Arthroscopic management of temporomandibular joint disc perforations and associated advanced chondromalacia by discoplasty and abrasion arthroplasty: a supplemental report.

PURPOSE: This article describes the results of treating temporomandibular joint (TMJ) articular disc perforation and advanced chondromalacia arthroscopically by the use of discoplasty and abrasion arthroplasty. PATIENTS AND METHODS: Forty-four joints were treated in 25 patients (23 females and 2 males). Twenty-nine disc perforations were present, 24 joints had grade III chondromalacia (fibrillated cartilage), and 14 joints had grade IV chondromalacia (exposed bone). Surgical procedures included 14 abrasion arthroplasties and 24 motorized shavings or holmium laser vaporizations. Holmium laser discoplasty with mobilization was used in 29 joints. Patients were followed-up for an average of 40.8 months (11 to 74 months). RESULTS: Preoperative pain on the visual analog scale (VAS) (1 to 10 cm) ranged from 5 to 10 cm, with an average of 7.4 cm. Postoperatively, nine patients had no pain and 16 patients had an average VAS of 2.7 cm (range, 1 to 5 cm). Preoperatively, 30 joints had clicking, and 14 joints had crepitation. Postoperatively, 25 joints had no noise, 12 joints had slight intermittent clicking, and seven joints had crepitation. The preoperative range of motion averaged 29.7 mm. Postoperatively, the range of motion averaged 37.7 mm (range, 33 to 42 mm). All patients could masticate a regular diet except hard food after an average of 40.8 months (11 to 74 months). CONCLUSIONS: These findings seem to justify the arthroscopic surgical procedures of discoplasty for disc perforations, motorized shaving, or holmium laser vaporization of grade III chondromalacia, and abrasion arthroplasty for bone exposure. The results also question the need for discectomy in the treatment of disc perforation.

Selective deafferentation of convergent inputs to trigeminal subnucleus caudalis: effects on calcitonin gene-related peptide distribution.

Electrophysiological studies (Sessle, 1987, 1991) suggest that trigeminal deafferenting injuries can cause an "unmasking" of existing but normally suppressed convergent inputs to the spinal trigeminal nucleus, including many that arise from the cervical spinal cord. However, the spatial arrangement of this projection has not been examined, particularly with reference to nociceptive components that might become involved in pathological changes leading to chronic pain. Therefore, the purpose of this study was to apply selective interruptions of the trigeminal and/or cervical primary afferent inputs to the spinal trigeminal subnucleus caudalis (Vc) in the cat, followed by (1) demonstration and quantification of axonal degeneration in the spinal trigeminal tract to determine the extent of trigeminal-cervical primary afferent overlap; and (2) an analysis of lesion-induced alterations in the distribution of calcitonin gene-related peptide immunoreactivity (CGRP-IR) in laminae I and II of Vc, since recent evidence strongly suggests that CGRP is involved in pathophysiological elevations of central nervous system neuronal excitability. Degenerating fibers were found throughout the spinal tract following a trigeminal rhizotomy or tractotomy, with the largest numbers adjacent to the rostral two-thirds of Vc, but with a significant number extending caudally to at least the level of C2. CGRP-IR was reduced or eliminated from the rostral one-third and periobex region of Vc, except for a dorsomedial zone that was minimally affected. Retention of CGRP-IR was greater at more caudal levels. Following a combined trigmeninal and cervical tractotomy, fiber degeneration was massive throughout the spinal tract, yet a population of small myelinated fibers persisted at 60 days after surgery. Concomitantly, CGRP-IR was profoundly reduced throughout Vc, except for a small dorsomedial zone of retention, which became more extensive caudally. A cervical tractotomy resulted in moderate numbers of degenerating fibers adjacent to the caudal one-third of Vc, and this number declined rostrally; however, degenerating fibers could be seen at the level of the obex. CGRP-IR was reduced in the dorsomedial and ventrolateral zones of Vc, particularly in its caudal one-third. Electron-microscopic analysis revealed a population of CGRP-IR boutons, most of which were of the simple axodendritic type with asymmetrical contacts. A few examples of axoaxonic contacts were observed. Loss of labeled boutons observed with the electron microscope was consistent with light-microscopic quantitative results. Those boutons that were retained were variable in size and displayed simple axodendritic contacts.(ABSTRACT TRUNCATED AT 400 WORDS)

Ultrastructural characterization of substance-P-immunoreactive synaptic terminals in the cat's normal and rhizotomized trigeminal subnucleus caudalis.

Deafferenting injuries often cause transient or permanent physiological alterations within the central projection field of affected primary afferent fibers. Aberrant sensory perceptions, dysesthesias, and hyperalgesias represent the clinical sequelae of such injuries; however, the results of experimental deafferentations have been subject to a variety of interpretations (Rodin and Kruger, 1984b). Neurochemical studies show an increased sensitivity of partially deafferented neurons to substance P (SP). Our previous studies (Hoffmann et al., 1991) documented, primarily at the light-microscopic level, a moderate transient loss of SP-immunoreactive (SPIR) boutons in the trigeminal subnucleus caudalis (Vc)--a loss that seemed to preferentially affect the slightly larger, possibly complex boutons with multiple contacts. However, despite the elimination of the trigeminal input, the larger boutons reappeared. In the present study, therefore, we examined Vc using electron-microscopic immunocytochemistry, in order to document these changes over time and to clarify the structure and relationships of this population of boutons. SPIR boutons occurred in lamina I and II degrees of the substantia gelatinosa of Vc, ranged in size from 1 to 5 microns in diameter, and displayed mixed populations of clear and dense-core vesicles. Most formed single or multiple axodendritic junctions, but a significant number engaged in axoaxonic contacts with both SPIR-labeled and unlabeled terminals. A small number appeared to be the central element of a typical glomerulus, particularly in lamina II degrees. Three to seven days following an ipsilateral retrogasserian rhizotomy, synaptic degeneration was evident in the substantia gelatinosa and often involved glomerular terminals. However, most of these were SPIR-negative and occurred primarily in lamina II degrees. Those SPIR boutons that displayed degenerative features often made single or multiple axodendritic contacts, and in some instances were scalloped. By 30 days, most remaining SPIR boutons were small, with a lower incidence of contacts; however, some of these were axoaxonic. In addition, many SPIR terminals were only very lightly stained--a feature not encountered to such an extent in the contralateral Vc. At 45 days, complex SPIR boutons were again evident in the field, and some showed densely packed vesicles. An increased incidence of clusters of two to four SPIR axoaxonic contacts was also observed. Finally, almost all SPIR boutons encountered at this stage were intensely stained. It is suggested that these alterations represent a compensatory neuroplastic response on the part of overlapping cervical and cranial primary afferents to the partial deafferentation resulting from the interruption of the trigeminal root.(ABSTRACT TRUNCATED AT 400 WORDS)