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Biomedical subjects

William M Bourne

Publications and source records attributed to William M Bourne.

At least 19 recordsLinked to original sources

Corneal endothelium and postoperative outcomes 15 years after penetrating keratoplasty.

PURPOSE: To determine changes in the central endothelium and thickness of grafted corneas and the cumulative probability of developing glaucoma, of graft rejection, and of graft failure 15 years after penetrating keratoplasty. DESIGN: Longitudinal cohort study of 500 consecutive penetrating keratoplasties by one surgeon. METHODS: Regrafted eyes, fellow eyes of bilateral cases, and patients not granting research authorization were excluded, leaving 388 grafts for analysis. At intervals after surgery, we photographed the endothelium and measured corneal thickness using specular microscopy. The presence of glaucoma, graft rejection, and graft failure were recorded. RESULTS: The 67 patients examined at 15 years represented 30% of the available clear grafts. Endothelial cell loss from preoperative donor levels was 71 +/- 12% (mean +/- standard deviation, n = 67), endothelial cell density was 872 +/- 348 cells/mm(2), and corneal thickness was 0.59 +/- 0.06 mm. Endothelial cell density was unchanged between 10 and 15 years, whereas corneal thickness increased (P = .001, n = 55). The mean annual rate of endothelial cell loss from 10 to 15 years after surgery was 0.2 +/- 5.7% (n = 54). The cumulative probability of developing glaucoma, graft rejection, or graft failure was 20%, 23%, and 28%, respectively, and 6 of the 8 graft failures after 10 years resulted from late endothelial failure. CONCLUSIONS: From 10 to 15 years after penetrating keratoplasty, the annual rate of endothelial cell loss was similar to that of normal corneas, corneal thickness increased, and late endothelial failure was the major cause of graft failure.

Adolescent↗

Keratocyte density: comparison of two confocal microscopes.

PURPOSE: The ConfoScan 3 clinical confocal microscope provides sharper images of cells in the stroma than the Tandem Scanning confocal microscope does. In this study, we compared volumetric densities of stromal cells determined from images recorded by these two instruments. METHODS: Fifty corneas of 25 normal subjects were examined by confocal microscopy, first by using a Tandem Scanning confocal microscope and then by using a ConfoScan 3 confocal microscope. Bright objects, assumed to represent keratocytes, were counted in a known area of two frames selected from the mid-stroma. The effective depth of the sample volume represented by each frame was estimated from the number of consecutive frames and the corresponding distance that selected cells were visible and countable during a scan. Density was the number of visible cells in the sample area divided by the effective sample volume. RESULTS: The effective focal depth of the Tandem Scanning microscope was 11.9 +/- 2.6 microm (mean +/- SD), and was 25.9 +/- 7.1 microm for the ConfoScan 3. Mean cell density at mid stroma was 23,013 +/- 4,420 cells/mm(3) with the Tandem Scanning microscope and 23,996 +/- 2,898 cells/mm(3) with the ConfoScan 3. This difference was not significant (P = 0.15). CONCLUSIONS: In normal corneas, the ConfoScan 3 and the Tandem Scanning confocal microscopes indicate stromal cell densities that are not significantly different from each other. Estimates of cell density from both instruments require an accurate estimate of the effective depth of the sample volume; this depth is approximately 2.2 times greater with the ConfoScan 3. This difference must be considered when comparing results from studies that use one instrument with results from studies that use the other.

Adult↗

Corneal thickness measurement by confocal microscopy, ultrasound, and scanning slit methods.

PURPOSE: To measure corneal thickness by using a calibrated confocal microscope and to compare this measurement to thickness determined by ultrasonic and noncontact scanning slit pachymetry. DESIGN: Comparison of corneal thickness measured by using four instruments in normal subjects. METHODS: Thickness measured by a clinical confocal microscope (Tandem Scanning) was calibrated from measurements of polymethylmethacrylate contact lenses with known thickness. Corneal thickness was measured in one eye of 24 normal subjects by using this instrument, two ultrasonic pachymeters (DHG-1000 and Sonogage), and a noncontact optical scanning slit pachymeter (Orbscan II). RESULTS: Mean corneal thickness measured by confocal microscopy was 516 +/- 30 microm (+/-SD). This was less than the mean thickness measured by both ultrasonic pachymeters, 554 +/- 28 microm by the DGH, and 555 +/- 28 microm by the Sonogage (P <.001). Thickness measured by the Orbscan II pachymeter was 540 +/- 35 microm (P <.001, compared with either confocal or ultrasound) after applying an "acoustic factor" of 0.92, a default correction of the software. CONCLUSION: Corneal thickness measured by calibrated confocal microscopy is approximately 39 microm (7.0%) less than thickness measured by two commonly used ultrasonic pachymeters and approximately 24 microm (4.4%) less than thickness measured by the corrected Orbscan II pachymeter. These differences are important for planning and measuring the effects of refractive and other surgical procedures. The precision of confocal microscopy is limited by corneal motion in an anterior-posterior direction. The difference between instruments suggests that verification of clinical ultrasonic pachymeters should be revisited.

Adult↗

Clinical responses of the corneal endothelium.

The corneal endothelium maintains corneal deturgescence and clarity by a pump-leak mechanism first described by David Maurice. This cell layer can be investigated clinically with specular microscopy, fluorophotometry, and pachymetry. We describe the clinical responses of the corneal endothelium to aging, drugs, glaucoma, contact lens wear, trauma, disease, and surgery.

Aging↗

Confocal microscopy evaluation of stromal ablation depth after myopic laser in situ keratomileusis and photorefractive keratectomy.

PURPOSE: To compare the measured ablation depth after myopic laser in situ keratomileusis (LASIK) and photorefractive keratectomy (PRK) with the predicted ablation depth. SETTING: Mayo Clinic, Rochester, Minnesota, USA. METHODS: Twenty-five eyes of 15 patients had PRK and 25 eyes of 15 patients had LASIK to correct refractive errors between -1.50 diopters (D) and -11.00 D. The corneas were examined by in vivo confocal microscopy before and 1 month after both procedures. Thickness measurements were obtained from digital-image analysis of confocal scans. The measured ablation depth, an estimate of the actual photoablation depth, was obtained as the surgically induced stromal thinning between the preoperative and the 1-month post-PRK or post-LASIK central stromal thickness. The predicted ablation depth was recorded from the laser's software program. RESULTS: In LASIK, the measured ablation depth (81 microm +/- 34 [SD]) was 25% greater than the predicted ablation depth (65 +/- 13 microm, P =.007) and the difference between the measured and predicted ablation depths was positively associated with the mean ablation depth (r = 0.81, P<.001). In PRK, there was no difference between the measured ablation depth (48 +/- 19 microm) and the predicted ablation depth (47 +/- 18 microm, P =.84). CONCLUSION: Significantly more tissue than predicted was removed by LASIK than by PRK excimer photoablation with the laser system used in this study.

Adult↗

Long-term keratocyte deficits in the corneal stroma after LASIK.

PURPOSE: To determine changes in keratocyte density up to 3 years after LASIK. DESIGN: Prospective, nonrandomized, comparative trial. PARTICIPANTS: Seventeen eyes of 11 patients received LASIK with a planned 180-microm flap to correct refractive errors between -2.0 diopters (D) and -11.0 D (mean, -6.56+/-2.44). METHODS: Corneas were examined by using confocal microscopy before LASIK and 1, 3, 6, 12, 24, and 36 months after LASIK. Bright objects that resembled keratocyte nuclei were manually counted by a masked observer. Cell densities were determined in anterior and posterior halves of the stromal flap, anterior and posterior halves of the 100-microm-thick layer immediately behind the ablation (retroablation layer), and the posterior third of the stroma. The region of stroma that was ablated (as measured 1 month after LASIK) was omitted from preoperative analysis. Cell densities after LASIK were compared (using1-factor repeated-measures analysis of variance) with densities in the corresponding layer of the normal preoperative stroma (which served as its own control). MAIN OUTCOME MEASURE: Corneal keratocyte density. RESULTS: Before LASIK, keratocyte densities in the anterior and posterior stromal flap and the anterior retroablation layer were 34 818+/-5108 cells/mm(3) (mean +/- SD), 25 390+/-4045 cells/mm(3), and 21 328+/-2980 cells/mm(3), respectively, and densities in these layers decreased 14% to 20% at 1 month after LASIK (P<0.001). Keratocyte densities in these layers remained stable at 3 and 6 months, and then gradually decreased further (P<0.001) to 26% to 36% below pre-LASIK densities by 3 years. Keratocyte densities in the remaining stromal layers did not change after LASIK. CONCLUSION: Keratocyte densities in the stromal flap and in the anterior retroablation layer decrease during the first 6 months after LASIK and then decrease further during the next 2.5 years. Further studies on these patients and others are warranted to confirm these findings and learn their significance.

Adult↗

Corneal reinnervation after LASIK: prospective 3-year longitudinal study.

PURPOSE: To measure the return of innervation to the cornea during 3 years after LASIK. METHODS: Seventeen corneas of 11 patients who had undergone LASIK to correct myopia from -2.0 D to -11.0 D were examined by confocal microscopy before surgery, and at 1, 3, 6, 12, 24, and 36 months after surgery. In all available scans, the number of nerve fiber bundles and their density (visible length of nerve per frame area), orientation (mean angle), and depth in the cornea were measured. RESULTS: The number and density of subbasal nerves decreased >90% in the first month after LASIK. By 6 months these nerves began to recover, and by 2 years they reached densities not significantly different from those before LASIK. Between 2 and 3 years they decreased again, so that at 3 years the numbers remained <60% of the pre-LASIK numbers (P <0.001). In the stromal flap most nerve fiber bundles were also lost after LASIK, and these began recovering by the third month, but by the third year they did not reach their original numbers (P <0.001). In the stromal bed (posterior to the LASIK flap interface), there were no significant changes in nerve number or density. As the subbasal nerves returned, their mean orientation did not change from the predominantly vertical orientation before LASIK. Nerve orientation in the stromal flap and the stromal bed also did not change. CONCLUSIONS: Both subbasal and stromal corneal nerves in LASIK flaps recover slowly and do not return to preoperative densities by 3 years after LASIK. The numbers of subbasal nerves appear to decrease between 2 and 3 years after LASIK. The orientation of the regenerated subbasal nerves remains predominantly vertical.

Adult↗

Corneal endothelium and postoperative outcomes 15 years after penetrating keratoplasty.

PURPOSE: To determine changes in the central endothelium and thickness of grafted corneas, and the cumulative probability of developing glaucoma, graft rejection, and graft failure 15 years after penetrating keratoplasty. METHODS: In a longitudinal cohort study of 500 consecutive penetrating keratoplasties by one surgeon, regrafted eyes, fellow eyes of bilateral cases, and patients not granting research authorization were excluded, leaving 388 grafts for analysis. At intervals after surgery, we photographed the endothelium and measured corneal thickness by using specular microscopy. The presence of glaucoma, graft rejection, and graft failure was recorded. RESULTS: The 67 patients examined at 15 years represented 30% of the available clear grafts (107 patients had died, 76 grafts had failed). Endothelial cell loss from preoperative donor levels was 71 +/- 12% (mean +/- SD, n = 67), endothelial cell density was 872 +/- 348 cells/mm2, and corneal thickness was 0.59 +/- 0.06 mm. Endothelial cell density was unchanged between 10 and 15 years (minimum detectable difference was 96 cells/mm2, alpha = .05, beta = .20, n = 54), whereas corneal thickness increased (P = .001, n = 55). The mean annual rate of endothelial cell loss from 10 to 15 years after surgery was 0.2 +/- 5.7% (n = 54). The cumulative probability of developing glaucoma, graft rejection, or graft failure was 20%, 23%, and 28%, respectively, and six of the eight graft failures after 10 years resulted from late endothelial failure. CONCLUSIONS: From 10 to 15 years after penetrating keratoplasty, the annual rate of endothelial cell loss was similar to that of normal corneas, corneal thickness increased, and late endothelial failure was the major cause of graft failure.

Adolescent↗

Keratocyte density in the human cornea after photorefractive keratectomy.

OBJECTIVE: To perform a quantitative analysis of keratocyte density in human corneas after photorefractive keratectomy (PRK). METHODS: In a prospective comparative trial, 24 eyes of 14 patients received PRK to correct refractive errors of between -1.25 diopters (D) and -5.75 D. Corneas were examined by using confocal microscopy before and 1 day, 5 days, and 1, 3, 6, 12, 24, and 36 months after PRK. Keratocyte nuclei were counted in 5 stromal layers in 3 to 6 scans per eye per visit. Keratocyte density in each layer post-PRK was compared with the density in the corresponding layer of the pre-PRK full stroma (included stroma that would later be photoablated) and the pre-PRK future unablated stroma (thickness adjusted by omitting the future ablation depth) (Bonferroni-adjusted paired t test). RESULTS: Keratocyte density in the anterior 10% of the post-PRK stroma decreased by 25% (P =.002), 41% (P<.001), 40% (P<.001), 43% (P<.001), and 45% (P<.001) at 3, 6, 12, 24, and 36 months compared with the anterior 10% of the pre-PRK full stroma and was reduced by 15% at 36 months (P =.02) compared with the anterior 10% of the pre-PRK future unablated stroma. CONCLUSION: After PRK, keratocyte density in the anterior stroma is not restored to the high-density levels found in the preoperative stroma.

Adult↗

Aberrant corneal nerve regeneration after PRK.

PURPOSE: To report a case of aberrant corneal nerve regeneration after myopic photorefractive keratectomy (PRK). METHODS: One patient underwent bilateral PRK to correct a refractive error of -5.50 D in each eye. Thirteen months after the original PRK, the left eye underwent an uncomplicated PRK reoperation to correct a regression of -1.00 D. The central corneas were examined by confocal microscopy preoperatively in both eyes, at 1 and 2 years after the original PRK in the right eye, and before and 1 and 2 years after the PRK reoperation in the left eye. RESULTS: Aberrant anterior stromal nerves with a coiled course and irregular branching pattern were identified 22 micro m deep to the most anterior keratocyte layer at 1 year after the PRK reoperation in the left eye and remained unchanged 2 years after reoperation. No abnormal stromal nerves were identified in the left eye before the reoperation or at any time in the right eye. CONCLUSION: Aberrant regeneration of corneal stromal nerves may occur after myopic PRK reoperation.

Adult↗

Keratometric astigmatism after suture removal in penetrating keratoplasty: double running versus single running suture techniques.

BACKGROUND AND OBJECTIVE: To compare astigmatism after suture removal in a retrospective sequential series of patients who had penetrating keratoplasty with either a double running suture technique or an adjustable single running suture technique. During the first year postkeratoplasty, when sutures were in place, the latter technique had produced less astigmatism. MATERIALS AND METHODS: Keratometry and keratometric astigmatism were measured before and after suture removal. We compared these variables in 30 grafts with the double running suture technique to the same variables in 24 grafts with the single running suture technique. RESULTS: The final portion of the double running suture was removed 408 +/- 177 (mean +/- SD) days after keratoplasty, whereas the single running suture was removed 611 +/- 224 days after keratoplasty (P<0.001). After suture removal, there was no difference between the double running and single running groups in either mean keratometry [46.5 +/- 1.8 diopters (D) versus 45.6 +/- 2.0 D, P=0.09, minimum detectable difference (MDD)=1.5D] or mean astigmatism (4.6 +/- 2.7 D versus 5.2 +/- 3.2D, P=0.72, MDD=2.3). CONCLUSION: In this consecutive series of corneal transplants performed by one surgeon, the results suggest no difference in astigmatism between the two suturing techniques after all sutures have been removed.

Astigmatism↗

Predicting endothelial cell loss and long-term corneal graft survival.

PURPOSE: To evaluate a biexponential decay model for describing the loss of corneal endothelial cells with age as well as the increased loss of cells after cataract surgery and penetrating keratoplasty. METHODS: Data from previous studies were identified and the sum of two exponentials, d = p. exp(-at) + q. exp(-bt) (where d is cell density at time t, p and q are constants the sum of which is equal to the initial cell density, and a and b are exponential rate constants), fitted to each data set by a nonlinear least-squares algorithm. Goodness of fit was indicated by the residual standard deviation. Half times were calculated from the exponential rate constants. RESULTS: The model identified in each instance a rapid and a slow component to the cell loss. The half time for the slow component of the loss with age was 224 years, underlining the excess endothelial capacity in normal eyes. After surgery, the rapid component of the cell loss was probably due to surgical trauma and, after penetrating keratoplasty, cell-mediated rejection and other complications. The half times of the slow component were only 26 years after cataract surgery and 21 years after penetrating keratoplasty. DISCUSSION: The loss of endothelial cells followed a biexponential decay and could thus be described by a single equation. The half times of the slow component of the cell loss after surgery were substantially less than for the loss with age, indicating a markedly increased rate of cell loss that persisted for many years after surgery. A mechanism for this accelerated cell loss is suggested that involves a nonspecific, innate response initiated by the breakdown of the blood-ocular barrier. The model was used to calculate endothelial cell loss in the long term after penetrating keratoplasty and to predict when cell density would reach levels that are incompatible with maintenance of transparency and graft function. Thus, a rationale is presented for the setting of minimum donor cell densities by eye banks.

Adolescent↗

Keratocyte density of central human cornea after laser in situ keratomileusis.

PURPOSE: To determine changes in keratocyte density in the first year after laser in situ keratomileusis (LASIK). DESIGN: Prospective interventional cohort study. METHODS: Seventeen eyes of 11 patients received LASIK with a planned 180-microm flap to correct refractive errors between -2.0 diopters and -11.0 diopters. Images of the full-thickness cornea were obtained by using confocal microscopy in vivo before LASIK and at 1 week, 1, 3, 6, and 12 months after LASIK. Bright objects (that resembled keratocytes) in images without motion blur were manually counted by one observer. Cell densities were determined in anterior and posterior halves of the stromal flap, anterior and posterior halves of the layer 100 microm-thick immediately deep to the ablation (retroablation layer), and in the posterior third of the stroma. The region of stroma that was ablated (as measured 1 month after LASIK) was omitted from the preoperative analysis. RESULTS: Keratocyte density in the anterior flap was 28,978 +/- 5849 cells/mm(3) (mean +/- SD) pre-LASIK, and was decreased at all postoperative examinations, but the difference was not significant until 12 months after LASIK (22% decrease). Keratocyte densities in the posterior flap were 20,397 +/- 4215 cells/mm(3) pre-LASIK and were decreased by 20%-40% at all postoperative examinations 1 week to 1 year after LASIK. Keratocyte densities in the anterior half of the retroablation layer were 16,605 +/- 3595 cells/mm(3) pre-LASIK and decreased by 16%-30% between 3 and 12 months after LASIK. Keratocyte densities in the posterior half of the retroablation layer and posterior stroma did not change. CONCLUSIONS: Keratocyte densities in the posterior flap and anterior retroablation layer (regions adjacent to the lamellar cut) decrease at 1 week and 3 months, respectively, after LASIK and remain decreased in these regions at 12 months after LASIK. In the anterior flap, keratocyte density decreases 1 year after LASIK. The long-term effects of these cellular deficits, if any, require further study.

Adult↗

Keratocyte density in keratoconus. A confocal microscopy study(a).

PURPOSE: To estimate keratocyte density in human corneas with keratoconus by confocal microscopy. DESIGN: Prospective, observational cohort study. METHODS: Twenty-nine unscarred corneas of 19 patients with keratoconus and 29 corneas of 19 controls matched for age (+/-3 years) and contact lens wear were examined by using confocal microscopy. Images were recorded from the full-thickness central cornea. A masked observer manually counted bright objects (keratocyte nuclei) in images without motion blur. Cell densities in anteroposterior stromal layers of keratoconus corneas were compared with densities in corresponding layers of control corneas. RESULTS: In keratoconus patients, age 40 +/- 15 years (mean +/- standard deviation), keratocyte density was 19% lower in those who wore contact lenses (16,894 +/- 4032 cell/mm(3), n = 12) than in those who did not wear contact lenses (20,827 +/- 4934 cell/mm(3), n = 17, P =.03). In control patients, age 39 +/- 16 years, there was no difference in keratocyte density between those who wore contact lenses (n = 12) and those who did not wear contact lenses (n = 17, P =.80). Among contact lens wearers, keratocyte density was 25% lower in keratoconus corneas (16,894 +/- 4, 032 cell/mm(3), n = 12 [9 = rigid gas-permeable lenses, 3 = soft lenses]) than in control corneas (22,579 +/- 2, 387 cell/mm(3), n = 12 [3 = rigid gas-permeable lenses, 9 = soft lenses], P =.002), the result of cell density being lower in the most anterior keratocyte layer (P =.001) and the layers between 0% to 10% (P <.001), 67% to 90% (P <.001), and 91% to 100% (P <.001) of stromal thickness. Among noncontact lens wearers, there was no difference in cell density between keratoconus and controls (P =.41). CONCLUSION: Keratocyte density is decreased in the anterior and posterior stroma of keratoconus patients who wear contact lenses.

Adult↗

Transplantation of cryopreserved human corneas in a xenograft model.

An ideal model to test methods of corneal storage for transplantation would simulate the environment of the grafted human cornea and predict the success of clinical corneal transplants (human to human). In this study, we tested such a model, the corneal xenograft (human to cat). Nine pairs of human corneas were transplanted into both eyes of nine recipient cats. One cornea of each pair was cryopreserved at -196 degrees C in 2.5 M dimethyl sulfoxide while the other was stored in preservative medium at 4 degrees C (control) for 6 +/- 2 (mean +/- SD) days before transplantation. One week after transplantation, the cats were euthanized and the eyes were examined. Three of the grafts (all cryopreserved) were clinical failures and showed no survival of donor corneal endothelial cells on scanning electron microscopy. The remaining six pairs of grafts were examined with a specular microscope and showed endothelial cell losses of 48 +/- 16% in cryopreserved and 8 +/- 16% in control corneas (p < 0.05). This survival is similar to survival in an earlier corneal perfusion model. The nine cryopreserved grafts were thicker than the control grafts, had fewer surviving keratocytes in the central stroma, and had more apoptotic central keratocytes (TUNEL assay). This failure rate in cryopreserved corneas clearly shows that this technique of cryopreservation was not adequate for clinical use. The corneal xenograft model can be used to study cellular survival and apoptosis in vivo after preservation as well as to test new methods of corneal preservation before initiating clinical trials.

Adolescent↗

Effect of myopic laser in situ keratomileusis on epithelial and stromal thickness: a confocal microscopy study.

PURPOSE: To determine changes in central epithelial and stromal thickness in human corneas in vivo after laser in situ keratomileusis (LASIK). DESIGN: Prospective, nonrandomized, comparative trial. PARTICIPANTS: Eighteen eyes of 12 patients received LASIK (performed using the VISX Star laser [VISX, Santa Ana, CA]) with a planned 180- micro m flap (created using an automated Hansatome microkeratome [Bausch & Lomb, Irvine, CA]) to correct refractive errors between -2.0 diopters (D) and -11.0 D. METHODS: Corneas were examined by using confocal microscopy in vivo before LASIK and at 1 week and 1, 3, 6, and 12 months after LASIK. Epithelial thickness was the distance between images of the surface epithelium and subbasal nerve plexus or, when nerves were not visible, the subbasal peak (if present in the light intensity profile). Total flap thickness was the distance between images of the surface epithelium and interface debris (or peak), and total stromal thickness was the distance between images of the most anterior keratocytes and endothelium. MAIN OUTCOME MEASURES: Corneal epithelial and stromal thickness. RESULTS: Epithelial thickness before LASIK was 46 +/- 5 micro m (mean +/- standard deviation) and increased 22% by 1 month after LASIK (56 +/- 5 micro m; P = 0.01). Thereafter, epithelial thickness did not change, but remained thicker at 12 months after LASIK (54 +/- 8 micro m) than before LASIK (P = 0.02). Total flap thickness at 1 month after LASIK was 160 +/-28 micro m and did not change thereafter. Changes in total stromal thickness between 1 and 12 months after LASIK were not significant. CONCLUSIONS: The central corneal epithelium was thicker in the first year after LASIK than before LASIK. There was no change in central stromal thickness between 1 month and 12 months after LASIK.

Adult↗

Confocal microscopy in vivo in corneas of long-term contact lens wearers.

PURPOSE: To compare keratocyte density, stromal backscatter, epithelial thickness, and corneal sensitivity between corneas of long-term contact lens wearers and those of non-contact lens wearers. METHODS: Twenty corneas of 20 daily contact lens wearers (>10 years' duration) and 20 corneas of 20 age-matched (+/-5 years) control subjects who had never worn contact lenses, were examined by confocal microscopy in vivo. The contact lens wearers removed their lenses 12 to 24 hours before the examination. Full-thickness images were recorded from the central and temporal cornea, and bright objects (keratocyte nuclei) in images were manually counted to calculate keratocyte density. Stromal intensity (backscatter) was measured by calculating the mean grayscale value (corrected for camera and light source variations) from the center of stromal images. Epithelial thickness was determined from the distance between images of the surface epithelium and subbasal nerve plexus. Central corneal sensitivity was measured by Cochet-Bonnet esthesiometry and correlated with the number of nerve fiber bundles in the subbasal nerve plexus. RESULTS: Full-thickness central and temporal keratocyte densities in contact lens wearers were 22,122 +/- 2,676 cells/mm(3) (mean +/- SD) and 20,731 +/- 2,627 cells/mm(3), respectively, and were not significantly different from central and temporal keratocyte densities in control subjects (P = 0.29). The minimum detectable difference in cell density was 11% (2346 cells/mm(3) and 2235 cells/mm(3) in central and temporal stroma, respectively). Temporal epithelial thickness was 46.3 +/- 4.7 microm in contact lens wearers and 50.9 +/- 4.7 microm in control subjects (P = 0.02). Central epithelial thickness and stromal backscatter did not differ between contact lens wearers and control subjects (P > 0.05). Corneal sensitivity was lower in contact lens wearers than it was in control subjects (P = 0.05) and did not correlate with the number of nerve fiber bundles in the subbasal nerve plexus. CONCLUSIONS: Long-term daily contact lens wear and its associated stromal hypoxia and acidosis have no demonstrable effect on keratocyte density. The temporal epithelium is thinner in corneas of long-term contact lens wearers than in control subjects. Decreased corneal sensitivity in contact lens wearers is not accompanied by decreased nerve fiber bundle density.

Adult↗