According to Christenson R.H. [24], the bone structure, metabolism, and regulation are reflected by markers of resorption, formation, and/or turnover. Among the markers of bone resorption is the type 1 collagen degradation and maker of bone formation: Osteocalcin. Bone formation markers derive from the osteoblastic activity, formed during the different stages of osteoblasts proliferation, differentiation, and osteoid synthesis [6, 51–53], namely the bone osteocalcin, alkaline phosphatase, and other makers. Osteocalcin is expressed during mineralization by osteoblastic cells. [24, 54–56]. Those evidences supported us to analyze the expression of bone extreme activities: resorption (collagen I) and formation (osteocalcin). Our immunohistochemistry results expressed the bone repair because it showed higher expression of osteocalcin at the 9M specimens. Since the titanium implants were fixed for 9 months, peri-implant bone was submitted to masticatory tension [23] and that causes bone activity, stimulating osteocalcin expression, because it occurs during mineralization. Notwithstanding, collagen I expression did not show statistical difference between both experimental conditions, in spite of all numerical values were higher to IR experiment. It can also be explained by the healing time evaluated. Immediate implant removal caused histological evidence but has no time enough to express changes in the expression of collagen type I. The healing time was not extended because immediate removal represents a clinical situation in titanium implant procedures, when failure is detected just after its installation. The higher numerical values of collagen I expression to IR experiment condition indicate more protein activity than 9M. It also represents no removal torque influence in the healing process leading to the understanding that this does not hinder the immediate installation of a new implant in the same socket.