Principles of Dentoalveolar Extractions. Seth Delpachitra
‘decision’ shares a common root with another word often associated with surgery: incision. Both are derivatives from the Latin word caedis, meaning ‘to cut’. Incision means to cut into something, such as the operative site; decision literally means ‘to cut away’. A decision thus precludes other options, and sets one upon a particular course of action. A skilled surgeon will be able to make treatment planning decisions that are in the best interests of their patients.
1.1 Wound Healing
Good outcomes following surgery depend on satisfactory wound healing. This involves a range of inflammatory, biochemical, and physiologic changes at the operative site, which will ultimately lead to resolution, healing, and bone remodelling. Wound healing does not always follow a predictable course, and therefore an understanding of its key aspects will serve as a foundation for interpreting clinical signs and determining when it is compromised.
There are four key stages in wound healing (Figure 1.1):
1 Haemostasis.
2 Inflammatory phase.
3 Proliferative phase.
4 Remodelling and resolution.
Figure 1.1 Phases of wound healing.
An interruption at any one of these stages will lead to a protracted recovery period.
1.1.1 Haemostasis
Any tissue trauma will result in bleeding from the local vasculature supplying the tissues. The immediate physiologic reaction is haemostasis, which involves reactive vasospasm, formation of a platelet plug, and activation of the coagulation cascade.
Reactive vasospasm occurs in the seconds to minutes following damage to the blood vessels. This is mediated through neurologic mechanisms, as well as the local release of endothelin. It rapidly reduces blood loss from trauma. In surgery, exogenous vasoactive medications such as adrenaline utilise this response to improve visual access to the surgical field by reducing blood flow.
Damaged endothelial cells result in a conformational change in von Willebrand factor expressed on the cell surface. Von Willebrand factor interacts with glycoprotein Ib on circulating platelets, resulting in activation and aggregation of the platelets, forming links to fibrinogen via the GpIIb/IIIa receptor. This leads to the formation of the platelet plug. Antiplatelet medications inhibit aspects of platelet plug formation and increase the risk of bleeding during surgical procedures.
The coagulation cascade is a series of successive reactions that occur in order to activate thrombin and form a stable fibrin clot (Figure 1.2). There are two pathways in this cascade: intrinsic and extrinsic. The intrinsic pathway is activated within the vascular system through exposure to endothelial collagen, whilst the extrinsic pathway is activated by tissue trauma and release of intracellular tissue factor. Anticoagulant medications and coagulopathies increase the tendency to bleed by inhibiting aspects of the coagulation cascade, and awareness of these effects may be clinically relevant in surgical planning.
Figure 1.2 The coagulation cascade.
Coagulation studies used clinically can assess the function of either the intrinsic, the extrinsic, or the shared common pathway. Prothrombin time screens for factors II, V, VII, and X and fibrinogen; these are all part of the extrinsic pathway, which is used to guide treatment for patients treated with warfarin. Warfarin inhibits vitamin K‐dependent factors common to both pathways, but because factor VII has the shortest half‐life, the extrinsic pathway is used to determine coagulability. The partial thromboplastin time will screen for factors in the intrinsic pathway affected by medications such as heparin and low‐molecular‐weight heparin.
1.1.2 Inflammatory Phase
This will commence on day one after the procedure and will continue for approximately three days. Important aspects of the inflammatory response include the release of pro‐inflammatory mediators and vasoactive factors such as the prostaglandins, leukotrienes, interleukins, and histamine, and recruitment of phagocytes to remove dead tissue and foreign debris. The inflammatory mediators lead to the swelling, redness, heat, pain, and loss of function associated with inflammation. Anti‐inflammatory medications are commonly prescribed after dentoalveolar procedures in order to mitigate the postoperative pain and swelling.
1.1.3 Proliferative Phase
This typically starts around day three and lasts for up to three weeks. The proliferative phase relies on the formation of granulation tissue and type III collagen, mediated by fibroblasts; wound contraction starts due to the action of myofibroblasts. Angiogenesis takes place as new capillaries are formed to provide blood and nutrients in order to help the wound heal. A number of growth factors, including vascular endothelial growth factor (VEGF), are also involved. At the wound edges, epithelial cells proliferate and begin to grow over the granulation tissue scaffold that has formed. Bone healing starts to take place as osteoprogenitor cells arrive, differentiating into osteoblasts, which begin depositing an osteoid matrix. Note that any systemic conditions or medications which prevent or suppress components of angiogenesis or inflammation may delay or prolong healing.
1.1.4 Remodelling and Resolution
At the completion of three weeks of healing, granulation tissue and immature bone will fill the extraction site, and the socket should be completely covered by a layer of epithelium. Bone remodelling will continue to take place with active resorption and deposition mediated by osteoblasts and osteoclasts. This important step can be impeded by medications that inhibit osteoclast function, such as bisphosphonates or denosumab. Radiographic evidence of bone remodelling will not become evident until after six to eight weeks.
1.2 Patient Assessment
Any medical or dental intervention requires a comprehensive patient history. This includes: a detailed medical history, including current and past medical treatments; documentation of known drug allergies and reactions; a social history comprising occupation and use of alcohol, cigarettes, and illicit substances; prior surgeries, dental treatments, and adverse outcomes; and, finally, the patient's chief complaint or main concerns.
Secondary to this is the clinical assessment of the patient's orofacial region, including both extraoral and intraoral examination. This should include an assessment of the temporomandibular joint, soft and hard tissue pathologies, and the presence of any dental pathology. Simultaneously, a difficulty and risk assessment for dentoalveolar surgery can be undertaken, paying particular attention to mouth opening, gingival biotype, gag reflex, patient anxiety, and previous heavily restored dentition.
Diagnostic tests should be carried out as necessary, including pulp testing, palpation for mobility, and percussion testing. A periodontal probe can be used to examine partially erupted or unerupted teeth, to assess soft tissue opercula, or to explore other communications with the oral cavity.
The patient's psychological state and level of anxiety can be assessed by asking how well they have tolerated dental treatment in the past. This aspect of the assessment is important; by virtue of temperament, some patients will require a more detailed discussion about their treatment, and some may request or require treatment with sedation or general anaesthesia.