Discussion - References.
Calcium sulphate has been reported to be useful as a bone substitute because it is easy to apply, bioresorbable (Peltier 1961), and biocompatible (Sottosanti 1992b, Mesimeris et al.1995). In a case with infection, calcium sulphate drained out with the pus and did not result in any sequestrae (Peltier 1961). It has been used in bone without hazard or complications (Peltier1961). Calcium sulphate did not adversely affect the healing of surgical defects in one study (Calhoun et al. 1965), and did not cause any foreign body reaction in the others (Alderman 1969, Yamazaki et al.1988).
Bone healing in three types of osseous defects which are encountered clinically was evaluated in this study. type1defects, which were simulated endodontic-periodontal defects, were not evaluated morphometrically because bone had not yet formed on the buccal side of the root in either experimental or control teeth at 16 weeks after surgery. Some possible explanations for these findings include:
- calcium sulphate may have been dissolved in saliva or drained out in the pus from the gingival sulcus because some specimens showed inflammation
- the bone on the buccal side of the root in type 1 defects might not have been thick enough originally to allow healing.
It has been reported that calcium sulphate did not stimulate new bone formation in infrabony periodontal defects, and the thin walls of the defects were resorbed due to the shortage of the blood supply and osteogenic cells (Shaffer & App1971). Radiographic assessment of osseous remodeling has been shown to be in direct proportion to the number of bone walls (Bier1970). Hence, type1defects, which were surrounded with only a few bone walls, might have been unsuitable for bone healing with calcium sulphate filling.
BV/TV values in type 2 and 3 osseous defects showed that calcium sulphate was remarkably effective at encouraging bone repair. Pecora et al. (1997) have reported that calcium sulphate could exclude connective tissue as a barrier and allow bone regeneration during healing. Calcium sulphate, however, was unlikely to have acted as a barrier because it was resorbed from 4 to 8 weeks (Peltier1961, Radentz &Collings1965, Bahn 1966,Yoshikawa et al. 2002). In this study, calcium sulphate was not observed at 8 weeks in any specimens, and no foreign body reaction was found.
The mechanism for resorption of calcium sulphate has not been clarified. Calcium sulphate implanted into muscle was resorbed more quickly than autogenous bone and freeze-dried bone (Bell 1964). Serum calcium levels were elevated when associated with resorption of calcium sulphate in dogs, which may indicate that calcium sulphate has the potential to elevate local concentrations of inorganic calcium and phosphorus ions (Peltier et al.1957). On the other hand, Sidqui et al. (1995) reported that osteoclasts could attach to calcium sulphate, and resorb it in vitro.
MAR values on the experimental side were higher than those on the control side. These results revealed that calcium sulphate facilitated bone mineralization. Possible explanations for these findings include:
- the calcium ion from calcium sulphate might play some role in bone formation
- calcium phosphate arising from calcium sulphate may have created a scaffold for in growth of osteoblasts.
Dissolution of calciumsulphate might increase the concentration of calcium ions and stimulate bone mineralization. Damien et al. (1994) reported that a rich layer of calcium phosphate was formed on a calcium carbonate implant, and this layer allowed growth of bone in direct apposition to calcium carbonate. This might suggest the role of calcium ions in bone formation. Sulphate ions released from calcium sulphate might be transformed into phosphate ions from surrounding fluid. The surface of calcium sulphate might convert into calcium phosphate and this might become a scaffold for in growth of osteoblasts.
The biologic mechanisms forming the basis for bone grafting include two basic processes: osteoinductive (e.g. BMP) and osteoconductive (e.g. Hydroxyapatite). Calcium sulphate has been reported to be osteoconductive, not osteoinductive (Hadjipavlou et al. 2000). Some studies have reported that calcium sulphate itself did not induce bone formation (Coetzee 1980, Yamazaki et al.1988, Sottosanti 1992a), and it seemed to stimulate osteogenesis when implanted in contact with bone or periosteum (Peltier et al. 1957, Beeson 1981, Mckee & Bailey 1984). In type 2 and 3 defects, calcium sulphate was placed in contact with bone, whereas in type 1 defects, it was placed in contact with less bone surface compared to the other types of osseous defects. Calcium sulphate was effective on bone regeneration in osseous defects which were surrounded by enough bone; such as type 2 and 3 defects. On the other hand, the application of calcium sulphate alone in endodontic-periodontal osseous defects such as type 1 defects was not effective.
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