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This report describes a remission of rheumatoid arthritis (RA) of 16 years duration, apparently caused by the extraction of endodontically well-treated, healthy looking teeth. The only clue that the teeth were contributing to the disease pathogenesis in this case of RA was that the patient was able to reproducibly induce severe attacks of arthritis after prolonged, heavy pressure on some of his teeth treated with root canal fillings. After extraction, a small pus layer was found to cover the apices of the clinically healthy looking teeth. The rheumatoid factor (RF) became negative and the patient remained symptom free for the next 16 years. The possible connections between micro-organisms in closed dental foci under constant pressure and the chronicity and exacerbations of RA are discussed.

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AIMS: To investigate the long term relation between corneal thickness, endothelial morphometric variables, and endothelial permeability in patients with endothelial cell counts under 900 cells/mm2 as a result of endothelial cell destruction after cataract surgery. METHODS: Eighteen patients developed the so called toxic endothelial cell destruction (TECD) syndrome following routine cataract surgery because of the intracameral injection of a toxic detergent residue. Ten patients with a mean (SEM) initial cell loss of 72% (2%) were followed for 4 years. Data were obtained at 6 months and 4 years postoperatively and compared between TECD eyes and contralateral control eyes. RESULTS: Mean (SEM) endothelial cell density of the TECD eyes increased from 642 (41) cells/mm2 to 849 (50) cells/mm2 at 4 years postoperatively (p = 0.005). There was no difference in coefficient of variation or percentage hexagonals between 6 months and 4 years postoperatively. Mean (SD) corneal thickness of the TECD eyes and control eyes was similar, 0.51 (0.02) mm and 0.49 (0.01) mm, respectively (p = 0.65). Mean (SD) endothelial permeability was also similar for TECD eyes and control eyes (4.3 (0.9) x 10(-4) cm/min and 4.4 (0.6) x 10(-4) cm/min, respectively (p = 0.57). There was no correlation between endothelial cell density, coefficient of variation, or percentage of hexagonal cells and endothelial permeability in the TECD eyes. In three patients a permanent corneal decompensation occurred. CONCLUSIONS: Four years after TECD corneal endothelial wound healing is stable and the barrier function has been restored.

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Four black patients with Fuchs' heterochromic uveitis had multiple nodules in the iris. The iris nodules were small, transparent, and scattered across the whole surface of the iris (Busacca's nodules) but increased in density toward the pupillary border. All four patients also had nodules at the pupillary border (Koeppe's nodules). Repeated etiologic screening for systemic diseases in these patients was noncontributory. Unilateral multiple iris nodules without the formation of synechiae may be encountered as part of Fuchs' heterochromic uveitis syndrome and may be important in the identification of Fuchs' heterochromic uveitis, especially in black patients.

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The Janus green photometric technique and the Mosmann's colorimetric MTT-assay to quantify corneal endothelial cytotoxicity were compared. Detergents, studied before by in vitro corneal perfusion, proved to be toxic at the 1% level in the Janus green assay with human corneas and at the 0.4% level in the MTT-assay with bovine endothelial cells. These results correlated well with earlier findings in vitro and in vivo. The use of human corneas reduced the ability of the Janus green photometric technique as a fast screening method because of the heterogeneity and restricted availability of this tissue. With the MTT-assay, large test series could be performed at the same time using cultured cells. Both assays are good tools to screen the cytotoxicity of chemicals and reduce the number of animals needed for endothelial cytotoxicity testing.

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Many studies have described the presence of circulating antibodies against corneal components in patients with corneal disease or uveitis, and in patients with skin or systemic disease with or without ocular involvement. The role of such antibodies in the underlying immunopathological process remains obscure. Here we describe the induction of autoantibodies against the rat cornea. Our attempts to induce corneal autoantibodies by various forms of keratitis and corneal trauma failed. However, circulating corneal autoantibodies could be detected by Western blotting after immunization of BN rats and Lewis rats with bovine corneal protein 54 (BCP 54). Rats immunized with rat corneal extracts (RaCE) or human serum albumin (HSA) as (auto) antigen did not develop corneal autoantibodies. During the study period (greater than 4 months), it was observed that the presence of circulating corneal autoantibodies did not elicit corneal inflammation. Severe keratitis did develop when BCP 54-immunized rats were challenged intracorneally with BCP 54, but the clinical signs were not significantly different from HSA-immunized rats after an intracorneal HSA challenge. Injection of corneal autoantibodies into the corneal stroma did not provoke keratitis. To the best of our knowledge this is the first study demonstrating corneal autoantibodies in rats without actual manipulation of the eye. This model may provide further insights in the role and significance of corneal autoantibodies in disease.

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There are indications that complement activation may be involved in inflammatory processes of the cornea. To investigate the role of the complement system in experimental keratitis, rats were depleted of their plasma complement by treatment with cobra venom factor (CVF). intraperitoneal injection of CVF resulted in undetectable complement serum activity for 6 days when measured by a hemolytic assay. The corneal inflammatory response, induced by a single intracorneal injection of heterologous serum into nonsensitized CVF-treated rats, was suppressed significantly. The onset of the clinical symptoms of keratitis was delayed, and the severity was reduced. In addition, analysis of the serum antibody titers showed impaired antibody synthesis in the CVF-treated group. When keratitis was induced by an intracorneal antigen challenge in sensitized rats, no difference was observed when comparing the clinical signs of keratitis of CVF-treated animals with sham-treated animals. In addition, CVF treatment did not alter the course of lipopolysaccharide (LPS)-induced corneal inflammation. These findings suggest that the role of plasma complement activation in antigen- and LPS-induced keratitis appears to be limited. The implications for the immunopathologic mechanisms underlying keratitis are discussed.

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The immunopathologic response following the injection of various antigens into the rat cornea was evaluated. This reaction, known as Wessely's phenomenon, was believed to be primarily triggered by antibodies and complement activation. The keratitis model was originally described in rabbits, using heterologous serum or purified proteins. In rats only, heterologous serum induced corneal inflammation with the characteristics of Wessely's phenomenon, (ie, a quiescent period of several days between antigen injection and onset of clinical signs and corneal opacification). Using rats allowed us to characterize the cellular infiltrate with immunohistochemical methods. Marked infiltration of the cornea by macrophages was observed, as was infiltration by polymorphonuclear cells, although to a lesser extent. Furthermore, T lymphocytes of the helper phenotype were demonstrated. Antibodies to complement activation product C3c showed faint staining, whereas B lymphocytes and plasma cells were absent. In addition, inflammatory cells and ocular tissues, particularly the limbal and peripheral corneal epithelium, were found to express major histocompatibility complex class II antigens during the inflammatory response. After the inflammation had subsided, macrophages and T lymphocytes remained in the corneal stroma (at least until day 30). These findings suggest that antigen-induced keratitis in rats might be mediated, at least partially, by T helper lymphocytes.

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The pathogenesis of peripheral corneal lesions of immune aetiology, like Mooren's ulcer and catarrhal infiltrates, has been related to the formation or deposition of immune compkexes. The present investigation was undertaken to study the mechanisms involved in the elimination of immune precipitates from the cornea. Immune precipitates were induced by injecting human serum albumin (HSA) and rabbit anti-HSA serum into opposite sites of the rat corneal stroma. This resulted in a line-shaped opacity in the stroma, which remained visible by slit-lamp for 7 days, and disappeared without clinical signs of keratitis and uveitis. At the ultrastructural level, the immune precipitates were clearly visible. Keratocytes in the vicinity of the immune precipitates appeared activated, as suggested by their less flattened appearance and well-developed rough endoplasmic reticulum. The arrangement of the collagen fibrils was not affected. Cells with a macrophage-like morphology were also present and contained electron-dense material, closely resembling the precipitate, suggesting phagocytosis. Separate corneas were injected with latex beads, which is known to induce migration of Langerhans cells into the cornea. Immunohistochemical analysis revealed that both latex beads and immune precipitates induced migration of macrophages (ED1+) into the rat corneal stroma. However, differences were observed with regard to the expression of MHC class II antigens by these ED1+ cells and the presence of complement deposits in the corneal stroma. ED1+ cells in corneas injected with latex beads were all MHC class II positive (OX4+), whereas most of the ED1+ cells at the site of the immune precipitates were negative (OX4-).(ABSTRACT TRUNCATED AT 250 WORDS)

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The mechanisms involved in the clearance of immune deposits in tissues are not yet clear. The cornea was chosen as a model to examine this question due to its avascularity and transparency. Bovine serum albumin (BSA) and rabbit anti BSA serum were injected at opposite sites into the corneal stroma of unsensitized rabbits. Within a day, a sharp opaque line was seen macroscopically between the two injection sites. Sections of the corneas were examined by light microscopy and electron microscopy; furthermore, immunohistochemical techniques were used. With the light microscope, a precipitation line was seen in the corneal stroma, which was identified as an antigen-antibody complex by immunofluorescence techniques. In the same area infiltrating polymorphonuclear cells and swollen keratocytes were observed. In the ultrathin sections precipitates were seen lying between the collagen fibrils without affecting the structure of the collagen. The swollen keratocytes had an activated rough endoplasmic reticulum. In certain cases the precipitates appeared to be intracellular, both in the polymorphonuclear cells, as well as in the keratocytes. These findings suggest that stromal keratocytes may play an important role in the degradation of corneal immune deposits.

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The ocular inflammatory activity following different techniques of lens extraction and vitrectomy was studied in rabbits recovered from primary uveitis. Primary uveitis was induced by intravitreal injection of human serum albumin. After five to ten weeks, when the eyes were completely quiet, vitrectomy combined with lensectomy in one session or extracapsular lens extraction followed by vitrectomy was performed in different groups of rabbits. The most intense postoperative inflammatory process was encountered following removal of the lens independently of the route of extraction (via the ciliary body or via the anterior chamber). Vitrectomy via the ciliary body led to a minimal postoperative inflammation which resolved within 7 days. From these results we concluded that vitrectomy in primarily sensitized rabbit eyes can be performed without intense postoperative complications.

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Eighteen patients developed an acute corneal decompensation following normal intraocular surgery (cataract extraction in 17 patients), characterized by star-shaped endothelial folds, a twofold increase in corneal thickness, and a visual acuity of counting fingers during several postoperative days. In some cases, there was an additional iritis and transient hypotony. There was no effect of topical and/or subconjunctival corticosteroids on the course of the decompensation. Endothelial morphometric analysis showed a mean endothelial cell loss of 72%. Endothelial wound healing, as determined by coefficient of variation and percentage hexagonals, stabilized 6 months postoperatively. We coined the term toxic endothelial cell destruction for this syndrome. Epidemiological evaluation revealed the toxic endothelial cell destruction syndrome to be linked with the 10-fold increase of a detergent solution in the ultrasonic bath for cleaning the surgical instruments.

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Eighteen patients developed a toxic endothelial cell destruction syndrome following normal intraocular surgery, caused by a detergent residue originating from irrigating cannulas. The residue occurred after the concentration of a detergent solution has been increased from 0.4% to 4%, in combination with insufficient cleaning of the cannulas. Mass spectrometric analysis revealed the detergent to contain a nonionic ethoxylated fatty alcohol (6% vol/vol). Quantitative endothelial vital staining and in vitro corneal endothelial perfusion demonstrated endothelial toxic effects at the 1% and 0.06% level for the detergent and the pure ethoxylated fatty alcohol, respectively. Permeability studies showed that the toxic effects occurred as a result of endothelial barrier breakdown.

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The surgical management of cataract in patients with chronic posterior uveitis is described. Of 41 eyes, 88% acquired improvement of the visual acuity 4 months postoperatively, which then remained stable in most of the cases during a follow-up of one year. The type of cataract extraction, extracapsular or intracapsular, did not influence these results, nor did the implantation of an intraocular lens. Recurrence of the uveitis occurred in about one third of the cases. Postoperative complications consisted of macular edema, retinal detachment and vitreous hemorrhage.

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A secondary immune response in the rabbit eye can be provoked by intravenous injection of the antigen, previously injected intravitreally. The inflammation process consists of iris hyperemia, pericorneal redness and cellular and proteinous exudates in the anterior chamber and vitreous. The influence of vitrectomy combined with lensectomy or preceded by extracapsular lens extraction on the character of the secondary immune response has been studied in the rabbit eye. Both eyes of adult rabbits were injected intravitreally with human serum albumin. Five to ten weeks later, when the primary inflammation process had vanished, the vitreous and the lens were removed from the right eye in one group of animals. In a second group of rabbits, an extracapsular lens extraction was performed upon both eyes, later followed by vitrectomy of the right eye. Four weeks later all animals received an intravenous booster injection with human serum albumin. The eyes which still contained the vitreous developed a secondary inflammation consisting predominantly of cells and fibrin clots in the anterior chamber however without flare. On the contrary, the eyes which underwent vitrectomy developed a flare in the anterior chamber with only a few cells detectable. Analysis of cells and protein in the anterior chamber and histological evaluation supported the clinically observed differences between both eyes. These results suggest that the persistence of the vitreous is associated with the reactivation of a secondary immune response. Vitrectomy combined with lensectomy or preceded by extracapsular lens extraction leads to increased passive transfer of proteinous material through the vessels.

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Analysis of local toxoplasma antibody production to confirm a suspected clinical diagnosis of toxoplasma chorioretinitis is a valuable diagnostic tool. Determination of toxoplasma antibodies in the blood of the patient is of limited use. When blood toxoplasma tests are negative this indicates that toxoplasma as a causative organisms in the pathogenesis of uveitis is unlikely. A positive blood test is a sensitive test (100% patients positive) but not a specific test since so many healthy individuals already have undergone subclinical infection and have acquired humoral immunity against the parasite. We analysed 93 paired aqueous and serum samples for toxoplasma antibodies and total IgG and determined the Goldmann-Wittmer coefficient. In patients retrospectively diagnosed as having toxoplasma chorioretinitis 16 out of 22 had a positive coefficient, indicating local parasite antibody production. In one patient with AIDS we also found a positive toxoplasma coefficient. Three out of 15 patients with posterior uveitis of unknown origin also had a positive coefficient. None of the cataract patients tested (n = 32) had a positive coefficient. Major drawbacks of aqueous humor analysis are that a false negative antibody coefficient can occur when a massive blood aqueous barrier breakdown has occurred.

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We reviewed 121 consecutive patients with biopsy-proven sarcoidosis who visited the sarcoidosis clinic of the University Hospital in Amsterdam, to determine the risk factors for the development of ocular manifestations. Of 121 patients 52 (43%) were black. Ocular disease developed in 50 (41%) patients and was more common in female and in black patients. uveitis was the most frequent manifestation of ocular sarcoidosis (29 out of 50 or 58%). There were no differences in the extra-ocular manifestations of the sarcoidosis between patients with and without ocular disease or between uveitis and non-uveitis patients. This study covered a mixed racial population and shows that different types of uveitis are seen in white and black patients. Anterior uveitis was more frequent in black patients (P less than .001), whereas posterior uveitis was more common in white patients (P less than .01). Chronic posterior uveitis with complications occurred most frequently in white female patients with late onset of the systemic disease. Uveitis was an early feature of sarcoidosis (25 out of 29 or 86%); moreover in 9 out of 29 (31%) cases, uveitis preceded the non-ocular detectable signs of sarcoidosis by more than one year. This emphasizes the importance of periodic re-evaluation of uveitis patients for sarcoidosis.

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HPLC analysis of human tears allows tear protein profiles to be obtained within ten minutes. A tear protein profile normally consists of 4 major peaks: IgA, lactoferrin, protein G and lysozyme. Although it is a rapid method, the use of High Performance Liquid Chromatography in the (quantitative) determination of proteins in tears is influenced by various factors. The day to day variability of the quantitative use, ranges between 7 and 9% for the various tear proteins. Combining the HPLC method with a convenient collection method such as sponges or Schirmer strips, showed that the sponges and some of the Schirmer strips used in this study eluted significant material absorbing light at 280 nm. No statistical difference was observed in the HPLC protein profiles of tears collected with Schirmer strips or with sponges. Using sponges has the advantage that they can absorb almost twice as much tears in a same period of time as Schirmer strips. HPLC analysis of human tear proteins is not accurate when there is albumin leakage as in traumatic sampling with Schirmer strips or in inflammatory states. The I-125 column which was used in our study is not able to separate lactoferrin and albumin, which may cause an overestimation of lactoferrin in inflammatory conditions. The study presented here indicates that for quantitative use of HPLC in epidemiological tear protein research better separating protein gel filtration columns are needed.

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