Biocompatibility of surface-sealed dental materials against exposed pulps.
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Biomedical subjects
Publications and source records attributed to C F Cox.
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Past studies dealing with the vascular supply to surgically mobilized dentoalveolar segments have mentioned occasional encounters with vital root transection and have noted varying degrees of pulpal response to this insult. The purpose of this investigation was to observe the pulpal and periapical responses of monkey dental tissues to intentional vital root transection over a 1-year postoperative period. Four adult Macaca mulatta monkeys were used in this study. All roots were surgically transected within the apical third with a bur. Maxillary and mandibular quadrants for 1, 2, 3, 4, 6, 12, 24, and 52 weeks following surgery were obtained after the animals were killed by perfusion of the left ventricle. The tissue blocks were prepared by routine histologic methods. The results demonstrated a disruption of the normal pulpal architecture, with initial pulpal degeneration and subsequent early replacement by the periodontal ligament tissue. A cellular cemental lining of the root canal occurred in all specimens. The periodontal ligament-like tissue continued to deposit cementum, resulting in almost total obliteration of the root canal and pulp chamber and leaving an intact but much reduced blood supply to the pulp chamber containing periodontal tissues.
Four adult Rhesus monkeys provided 120 teeth for buccal Class V cavities. Twenty-nine were non-exposed controls and 91 were exposed for 3 intervals. All 120 teeth were capped with a hard set Ca(OH)2 medicament, restored with amalgam, 57 evaluated after 1 year and 63 after 2 years. Of the 91 exposed pulps, 45 showed complete healing, 25 showed pulpal inflammation varying from acute to chronic, 12 showed severe pulpal breakdown and abscess formation and 9 were necrotic. No difference was observed in the healing response between the 3 exposure times. New hard tissue formed at, or subjacent to, the medicament in 77 of 91 exposed pulps with a tunnel defect frequently present, running from the medicament interface to the pulp. This study demonstrates that recurring pulp inflammation observed after 1 & 2 year direct pulp capping, is associated with bacterial contamination.
Several studies have reported devitalization of teeth following surgical procedures in the area of the root apices. The purpose of this investigation was to observe the 1-4-week wound healing pattern in monkey dental tissues following intentional vital apicoectomy (IVA). Two adult Macaca mulatta were used in this study. All of the teeth were surgically transected within the apical one-third with a bur. The soft tissues were then closed. At death, a maxillary and a mandibular quadrant for 1, 2, 3 and 4 weeks following surgery were obtained after vascular perfusion. Each quadrant was demineralized in EDTA, processed, serially sectioned at 7 microns and alternately stained with hematoxylin and eosin, Preece's modified trichome, and McKay's bacterial stains. Examination of sequential IVA cuts showed an initial disruption of the pulpal neurovascular supply resulting in pulpal necrosis. The pulpal tissues underwent a process of replacement with PDL-like connective tissues and deposition of cementum on all cut dentin surfaces of the tooth roots as well as in some of the pulp chambers. No abscesses, external resorption or ankylosis were found.
The healing capacity of mechanically exposed and bacterially contaminated dental pulps was assessed in monkeys after capping with 2 commercial Ca(OH)2 containing compounds. One hundred eighty teeth in 7 monkeys were employed, 45 as untreated controls and 135 as treated exposures. Class V buccal cavity preparations resulting in pulpal exposure were prepared, left open to the oral cavity for 0, 1, 24 h or 7 days and employed as controls, or debrided, capped, restored with amalgam and left undisturbed for 5 weeks as treated exposures. Zero and 1 h untreated exposures presented damage from the mechanical trauma only, whereas 24 h and 7 day pulp wounds exhibited pronounced infiltrations of polymorphonuclear and mononuclear leukocytes. In addition, the 7 day exposures demonstrated several teeth with partial and total necrosis. Treated 0, 1 and 24 h exposures demonstrated wound healing, minimal pulp tissue inflammation, reorganization of soft tissue and formation of new hard tissue at the exposure site in 86 of 99 teeth. Treated 7 day exposures healed less frequently, showing signs of dentin bridging in 15 of 27 teeth. This study indicated that mechanically exposed and orally contaminated dental pulps in monkeys have a high capacity to resolve inflammation and initiate healing with new dentin formation at the exposure site when treated as described.
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The results from this study showed a variety of pulpal responses to various calcium hydroxide materials when placed directly on the dental pulp. Two of the materials proved to be more successful at stimulating reparative dentin bridging and healing of the underlying pulp tissue. The remainder of the pulp capping agents were ineffective at healing the pulp and forming a reparative dentin bridge. When teeth were capped with these other agents, the pulp showed necrosis and chronic inflammation.
In all, 30 adult (45-day-old) Swiss Webster mice were used for light and electron microscopic examination of the presence, number, and location of adrenergic endings in the first molar teeth. Prior to sacrifice, 10 animals received i.p. injections at 8, 6, 4, and 2 hours of 0.5 cc of 20 mg/kg solution of 5-hydroxydopamine (5-OH-DA) as a label for adrenergic endings. The animals were then anesthetized, perfused with Karnovsky's fixative, and the teeth were postfixed in Osmic acid, decalcified, embedded in methacrylate, and serial-sectioned. The sections were surveyed by light microscopy, and the number and location of nerve endings containing the reduced 5-OH-DA were recorded. Ten control mice were injected with the vehicle solution and prepared in the same manner. A third series of mice were given a single injection of 5-OH-DA, sacrificed, and prepared for ultrastructural study. The molar pulps were divided into four areas to facilitate examination: pulp horns, coronal pulp, bifurcation area, and root pulp. These four areas were further divided into three zones: odontogenic, vascular-related, and nonvascular-associated. The location and number of endings were evaluated, and an average of approximately 70 endings containing the 5-OH-DA were found in each tooth using light microscopy. These represented 35.5 +/- 5.2 in the pulp horns; 26.1 +/- 2.4 in the central coronal; 5.4 +/- 0.7 in the bifurcation, and 5.6 +/- 0.9 in the root pulp per tooth. Vascular related endings were found in greatest number, the odontogenic zone next, and free endings lease. Verification of location of 5-OH-DA by ultrastructural analysis revealed the false transmitter in vesiculated endings in the four areas and zones of the pulp.
Dentinal bridge formation and pulpal responses of four calcium hydroxide materials, pulp capping medicaments, MPC, Experimental MPC-12, Dycal and Pulpdent, were evaluated in primary and permanent monkey teeth. A total of 60 primary and 60 permanent teeth were used with each material placed in a Class V cavity exposure in Rhesus monkey teeth. The materials were placed on the exposed pulp tissue and were histologically evaluated at 3 days, 5 weeks and 8 weeks. After perfusion the teeth were processed using routine histological procedures. The 3-day pulpal responses in both primary and permanent teeth were moderate, characterized by disruption of the pulpal tissue directly beneath the exposure site and a zone of acute inflammation and hemorrhage in the underlying pulp. The 5-week response showed histological differences between the four medicaments, with Dycal producing the least amount of pulpal irritation with reparative dentin bridges occurring in 50% of the permanent teeth. Experimental MPC-12 stimulated one reparative dentin bridge, while Pulpdent and MPC showed no evidence of bridge formation. Pulpal responses to Dycal were moderate and moderate to severe for the other calcium hydroxide compounds. No reparative dentin bridges were seen in the primary teeth at 5 weeks with any of the materials, and the pulpal responses were of a moderate degree at that time. Eight-week responses were similar to the 5-week responses Dycal provoked a slight to moderate pulpal response with 50% success at bridging. Experimental MPC-12 initiated pulpal responses in the moderate to severe range with some bridging evident. Pulpdent incited moderate to severe histological responses with three teeth demonstrating bridge formation, and MPC provoked severe pulpal responses with no bridging. Primary teeth showed some bridging for all compounds except those treated with MPC, in which no evidence of bridging occurred, and moderate to severe pulpal responses were present.
This study showed a statistically significant difference between the microhardness of reparative and primary dentin at both five-and eight-week intervals. Reparative dentin from occlusal trauma is harder than reparative dentin underlying a cavity preparation at the 99% level. No statistical difference was noted in the hardness of reparative dentin underlying different materials, but trends were observed.
Sensory, sympathetic and parasympathetic ganglia located in the head and neck of rhesus monkeys were histologically examined after injection of H3-HRP into the right mandibular premolars and molars. The results showed positive labeling of ganglionic cell bodies located in the ipsilateral trigeminal, superior cervical, and otic ganglia, plus the ipsilateral mesencephalic nucleus of the trigeminal nerve.
In vivo pulpal responses in monkeys and in vitro bacterial inhibition studies were completed on new copper amalgams, Sybraloy, Dispersalloy, Tytin and a conventional Spheraloy amalgam. Amalgams were placed in cavities lined with ZOE and in unlined cavities. Silicate and ZOE were used as controls. A total of 165 adult monkey teeth were evaluated at 3 days, 5 and 8 weeks. At 3 days the pulpal responses elicited by the copper amalgams appeared similar to conventional Spheraloy, all showing a slight to moderate response. At 5 weeks the majority of amalgams exhibited a slight pulpar response with a tubular reparative dentin under each restoration. The 8 week pulpal response showed a reduction of the inflammatory response characterized by a tubular reparative dentin with a uniform zone of predentin. Lined ZOE controls exhibited a slight response while silicate showed a moderate response with some persistent chronic inflammation. In vitro bacterial tests revealed that the various amalgams had little to no inhibitory effect on the three serotypes of S. mutans that are most prominent in humans.
The interfaces and the relationships between collagen and oxytalan fibers were observed under light and electron microscopy. Guinea pig periodontal ligament was prepared for light and electron microscopy with perfusion using Peter's buffered formalin for light microscopy and GTA-S-collidine and OSO4 for electron microscopic studies. The tissue for light microscopy was stained with a modified Gomori's aldehyde fuchsin technique, in which pre-oxidization with potassium monopersulfate was carried out before staining so as to demonstrate the oxytalan fibers. EM tissues were routinely stained with lead citrate and uranyl acetate. Two different structural relationships were observed. First, the subcomponents of the collagen and oxytalan fiber types interweave with each other; and, second, some of these two-fiber subcomponents appear attached to each other. These relationships and the known orientation of oxytalan fibers as seen in the periodontal ligament provide insight as to the function of oxytalan fibers. The oxytalan fibers may provide increased structural integrity and increased distribution of forces over a wider area of the periodontal ligament. Because of their close relationship to blood and lymph vessels in the periodontal ligament, they may also help to stabilize these elements by the same structural relationships to collagen fibers.
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