Fissure Area Research Articles

Microbial Findings in Suture Erosion after Penetrating Keratoplasty

The purpose of the study was to evaluate the presence of microorganisms in eroded (broken or loose) sutures post-penetrating keratoplasty (PKP). Fifty-five consecutive episodes of eroded 10-0 nylon sutures post-PKP in 35 eyes were evaluated. Eroded sutures were removed and, along with a swab from the conjunctiva, studied for aerobic and anaerobic bacteria. Preoperative diagnosis, elapsed time since surgery, presence of symptoms, suture location, infiltration, vascularization, and mucous at the suture site were recorded. Student's t test was used for statistical analysis. The average time from PKP to suture removal was 31.6 months. Eyes treated with topical steroids presented earlier suture erosions (P = 0.05). Of the 55 sutures, 34 were sterile, and in 21, both Staphylococcus epidermidis and diphtheroids (mixed flora) were cultured. Of the 55 conjunctivas, 32 were sterile, 22 showed mixed flora, and 1 had Pseudomonas. Sutures eroded for more than 24 hours had more positive cultures than those eroded for 24 hours or less (P = 0.043). Sutures located superiorly had fewer positive cultures than did those in the palpebral fissure area (P = 0.044). Eyes with repeated suture erosions had more culture-positive sutures (P = 0.017) and conjuctivas (P = 0.014) at the first erosion in comparison with the second erosion. Infiltration, vascularization, or muscus at the suture site did not correlate with positive cultures. Bacteria are encountered at the site of eroded sutures. Patients with PKP should report symptoms immediately, and eroded sutures should be removed as early as possible.

Metabolic and functional mapping of the neural network subserving inferior collicular seizure generalization

The sensory-motor portion of the inferior collicular cortex is capable of seizure genesis that is characterized initially by coincident wild running behaviors and localized electrographic afterdischarge. With repeated stimulations, this seizure activity spreads into the forebrain, producing generalized tonic-clonic or myoclonic seizure activity. In order to characterize the neural network subserving this caudal-rostral seizure generalization, three mapping techniques were used: 2-deoxyglucose (2-DG) utilization, c-fos expression and local anesthetic microinjection. Kindled seizure generalization from the inferior collicular cortex produced a global increase in 2-DG accumulation, while relative 2-DG increases were found in the inferior collicular cortex, dorsal lateral lemniscus, dorsal central gray, peripeduncular nucleus, medial geniculate nucleus, substantia nigra, entopeduncular nucleus, ventroposterior and centromedian thalamus and tenia tectum, as well as the perirhinal, somatosensory and frontal cortices. Kindled seizure generalization also increased c-fos-like immunoreactivity (FLI) in the inferior collicular cortex, cuneiform nucleus, dorsal lateral nucleus of the lateral lemniscus, peripeduncular nucleus, caudal central gray, dentate gyrus of the hippocampus, rhinal fissure area of the perirhinal cortex and the frontal cortex. Microinjections of procaine into the amygdala, perirhinal cortex, entopeduncular nucleus, substantia nigra, peripeduncular nucleus, dorsal central gray, and pontine reticular nucleus all prevented generalized seizure behaviors, but had no effect on the wild running seizures. Conversely, procaine microinjection into the area of the cuneiform nucleus/pedunculopontine tegmental nucleus prevented the wild running seizure but did not block the generalized seizure activity. Neither wild running, nor generalized seizures were altered following procaine microinjections into the anterior thalamus, sub-thalamus, lateral hypothalamus, hippocampus or deep superior colliculus. Thus, specific forebrain sites form a widespread neural network that mediates the generalization of seizure activity from the inferior collicular cortex into the forebrain.

The cranial attachment of the sphenomandibular (tympanomandibular) ligament.

AbstractThe sphenomandibular (tympanomandibular) ligament develops from Meckel's cartilage between the future petrotympanic fissure and the mandibular lingula. The superior attachment of this ligament has been described to attach to the sphenoidal spine.Fifty‐one cadaver half heads were dissected to study the superior attachment of this ligament. Forty‐five of the 51 ligaments were found to be attached in the area of the petrotympanic fissure, not directly to the sphenoidal spine. Six of the specimens had a thin fibrous slip which fanned out medially to the sphenoidal spine.Twelve additional cadaver specimens were decalcified and cut in various planes through the temporomandibular joint. All specimens showed a fibrous continuation of the ligament through the petrotympanic and/or squamotympanic fissures with an attachment to the malleus in the middle ear. When tension was applied to the ligament the malleus was seen to move.A 115 mm human fetus head was dissected. A ligamentous structure was seen to run from the medial side of the mandibular ramus to the future squamotympanic fissure area. When observed microscopically the ligament was continuous through the fissure and attached to the malleus.

Thickness of Enamel at the Base of Pits and Fissures in Human Molars and Bicuspids

The anatomy of pit and fissure areas* in human posterior teeth has long been a subject for dental research. In 1841, W. Robertson, in his book A Practical Treatise on the Human Teeth,2 stressed the possibility of small openings on the occlusal surface leading into large cavities and published a drawing illustrating a fissure extending to the dentin. In 1870 James Truman3 suggested that fissures predispose to dental caries. A year later J. H. McQuillan4 made the observation that minute fissures may extend almost to the dentin, and he supported this with an illustration of a ground section showing a fissure leading through a small opening into an oval space in the enamel. In 1899 R. R. Andrews,5 quoting Tomes, stated: From the natural depressions which separate the cusps of the molars, minute but deep fissures may be extended through the enamel to within a short distance of the dentin, and they may become larger as they recede from the surface of the tooth. Hopewell Smith6 in 1926 published a series of articles on enamel with numerous illustrations of deeply invaginated pit and fissure areas. Hyatt and Bodecker7-19 have both contributed voluminously to the subject and regarded these areas as faults in the enamel. Standard texts support this view.20' 21 More recently, Hodson22, 23 published several papers on investigations of T hypoplasia, his term for the deep invaginations he found in posterior teeth, using a technique of slow decalcification, followed by microdissection. He stated that these areas were manifestations of arrested amelogenesis, often associated with defective matrix formation. Reviews on the pit and fissure area and the associated subject of occlusal caries have been published by Hyatt12 in 1922 and by Brucker24 in 1944, the latter containing many references. Since decay often starts in pit or fissure areas, the presence of deep invaginations of the enamel is thought by many to be an important predisposing factor. Moreover, clinical studies have demonstrated the susceptibility of these areas to caries.25-28 Methods for caries prevention have been directed at limiting the accumulation of