إعداد الأستاذ المساعد الدكتورة فيحاء أزهر المشهداني
قسم علوم طب الأسنان الأساسية، جامعة الموصل، العراق
الإشراف والتدقيق العلمي الدكتور رامز القضماني
Given the millions of dental implants and dental surgery involving bone, plus the frequent use of analgesic drugs for postoperative analgesia and inflammatory conditions. The effect of analgesic drugs on bone density and healing should not be missed. Non-steroidal anti-inflammatory drugs (NSAIDs) have been used by humans in various forms for more than 3500 years, their popularity is still enormous. Despite this long history, the mechanisms of how NSAIDs achieve their all actions are still not completely understood (Vane, 2000). From 30 years ago, it was first revealed that these drugs reduced the formation of prostaglandins and that this ability was associated with inhibition of the enzyme cyclooxygenase (COX).
In the early 1990’s the existence of two isoforms of COX, COX-1, and COX-2 were demonstrated, leading to the categorization of all NSAIDs according to their specificity to each of these isoforms (Warner and mitchell, 2002., Raffa et al., 2014). NSAIDs usually are classified as mild analgesics, however, consideration of the type of pain, as well as its intensity, is important in the assessment of analgesic efficacy. NSAIDs are particularly effective when inflammation has caused sensitization of pain receptors to normally painless mechanical or chemical stimuli. Pain that accompanies inflammation and tissue injury probably results from local stimulation of pain fibers and enhanced pain sensitivity (hyperalgesia), in part a consequence of increased excitability of central neurons in the spinal cord (Hyungsuk and Raymond, 2011; Clark et al., 2012).
NSAIDs are widely prescribed for dental implant patients, not only for postoperative pain relief but also for other systemic diseases like muscular and skeletal disorders. Given their frequency of use, likely cross-correlation of NSAIDs with implant failure could indicate that they cannot be used safely for pain relief during the early postoperative period and a possible increased risk of implant failure if performed for the patient after chronic use of such drugs (Demos and Maria, 2008). Although the effects of NSAIDs in maxillofacial surgery have not been adequately investigated, their negative effect on bone healing has been confirmed in orthopedics (Aspenberg, 2002; Kjaersgaard and Jensen, 2003; Jeffcoach et al., 2014).
Until recently, the adverse effects of NSAIDs on the osseointegration of dental implants were unknown (Cai et al., 2014). Studies showed delayed in the healing of dental implants in diclofenac treated animals compared to other animals, was associated with a decline in osteocyte lacunar density. An impaired bone remodeling process is reflected in a reduced number of osteocytes and the presence of bone necrosis areas in the diclofenac group compared to other groups (Krischak et al., 2007; Bjőrn et al., 2010). Diclofenac may arrest the favorable effects of increased roughness on cells at the bone-implant interface. In the culture of osteoblast-like cells, isolated from humans, the presence of indomethacin caused inhibition of the cell roughness at the bone-implant interface (Batzer et al., 1998).
The health of the host bed (the bone and soft tissues) into which the implant is placed is important for osseointegration. The amount of blood in the bone site i.e. vascularity and the quality of the bone into which the implant is being placed are crucial factors that determine how well the implant will integrate into the bone. The vascularity determines how many bone cells are available to help with the osseointegration process. If the blood supply is reduced or compromised, the rate at which osseointegration can occur will be affected due to the reduced number of cells that can be transformed into bone-forming cells. The bone quality is assessed by the density of the bone. The bone density helps to determine the extent of the initial healing period. Bone volume dose not itself influences osseointegration, but it is an important determinant of implant placement (Kuzyk et al., 2011).
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