Two recent studies confirm some of the points we have made about how to regenerate bone in an extraction socket. Let’s start with the first:
The effect of hemostatic agents on early healing of the extraction socket
This study evaluated the effects of placing collagen or oxidized cellulose in an extraction socket. In dentistry, many animal collagen products are made for filling extraction sockets and are usually marketed as collagen plugs with or without graft material embedded in the bovine collagen. Two products that are composed of oxidized cellulose are BenaCel and Surgicel, marketed for surgical hemostasis. In the article, they provide a good literature review of these materials.
“However, in a cutaneous wound healing model, Anselme reported that the remaining collagen sponge was surrounded by foreign body giant cells with granulation tissue 1 month after insertion into the pocket under the skin in the dorsal median zone (Anselme et al., 1990). Moreover, residual collagen in bone was noted 2 months after surgery in a dog iliac crest defect healing model (Finn, Schow, & Schneiderman, 1992). Thus, collagen is not a good biodegradable material. Oxide cellulose has been considered to be a good socket-filling material for its absorbability, as it can be completely absorbed in 28 days as reported by Howk et al. in a swine bleeding model (Howk, Fortier, & Poston, 2016). However, due to its highly acidic properties, this material leads to the lysis of erythrocytes (Achneck et al., 2010; Bjorenson, Grove, List, Haasch, & Austin, 1986) and promotes an inflammatory response (Jamborova et al., 2008). Furthermore, Armstrong and Ibarrola have demonstrated that oxide cellulose inhibits the healing of bone defects in the tibia of rabbits and rats (Armstrong et al., 2010; Ibarrola, Bjorenson, Austin, & Gerstein, 1985).”
Study Results
The data demonstrated that the haemostatic agents delayed early extraction socket healing via compressing the periodontal ligament, inducing apoptosis (cell death) of periodontal ligament cells and retarding the migration, proliferation and osteogenic differentiation of stem cells from the PDL.
The extraction socket was almost filled with newly formed bone on day 14 in the control group (no graft) (below, Figure 1e). However, the insertion of hemostatic agents compromised early socket healing with residual materials detected in the sockets on day 14.
Runx2 and Osterix are two main transcription factors involved in osteoblastic differentiation and bone formation, and the significantly reduced expression of these two molecular markers on day 3 and day 7 in the collagen and cellulose groups supported a compromise by the materials of the osteogenic differentiation of BMSCs and many other cells committed to the osteoblastic phenotype. Thus, the reduced fiber density in the collagen and cellulose groups was associated with the compromised activity (i.e., migration, proliferation and differentiation) of the cells, which in turn impeded the subsequent woven bone formation.
Compression was generated on the PDL by each material which may be a significant causal factor of the apoptosis (death) of PDL cells. On the other hand, the pH dynamics and live/dead cell staining results indicated that oxide cellulose would result in a highly acidic socket, which was another potential factor leading to the apoptosis of PDL cells. It has been established that apoptotic cells are detrimental factors for cellular biological behaviors due to their effect on the microenvironment which would consequently delay the healing of the extraction socket.
