Oral and Maxillofacial Surgery in Dogs and Cats - E-Book

Frank JM Verstraete, Milinda J Lommer, Boaz Arzi

• Publisher: Elsevier
• Year: 2019
• ISBN:
  9780702076763
• Edition: 2
• Topic: Médecine
• Subtopic: Médecine vétérinaire

Learn to master a highly specialized form of animal surgery. Oral and Maxillofacial Surgery in Dogs and Cats, 2 nd Edition offers a unique, detailed, comprehensive and highly illustrated account of surgical procedures that will improve outcomes for all surgical and dental specialists. The second edition of this text is a collaborative effort from both human and veterinary oral surgeons – each considered an expert in their field. With in-depth clinical photos, and illustrations, this indispensable resource is perfect for both general practitioners and students alike.

• An authoritative collaboration between human and animal surgeons includes over 30 international contributors whorepresent the peak of professional expertise in the field.
• UNIQUE! Only book on the market devoted to a surgical specialty of growing relevance provides you with a look at a highly specialized practice.
• High-quality illustrations combined with step-by-step textual guidance give you a clear understanding of the material.
• In-depth descriptions of surgical conditions provide you with detailed explanations of surgical procedures.

• NEW! Expert Consult site provides you with digital access to the full textbook.
• NEW! Additional chapters on the latest discoveries and techniques cover Diagnostic imaging in oral and maxillofacial surgery, Piezosurgery, Temporomandibular ankyloses and pseudoankylosis, and Regenerative techniques in maxillofacial surgery.

Section 1:

Surgical Biology

Outline

• 1. Oral soft tissue wound healing
• 2. Maxillofacial bone healing
• 3. Use of antibiotics and antiseptics
• 4. Anesthesia and pain management
• 5. Enteral nutritional support

Chapter 1

Oral soft tissue wound healing

Vivek Shetty, Anh D. Le

Definitions

A wound, regardless of the cause of injury, is a disruption of normal tissue continuity and integrity. Healing is simply the process of restoring the integrity of the wounded tissue. If the result is tissue that is structurally and functionally the same as the original tissue, then regeneration has taken place. However, if tissue integrity is reestablished primarily through the formation of a fibrous, connective-tissue scar, then repair has occurred. The nature of the native tissue involved determines whether regeneration or repair will ensue, and the surgeon’s expectations should be correspondingly realistic. Whereas a fibrous scar may be normal for dermal healing, it is suboptimal in the case of bone healing.

General considerations

Every injury initiates an orderly, but complex sequence of orchestrated events that reestablish the integrity of the damaged tissue. Despite the body’s innate ability to heal, surgical intervention is often used to optimize the healing process and favorably modulate the outcome. Interventions may include adequate debridement of devitalized tissue, removal of diseased tissue or foreign materials, securing adequate hemostasis, and apposing severed tissues with mechanical means until such time the wound is capable of withstanding functional stresses.

From a surgical viewpoint, the nature of wound healing depends upon the site, type of tissue involved, and the surgeon’s ability to approximate the wound margins. Healing by first intention usually occurs when early primary closure can be achieved by accurately reapproximating the wound margins. Such a wound heals quickly with no separation of the wound edges, and with minimal scar formation. Absent favorable conditions, wound healing is prolonged and occurs through a filling of the tissue defect with granulation and connective tissue. This process is called healing by second intention and is frequently encountered following avulsive injury, wound infection, or poor apposition of the wound margins. In instances of infected or contaminated traumatic wounds with severe tissue loss, the surgeon may attempt healing by third intention. This is a staged procedure wherein the wound is allowed to granulate and heal by second intention before a delayed primary closure is carried out by bringing together the two surfaces of granulation tissue.

Wound-healing phases

The healing process in different tissues occurs in a cascade of overlapping phases best represented by cutaneous wound healing. Beginning with the inflammatory phase precipitated by the injury, the wound eventually restores itself through sequentially occurring proliferative and remodeling phases. While the rates and patterns of healing depend on a host of local, systemic, and surgical factors, the phases of oral soft-tissue healing are typical for all other tissues as well. In general, wounds in the oral cavity seem to heal faster than wounds to the skin. Oral wounds, despite being exposed to a bacteria-laden, moist, seemingly hostile environment, heal perfectly well and reepithelialize rapidly with minimal or no scar formation.

Inflammatory phase

The wounded area attempts to restore its normal state (homeostasis) immediately following injury. Disrupted blood vessels constrict and thrombose, and the thromboplastin released by the injured cells initiates the coagulation process. The accumulating platelets help form a fibrin clot to control bleeding. Additionally, the injured tissue and platelets begin to release key mediators of wound healing, particularly platelet-derived growth factors (PDGFs) and transforming growth factor β (TGF-β). These chemoattractants recruit inflammatory cells that begin to remove damaged tissue and bacteria from the injured area. Clinical signs include localized edema, pain, redness, and increased warmth at the wound site. Neutrophils are the predominant inflammatory cells during the initial 2 to 3 days following injury but are rapidly outnumbered by macrophages derived from mobilized monocytes. As the primary source of modulating cytokines such as PDGF and vascular endothelial growth factor (VEGF), the macrophages regulate the formation of the granulation tissue that is distinctive of the proliferation phase.¹

Proliferation phase

The proliferation phase is a period of intense replication of cells and is characterized by the migration and proliferation of fibroblasts and smooth muscle cells into the wound milieu. The fibroblast is the major cell responsible for the production of collagen and proteoglycans. Fibroblasts interact with their surrounding matrix via receptors known as integrins that regulate the level of collagen gene expression and collagenase induction. Collagen restores the strength and integrity of the repaired tissue, whereas the proteoglycans function as moisture storage. Concurrent with these events is the process of angiogenesis, whereby new blood vessels are formed and lymphatics are recanalized in the healing tissues. This essential process reestablishes transport of the nutrients and oxygen to the local injured site. In a synergistic way, the new capillaries supply nourishment to the developing collagen, while the collagen fibers structurally support the new capillary beds. Epithelial cells originating from hair follicles, sebaceous glands, and margins of the wound edges proliferate and resurface the wound above the basement membrane. In contrast to skin, the process of reepithelialization progresses more rapidly in the oral mucosal wound. The oral epithelial cells migrate directly onto the moist, exposed surface of the fibrin clot instead of under the dry exudate (scab) of the dermis as in dry skin.² The rapid reepithelialization limits further insults from the oral cavity environment such as food debris, foreign particles, and microorganisms.

Maturation/remodeling phase

The remodeling phase is the final stage of tissue repair and is distinguished by a continual turnover of collagen molecules as precursor collagen is broken down and new collagen synthesized. The tensile strength of the wound gradually restores as the collagen fibers are realigned and increasingly cross-linked to each other. The maximal tensile strength of a healed wound is reached in 6 to 12 months following injury but never reaches the strength of unwounded tissue. Eventually, active collagen synthesis achieves equilibrium with collagenolysis. However, disruptive processes such as poor oxygen perfusion, lack of nutrients, and wound infection can shift the balance to favor collagen breakdown and wound dehiscence.

Healing of extraction wounds

The healing of a dental extraction wound is a specialized example of healing by second intention (Fig. 1.1).³ Immediately after the removal of the tooth from the alveolus, blood fills the extraction site. Both intrinsic and extrinsic pathways of the clotting cascade are activated. The resultant fibrin meshwork containing entrapped red blood cells seals off the torn blood vessels and reduces the size of the extraction wound. Organization of the clot begins within the first 24 to 48 hours with engorgement and dilation of blood vessels within the periodontal ligament remnants, leukocytic migration, and formation of a fibrin layer. In the first week, the clot forms a temporary scaffold upon which inflammatory cells migrate. Epithelium at the wound periphery grows over the surface of the organizing clot. Osteoclasts accumulate along the alveolar bone crest (in humans) or margin (in animals) setting the stage for active crestal or marginal resorption. Angiogenesis begins in the remnants of the periodontal ligaments. In the second week, the clot continues to get organized through fibroplasia and neoangiogenesis that begin to penetrate towa...