice flashes of light in your side (peripheral) vision.

Sometimes, vitreous detachment causes more serious eye problems that need treatment right away. The only way to tell if vitreous detachment has caused a serious eye problem is to get a dilated eye exam. So if you notice symptoms of vitreous detachment, it’s important to go to your eye doctor right away.

If your vitreous detachment doesn’t cause a serious eye problem, you’ll probably stop noticing symptoms as much after a few months.


Abstract

Initial triggers for diabetic retinopathy (DR) are hyperglycemia-induced oxidative stress and advanced glycation end-products. The most pathological structural changes occur in retinal microvasculature, but the overall development of DR is multifactorial, with a complex interplay of microvascular, neurodegenerative, genetic/epigenetic, immunological, and secondary inflammation-related factors. Although several individual factors and pathways have been associated with retinopathy, a systems level understanding of the disease is lacking. To address this, we performed mass spectrometry based label-free quantitative proteomics analysis of 138 vitreous humor samples from patients with nonproliferative DR or the more severe proliferative form of the disease. Additionally, we analyzed samples from anti-VEGF (vascular endothelial growth factor) (bevacizumab)-treated patients from both groups. In our study, we identified 2482 and quantified the abundancy of 1351 vitreous proteins. Of these, the abundancy of 230 proteins was significantly higher in proliferative retinopathy compared with nonproliferative retinopathy. This specific subset of proteins was linked to inflammation, complement, and coagulation cascade proteins, protease inhibitors, apolipoproteins, immunoglobulins, and cellular adhesion molecules, reflecting the multifactorial nature of the disease. The identification of the key molecules of the disease is critical for the development of new therapeutic molecules and for the new use of existing drugs.


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Ageing processes in the vitreous

PVD is a process whereby the cortical vitreous gel splits away from ILL on the inner surface of the retina as far anteriorly as the posterior border of the vitreous base (Figure 4). 48 It occurs in approximately 25% of the population during their lifetime. 48, 49 PVD can be localised, partial, or ‘complete’ (ie up to the posterior border of the vitreous base). PVD results from a combination of vitreous liquefaction and weakening of post-basal vitreoretinal adhesion. During PVD, separation of the basal vitreous from the peripheral retina and ciliary body does not occur because of the particularly strong adhesion in this region.

Age-related vitreous liquefaction and PVD. Pockets of liquid appear within the central vitreous that gradually coalesce. There is a concurrent weakening of postoral vitreoretinal adhesion. Eventually, this can progress to PVD, where the liquid vitreous dissects the residual cortical gel away from the ILL on the inner surface of the retina as far anteriorly as the posterior border of the vitreous base.

While in a majority of subjects PVD occurs without major complications, in some it has sight-threatening complications. The concept of anomalous PVD was introduced by Sebag 50 to describe the situation where the extent of liquefaction exceeds weakening of vitreoretinal adhesion. This results in tractional forces being exerted upon the retina during PVD and/or incomplete separation, thereby leading to complications including haemorrhage, retinal tears and detachment, macular hole formation, and vitreomacular traction syndrome. Conversely, ‘complete’ PVD protects against proliferative diabetic retinopathy, 51 because the newly formed blood vessels require the collagenous network of the cortical vitreous as a scaffold for growth and invasion. 52 In the presence of a PVD or following surgical vitrectomy, abortive neovascular outgrowths have been observed in the eyes of diabetic patients. 51

Vitreous liquefaction

The human vitreous humour undergoes an inevitable process of liquefaction (or syneresis) with ageing. Studies by Balazs and Denlinger 10 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.

Ultrastructural studies have shown that collagen fibrils aggregate with ageing into macroscopic strands within the vitreous gel. 53, 54 Age-related vitreous liquefaction may be caused by this gradual and progressive aggregation of the collagen fibrils, resulting in a redistribution of the collagen fibrils, leaving areas devoid of collagen fibrils and thereby converted into a liquid, and the collagen aggregates concentrated in the residual gel. 7, 47 An alternative hypothesis is that age-related liquefaction is a result of destruction of vitreous collagen fibrils, possibly due to enzymatic activity. 55 However, recent data substantiate the former hypothesis and provide a unifying explanation for age-related vitreous liquefaction. 47

Bos et al 47 demonstrated that there is an age-related loss of type IX collagen from the surface of the heterotypic collagen fibrils of the human eye. Indeed, the half-life for the type IX collagen was found to be just 11 years of age. The CS chains of type IX collagen are thought to space the collagen fibrils apart and their loss allows the collagen fibrils to directly come into contact with one another (Figure 3b). Furthermore, the loss of type IX collagen results in the increased surface exposure of ‘sticky’ type II collagen so that when the type II collagen on adjacent fibrils comes into contact, there is a propensity towards fibril fusion. 47 These conclusions are supported by a study showing that digestion of the vitreous with chondroitin ABC lyase, an enzyme that degrades the CS chains of type IX collagen, resulted in the aggregation of collagen fibrils. 56

HA provides a swelling pressure to the collagen network and hence the vitreous gel. Complete (enzymatic) removal of the HA resulted in gel shrinkage, but not complete collapse so HA is not a prerequisite for the gel structure. 57 However, this study only looked at the short-term effects of the removal of the HA and in the longer term, it is likely to be important for the stability of the gel. It was subsequently shown that HA weakly associates with vitreous collagen fibrils and that the HA network ‘stiffens’ the collagenous network, as hyaluronidase digestion resulted in deflation and relaxation of the collagen network. 46

Weakening of the vitreoretinal adhesion

In young eyes there is a strong adhesion between posterior vitreous cortex and the ILL of the retina however, this weakens with ageing and this weakening is likely to be due to biochemical changes at the vitreoretinal interface. As the cortical vitreous collagen fibrils do not generally insert directly into the post-oral ILL, the basis of this adhesion may be interactions between components on the surface of the vitreous collagen fibrils and macromolecules on the inner surface of the ILL.

It has been shown that collagen type XVIII contributes towards vitreoretinal adhesion in the mouse eye, as a proportion of eyes from type XVIII collagen-knockout mice had vitreoretinal disinsertion, 58 this could be due to abnormal development at the vitreoretinal interface or due to type XVIII collagen being directly involved in vitreoretinal adhesion. Type XVIII collagen is an HS proteoglycan and opticin binds to HS. 36 Therefore, the opticin on the surface of cortical vitreous collagen fibrils could bind HS proteoglycans of the ILL, including type XVIII collagen, thus providing a molecular basis for vitreoretinal adhesion (Figure 5). This hypothesis is supported by the colocalisation of opticin and type XVIII collagen at the vitreoretinal interface. 59 However, opticin-knockout mice do not appear to have spontaneous vitreoretinal disinsertion (unpublished observations), suggesting that other molecular interactions also contribute to vitreoretinal adhesion, at least in the mouse eye.

Diagram representing the postbasal vitreoretinal junction. Weakening of the adhesion at this interface predisposes to posterior vitreous detachment. Vitreoretinal adhesion may be dependent upon intermediary molecules acting as a ‘molecular glue’ and linking the cortical vitreous collagen fibrils to components of ILL. It is possible that opticin, because it binds to both vitreous collagen fibrils and HS proteoglycans in the ILL, contributes towards this ‘molecular glue’.

Posterior extension of the vitreous base

During PVD, the vitreoretinal separation only extends as far anteriorly as the posterior border of the vitreous base, as there is an unbreakable vitreoretinal adhesion within the vitreous base. This unbreakable adhesion is due to basal vitreous collagen fibrils running perpendicularly through defects in the ILL to merge with a network of collagen fibrils on the cellular side of the ILL or passing into ‘crypts’ within the cellular layers. 13, 42

The posterior border of the vitreous base is at the ora serrata at birth. However, it gradually migrates posteriorly as the vitreous base expands to form an annular ring that straddles the ora serrata. 13 The maximum observed width of the postoral vitreous base in this study was 3.7 mm. The extension of the vitreous base into the peripheral retina is due to synthesis of new ‘vitreous’ collagen by retinal cells. This collagen either forms a layer on the cellular side of the ILL or penetrates through defects in the ILL to intertwine with the pre-existing cortical vitreous collagen thereby creating new ‘unbreakable’ adhesions and extending the vitreous base posteriorly (Figure 6). 13 If irregularities are introduced into the posterior border of the vitreous base during this process, there will be a predisposition to postoral retinal break formation and subsequent retinal detachment.

Diagram representing the vitreoretinal junction within the vitreous base. There is a very strong adhesion at the vitreoretinal interface within the vitreous base because vitreous collagen fibrils insert directly into the posterior ciliary body and peripheral retina. The vitreous base extends posteriorly into the peripheral retina with ageing as a result of the adult peripheral retina synthesising new collagen. This new collagen forms a layer on the cellular side of the ILL, but some breaks through defects in the ILL and intertwines with pre-existing cortical vitreous collagen thereby creating new adhesions and extending the vitreous base posteriorly.


Vitreous Humor In The Eye Helps To Establish Time Of Death

A team of researchers from the University of Santiago de Compostela has proposed a new method to estimate the approximate time of death. This is based on the analysis of several substances from the vitreous humour of the eye of cadavers, according to an article published in the journal Statistics in Medicine.

Using this system, scientists have developed a piece of software that makes it possible to establish precisely the post mortem interval (PMI), information that will make the work of the police and the courts of justice easier.

To apply this technique the researchers analyse initially potassium, urea and hypoxantine (a DNA metabolite) concentrations present in the vitreous humour of the eye of the human cadaver, and introduce these figures into a computer programme. The software that has been invented by these Galician scientists uses this information and is capable of establishing the time at which death occurred.

&ldquoThe equations we have developed now make it possible for us to estimate the PMI more precisely than before, and provide a useful and accessible tool to forensic pathologists that is easy to use&rdquo José Ignacio Munoz Barús, one of the authors of the study, explains to SINC, and who is also a specialist doctor from the Institute of Legal Medicine at the University of Santiago de Compostela.

The traditional techniques for estimating the PMI are based on the study of parameters such as the rectal temperature of the cadaver or one of the organs, such as the liver, in rigor mortis, or post mortem lividity examination. These methods are complemented by biochemical analyses of the body fluids. One of these is the vitreous humour, the gelatinous liquid that is found behind the crystalline lens of the eye.

Muñoz Barús points out that the study, published recently in Statistics in Medicine, suggests mathematical models that are &ldquomore flexible, useful and efficient&rdquo than those that have been applied until now. The doctor describes some of the previous techniques as &ldquonot very reproducible, not very precise and untested in the field&rdquo, such as the deterioration of DNA, immunoreaction or the traditional techniques based on the biochemistry of the vitreous humour.

In this last case the researcher specifies that previous studies used a &ldquolinear regression mathematical model&rdquo which assumes that the concentrations of potassium, hypoxantine and urea increase in a linear way that is more or less constant throughout the post mortem interval. However, the new analyses suggest that those premises are not valid and that the statistical models known as generalized additive models (GAM) or the support vector machine (SVM) models are more flexible and much more useful, since they avoid the assumption of linearity&rdquo.

The precision and usefulness of these two models have been confirmed by chemical analysis in more than 200 vitreous humour samples. The doctor and the two mathematicians who have performed the study have verified that the SVM method offers more precise data, although the GAM method is more easy to assimilate to the linear model and understand graphically and numerically, &ldquo for which reason both complement each other&rdquo.

The three scientists have incorporated all this information into the development of a free computer package (based on code &ldquoR&rdquo) which makes it possible to establish the PMI using four predictive variables: concentrations of potassium, hypoxantine and urea, and cause of death. In addition, the software makes it possible to show the results graphically. &ldquoIn this way the estimation of the time of death and expert examination are made easier when attending the courts of justice&rdquo, Munoz Barús points out to SINC

&ldquoThe precise determination of the exact time of death has been the subject of various studies going back to the 19th century, since this information is of paramount importance in the field of legal medicine, owing to its repercussions on crime and civil society. This new method offers an important contribution to this field&rdquo, the researcher concludes.

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Watch the video: Anatomy of the Vitreous (November 2022).