Healing of Extraction Socket
Healing of Extraction Socket
Healing of Extraction Socket
Introduction HEALING BY SECONDARY INTENTION SEQUENCE OF CHANGES FOLLOWING EXTRACTION-: IMMEDIATELY FIRST 24 TO 48 HOURS 1ST WEEK 2ND WEEK 3RD WEEK HISTOLOGICAL CHANGES FOLLOWING EXTRACTION-: Inflammatory Proliferative Remodelling
CONTENTS-
Factors affecting healing Complications of healing Guidelines to be followed for an Uneventful healing Importance of healing from prosthodontic point of view index
Introduction
The healing extraction socket is an overt
expression of an intricate and tightly choreographed sequence of biochemical responses directed toward restoring tissue integrity and functional capacity following extraction.
phenomenon of healing of extraction wounds is imperative to the dentists,since vast number of teeth are extracted because of pulp,peripical infection ,periodontal disease and there is an evert possibility of complications in the healing process. The healing of an extraction wound does not differ from healing of other wounds of the body except as it is modified by the peculiar anatomic situation which exists after the removal of the tooth.
Extraction Wounds
The healing of an extraction socket is a specialized example of healing by secondary intention.
Secondary intention,occurs when 1. wound edges are separated 2. gap between them cannot be bridged directly 3. extensive loss of epithelium, 4. severe wound contamination or 5. significant subepithelial tissue damage.
Healing occurs, slowly from the bottom of the wound towards the surface by the process of granulation resulting in a greater mass of scar tissue than healing by primary intention. In time, such scarring tends to shrink, resulting in wound contracture.
engorgement and dilation of blood vessels within the periodontal ligament remnants
followed by leukocytic migration formation of a fibrin layer.
The hours after tooth extraction are critical, for if the blood clot is dislodged , healing may be greatly delayed and may be extremely painful.
3. inflammatory stage White blood cells enter the socket to remove contaminating bacteria from the area and begin to break down any debris, such as bone fragments, that are left in the socket.
4. Fibroplasia also begins during the first week, with the ingrowth of fibroblasts and capillaries.
5. epithelial migration: down the socket wall until it either reaches a level at which it
6.contacts epithelium from the other side of the socket or it
7.encounters the bed of granulation tissue (i.e., tissue filled with numerous immature capillaries and fibroblasts) under the blood clot over which it can migrate.
8.Finally, during the 1st week of healing, osteoclasts accumulate along the crestal bone.
Osteoid deposition has begun along the alveolar bone lining the socket. In smaller sockets the epithelium may have become fully intact by this point.
Trabeculae of osteoid slowly extend into the clot from the alveolus, and osteoclastic resorption of the cortical margin of the alveolar socket is more distinct. The processes begun during the second week continue during the third and fourth weeks of healing, with
typically broken down into three distinct overlapping phases: inflammatory, proliferative, remodeling.
Inflammatory Phase
The inflammatory phase usually lasts for 3 to 5 days.
Vasoconstriction of the injured vasculature is the spontaneous tissue reaction to bleeding.
Initiation: Tissue trauma and local bleeding
activate factorXII (Hageman factor), which initiates the various effectors of the healing cascade including the complement, plasminogen, kinin, and clotting systems.
Aggregation: Circulating platelets (thrombocytes) rapidly aggregate at the injury site ,adhere to each other and the exposed vascular subendothelial collagen to form.
Early vascular responses to injury. Initial transient vasoconstriction (A) is soon followed by
vasodilation (B). Vasodilation is caused by the actions of histamine, prostaglandins, and other vasodilatory substances. Dilation causes intercellular gaps to occur, which allows egress of plasma and emigration of wbc
Inflammatory (lag) stage of wound repair. Wound fills with clotted blood, inflammatory cells, and plasma. Adjacent epithelium begins to migrate ,undifferentiated mesenchymal cells begin to transform into fibrobiasts
The clot secures hemostasis and provides a provisional matrix through which cells can migrate during the repair process.
Additionally the clot serves as a reservoir of the cytokines and growth factors that are released as activated platelets degranulate.
The bolus of secreted proteins: interleukins
(TGF-),
(PDGF), and (VEGF) regulate subsequent healing.
Proliferative Phase
The cytokines and growth factors secreted during the
weeks,
the proliferative phase is distinguished by the formation of pink
microcirculation to supply the oxygen and nutrients necessary for the elevated metabolic needs of regenerating tissues.
Remodelling
The proliferative phase is progressively replaced by an extended
deposited during the granulation phase is gradually replaced by stronger Type I collagen.
Local
wound sepsis Location poor blood wound tension foreign bodies previous irradiation
poor technique
Immobilization-so that formation of connective tissue is not hindered
Systemic
nutritional deficiencies-protein,vitamins(A,C,D)
systemic diseases
therapeutic agents Age-wounds in younger persons heal more rapidly
4.
5.
localized alveolar osteitis. delay In the absence of a healthy granulation tissue matrix, the apposition of regenerate bone to remaining alveolar bone takes place at a much slower rate. Compared to a normal socket the infected socket remains open or partially covered with hyperplastic epithelium for extended periods. Fibrous healing of extraction wound
figure is much higher if the definition of postextraction pain is used as the sole diagnostic criterion.
4.
5. 6. 7.
Infection Extraction trauma Blood supply Site Smoking Sex Systemic factors, e.g. oral contraceptives
extraction. Commonly occurs when extraction is accompanied by loss of both lingual and labial or buccal plates alongwith the periosteum radiographically -well circumscribed radiolucent area in the site of previous extraction site. Treatment is excision of the lesion.
summarsation
The removal of a tooth initiates the same sequence of inflammation, epithelialization, fibroplasia, and
consists of cortical bone (the radiographic lamina dura) covered by torn periodontal ligaments, with a rim of oral epithelium (gingiva) left at the coronal portion.
The socket fills with blood, which coagulates and seals the socket from the oral environment
.
The cortical bone continues to be resorbed from the crest and walls
of the socket, and new trabecular bone is laid down across the socket. It is not until 4 to 6 months after extraction that the cortical bone lining a socket is fully resorbed; this is recognized radiographically by a loss of a distinct lamina dura. As bone fills the socket, the epithelium moves toward the crest and eventually becomes level with adjacent crestal gingiva.
Radiographic evidence of bone formation does not become
reason for the introduction of virulent microorganisms into the wound. Minimal trauma-Transformation of contaminated wounds into infected wounds is also facilitated by excessive tissue trauma, remnant necrotic tissue, foreign bodies, or compromised host defenses. meticulous surgical technique -The most important factor in minimizing the risk of infection is meticulous surgical technique, including thorough dbridement, adequate hemostasis. proper postoperative -technique must be augmented by proper postoperative care, with an emphasis on keeping the wound site clean and protecting it from trauma.
fabricated. Ideally a waiting period of 4 to 6 months is advisable after extraction since there is increased resorption immediately following extraction. Cases of abused tissue ,hyperplastic tissue and an abnormally contoured ridge can compromise the success of replacement dentures.
The alveolar ridge following tooth extraction undergoes a
progressive,irreversible resorption.
force per unit area.systemic factors such as the menopause cause residual ridge resorption,but the evidence supports a multifactorial cause. sequence of changes in shape of residual ridges following tooth extraction-: the ridge at first becomes knife edged before becoming flat and finally totally resorbed. there are differences in the direction of ridge resorption in different areas of the mouth. in the anterior part of the jaws,it is vertical and labiolingual. posteriorly maxillary ridge resorbs vertically and buccopalatally while mandibular ridge is resorbed in a vertical direction.
index
PETERSON'S PRINCIPLES OF ORAL AND MAXILLOFACIAL
SURGERY TEXTBOOK OF GENERAL AND ORAL SURGERY,david wray,david stenhouse,lee,clark Complete dentures,hugh delvin