Inflammation and Pain after Surgery
Presnted by:
marwa bedier
Inflammation and Pain after Surgery
Periradicular surgury differs from peridontal surgury in purpose, procedures, manipulation of soft and osseous tissues and mechanism of wound healing.
Periradicular surgury entails surgical manipulation of normal healthy oral soft tissue and supporting bone.
The tissue wounded in the periradicular surgery are the oral mucoperiosteal tissues, periradicular (Bone +P.L) and radicular tissues(Dentin+Cementum).
Type of surgical wound include, incisional /blunt dissection and excisional.
Rate of healing is fastest in incisional and slowest in excisional, a reflection of fact that the former heals by primary intention.
Mucoperiosteal wound healing
Reflection of the mucoperiosteal flap requires incsional and dissectional wound.
INCISIONAL WOUNDS
Precise and least injury, Involves the epithelium and reapproximation of like tissues.
DISSECTIONA WOUNDS
Less precise,entail crushing force during reflection, does not involve the epithelium and reapproximation of dissimilar tissue.
(fibrous connective tissue to cortical bone)
Healing Phases:
Phase I: Clotting and Inflammation.
Phase II: Epithelial healing.
Phase III : Connective tissue healing.
Phase IV: Maturation and Remodeling.
INCISIONAL WOUNDS
Phase I: Clotting and Inflammation
Clotting:
§The first requirement in wound healing is hemostasis.(Ross 1969)
§
§Vascular injury release plasm fractions(albumin, gloublin,etc) and erythrocytes, platelets and leukocytes.
§
§ Also, the host mediators are activated causing initial vascular contraction followed by vasodilatation and increased permeability and platelet aggregation (platelet plug) then the intrinsic and extrinsic clotting mechanism triggered and clot is formed.
Proper post surgical tissue compression, the clot form thin gel occluding the narrow spaces of the wound and connecting the wound edges.
If blood continue to leak, formation of coagulum of serum, plasma fractions and fibrin fragments leading to delayed migration
of inflammatory and reparative cells into the wound site with secondary intention healing, excessive granulation tissue and scar formation (John 1991).
Phase I: Clotting and Inflammation
Inflammation :
Early inflammation:
As result of release of chemical madiators(chemoattractant) plymorphnuclaer neutophil begin to enter the wound site within 6h of clot stablization and reach the peak at 24-48h.
Late inflammation:
vBy approximately the third day macrophages begin to enter the wound site. Although the neutrophil initiate phagocytic process, macrophages are more efficient.
v
v Have longer life span and play a major role in decontamination through phagocytosis of bacteria and tissue debris and processing of antigen to T-lymphocytes.
v Directing Initiation wound healing by stimulation of fibroblast which begin synthesis the ground substance and collagen essential for macrophage-induced angiogenesis which provide bl. supply to the wound for active healing. Haunt 1984.
v
Phase II: Epithelial healing
Epithelium:
The first step is formation of epithelial seal on the surface of fibrin clot, this begins at the edges of the wound, where the basal and suprabasal prickle cell undergo mitosis and migrate 0.5-1mm per day across the clot by contact guidance then stop by contact inhibition of cells in opposite wound edge.
Phase III : Connective tissue healing
Fibroplasia:
Fibroblast migrate by the third day to the wound site, this stimulated by cytokines (FGF, IGF-1, PDGF produced by platelets, macrophages and lymphocytes.
As macrophages decline and fibroblast increase tissue in the wound transfer from Granulomatous to granulation tissue.
By the third day Collage type II is produced, then as wound mature type collagen type I is produced and become more organized.
Phase IV: Maturation and
Remodeling
Begin 5-7 days after injury.
Suffficient collagen produced, reduction in fibroblast and replacement of granulation tissue by young fibrous connective tissue.
As healing progress collagen reorganization require deaggregation (depolymerization) and reaggregation to inc. strenght of the wound.
Wound contraction:
Myofibroblast–fibronectin network
Myofibroblast attach to the surrounding tissue and to each other through powerful binding force of fibronectin on the cell membrane, plays significant role in wound contraction .
Lorena et al., 2002
DISSECTIONAL WOUNDS
The fibrin clot organized by granulation tissue derived from one wound edge only (mucoperiostesl)
Cortical retained periostium showed cellular destruction, collagen depolymerization.
It plays a protective role against clastic activity and necrosis of surface lamella under the cortical bone
Periradicular and radicular
wound healing
Excisional wound
Exposure of the root end by removal of bone, resection of the root-end,where tissues are removed from the surgical site.
Excisional wound become filled with coagulum contain widely spaced fibrin strands, serum exudate and inflammatory cells.
Apical dentoalveolar healing
Osseous Healing
Endosteal tissue proliferate into the coagulum, and osteoblast begin formation of woven bone.
About 3 to 4weeks after surgery, 75%to 80% 0f the osseous wound filled with trabecula surrounded by active osteoid and osteoblastic cells.
At 8 week trabecula are larger and osteoid less prononced and ostoblast dec.
Trabecula replaced by mature lamellar bone.
Reformed periostium can be seen in the outer surface.
Factors affecting wound healing:
1- Size of the lesion.
Rubinstein and Kim, 1999 showed that periapical defect of size <5mm might heal within few months, Nancy et al.,2004 reported that the preoperative lesion size affect the outcome.
2- Type of the flap.
The blood vessels in the mucoperiostium are oriented in vertical direction,so angled vertical or horizontal incision will disrubt the vascular supply.
3- Improper management of the supporting peridontium.
Traumatic reflection, longer time of retraction, improper repositioning and inadeguate suturing
(Gutmann and Harrison, 1985)
4-Quality of cleaning and shaping.
5-Quality of root-canal obturation and seal.
6- Root- end resection.
7-Type of root-canal filling or root-end filling.
MTA showed high incidence of cementum formation and osseous healing when used as root- end filling material. Torabinejad 2003.
8- Loss of the buccal cortical plate will render poor prognossis Wesson and Gale2003)
9- presence of endo-perio lesion will lower the success rate. Kim et al.,2008
10- Introduction of microsurgical techniques will improve the success rate (Von Arx,2005).
11- Guided tissue regeneration (GTR) and Bone augmentation : enhance the quality and quantity of bone regeneration and accelerate bone growth.
12- The use of antibiotics to manage potential infection and enhance healing Barnett et al 1988.
Pain after endodontic surgery
In periapical surgery, as in any surgical procedure, secondary effects such as pain and swelling may occur. Peñarrocha 2006
In majority of patients , pain following periradicular surgery is minimal.
post surgical pain is of short duration and reach its maximum intensity 6-8h following surgery.
pain and swelling during the first 2 days of periapical surgery were more distinct in patients with poor oral hygiene before surgery and in smokers. García et al 2007.
Low level laser therapy can be beneficial for the reduction of postoperative pain. Kreisler 2004.
Its unusual for patient to experience pain that can't be managed by mild to moderate analgesics (NSAIDs). Seymour and Meeghan 1986.
Another method to control postsurgical pain is the use of long-acting local anaethesia, such as bupivacine (Marcaine) or etidocaine (Duranest), which provide 6-8h of local anaethesia and up to 10h of local analgesic. Dunsky and Moore 1984.
They are not used alone because they contain low conc. Of VC so, they should be used in conjunction with lidocaine.