Anytime subretinal fluid accumulates in the space between the neurosensory retina and the underlying retinal pigment epithelium (RPE), a retinal detachment occurs. Depending on the mechanism of subretinal fluid accumulation, retinal detachments traditionally have been classified into rhegmatogenous, tractional, and exudative.
A tractional retinal detachment (TRD) is the second most common type of retinal detachment after a rhegmatogenous retinal detachment (RRD).
In TRD secondary to proliferative vitreoretinopathy (PVR) and penetrating trauma, contractile vitreoretinal, epiretinal, intraretinal (very rarely), or subretinal membranes pull the neurosensory retina away from the RPE. PVR can be considered to represent an inappropriate or uncontrolled wound healing response. Microscopic examinations of these membranes have revealed their cellular composition. RPE cells, glial cells, fibrocytes, macrophages, and collagen fibrils are important components of these membranes. RPE cells are the major players in these membranes. They gain access to the vitreous cavity during retinal break formation. It has been shown that the amount of RPE cells in the vitreous cavity correlates with the size of the retinal breaks. The larger the break, the larger the amount of RPE cells intravitreally.
In addition, RPE cells also may be dispersed into the vitreous cavity by excessive cryotherapy, cryotherapy on bare RPE, and scleral indentation following cryotherapy. Once in the vitreous cavity, the RPE cells undergo morphological changes where they attain fibroblastlike activity, secreting growth factors that stimulate collagen and fibronectin production.
Cryotherapy also causes breakdown of the blood-ocular barrier, allowing serum to enter the eye. Serum components fibronectin and platelet-derived growth factor (PDGF) are strong chemoattractants for other RPE cells, astrocytes, and fibrocytes. Thus, one can understand the risk that vitreous hemorrhage poses in the chances of periretinal membrane formation. Once collagen sheets form, the individual cells pull on them, leading to TRD. Transforming growth factor beta (TGF-ß) is also a potent chemoattractant for monocytes and fibroblasts.  TGF-ß stimulates fibronectin synthesis and collagen contraction by RPE cells. [2, 3] Fibronectin may serve as a provisional matrix and scaffold for RPE cells in PVR membranes. It also induces conversion of RPE cells toward a fibroblastlike phenotype. In a rabbit model of PVR, decorin used as an adjuvant during vitrectomy reduced the amount of fibrosis and TRD. 
TRD may occur in a number of ocular pathologic conditions, such as proliferative diabetic retinopathy (PDR), sickling hemoglobinopathies, retinal venous obstructions, and retinopathy of prematurity (ROP), that are characterized by progressive retinal ischemia. Examples are shown in the images below.
Progressive retinal ischemia leads to secretion of growth factors, especially vascular endothelial growth factor (VEGF). Neovascularization ensues, and the vitreous serves as a scaffold where strong vitreoretinal adhesions develop. With time, as the vitreous starts pulling away, a mechanical separation of the neurosensory retina from the underlying RPE occurs.
At the molecular level, VEGF is the main driver of angiogenesis and the resulting neovascularization. VEGF upregulates the profibrotic growth factor connective tissue growth factor (CTGF) in various cell types in the newly formed neovascular membranes. Increasing levels of CTGF inactivate VEGF, and when the equilibrium between these two factors shifts to a certain threshold ratio, the neovascular membranes become more fibrotic and less vascular. Fibrosis driven by excess CTGF leads to scarring and blindness. 
In the past few years, intravitreal anti-VEGF agents have gained popularity in the treatment of several diseases of the posterior segment of the eye characterized by macular edema and intraocular neovascularization such as proliferative diabetic retinopathy (PDR) and retinopathy of prematurity (ROP). In addition, they have been used as presurgical adjuvants in diabetic vitrectomies and ROP. Despite the advantages of such treatment, caution must be exercised in eyes with advanced PDR and ROP since a rapid involution of the fibrovascular proliferation may lead to the development or the progression of a tractional retinal detachment. In the largest study to date, the earliest development or progression of a TRD occurred 5 days after the injection. Timely surgery should be anticipated following intravitreal bevacizumab. Therefore, to be on the safe side, if bevacizumab is to be used as a vitrectomy adjunct, surgery should be performed no later than 4 days after injection. [6, 7]
PVR is responsible for most failures of retinal reattachment surgery. It occurs in about 7% of eyes after retinal reattachment surgery. In 1 year, approximately 1600 new cases of PVR are seen.
Approximately 500 cases of blindness secondary to ROP are reported per year in the United States.
Recent series have reported that the anatomical success rates of PVR are about 75-90%. However, the functional results are not that good since only about 40-50% of eyes attain 20/400 or better visual acuity.
ROP complicated by TRD is the leading cause of childhood blindness.
Diabetic retinopathy is the leading cause of blindness in the working age group. In the 1960s, prior to the advent of laser photocoagulation, up to 50% of patients with PDR were legally blind. With new techniques, currently only 5% of patients with PDR progress to legal blindness.
TRD related to sickle cell disease occurs mainly in blacks.
No studies exist that specifically refer to the incidence of TRD according to gender. However, it is well known that men are more susceptible to penetrating trauma than women.
The incidence of TRD according to age depends on the cause.
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