Tenderness, discharge and lymphatic involvement are also impor 8 Principles of Oral and Maxillofacial Surgery surgeon will need to consult. Text book of Oral and Maxillofacial Surgery. 94 Anand et al Testicular abscesses exhibits increased flow on the dynamic phase images along with a non specific. In the second edition of the book a detailed and authoritative exposition of basic principles of oral and maxillofacial surgery is presented in.

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Ramdas Balakrishna BDS, MDS Oral and Maxillofacial Surgeon and . Armamentarium and their Usage in Oral and Maxillofacial Surgery 45 UNIT II. Many textbooks have been written over the years aiming to introduce students and resi- dents to the fundamentals of oral and maxillofacial surgery. Some of. Challenging Concepts in Oral and Maxillofacial Surgery presents 26 complex case scenarios that are mapped to the OMFS syllabus. These are intended to.

Use anxiety reduction protocol. V solutions. Have nitroglycerin tablets or spray readily available use premedication if needed. Severe hypertension: Administer supplemental oxygen. Ensure profound local anesthesia before 1. Defer elective dental treatment until starting surgery hypertension is better controlled.

Consider use of nitrous oxide sedation 2. Consider referral to oral and maxillofacial 7. Monitor vital signs closely surgeon for emergency problems.

Possible limitation of amount of adrenaline to 0. Management of Patient with 1,00, adrenaline Myocardial Infarction 9. Maintain verbal contact with patient 1. Same as managing a patient with Angina. Defer surgery if possible for 6 months post MI attack.

Management of Patient with 3. Administer oxygen. Congestive Cardiac Failure 4.

Check if patient is taking anticogulants. Defer treatment until heart function has been medically improved and physician believes II. Features confirming respiratory disorders: Recommend that the patient seeks the respiratory tract infection. Listen to chest with stethoscope to detect therapy of hypertension.

Monitor the patients blood pressure at each procedures or sedation. Use anxiety reduction protocol, including adrenaline- containing local anesthesia nitrous oxide, but avoid use of respiratory surpasses 0. Consult physician about possible use of Management of a Patient with preoperative cromolyn sodium.

Chronic Obstructive Pulmonary 5. Defer treatment until lung function has insufficiency. Keep a bronchodilator — containing inhaler 2. Listen to chest bilaterally with stethoscope to easily accessible. Avoid use of nonsteroidal anti inflammatory 3. Afternoon or midday appointments are 4.

If patient is on chronic oxygen supplemen- preferred.

If patient is not on supplement oxygen therapy, Management of Patient with Acute consult physician before administering Asthmatic Episode Occurring during oxygen. Dental Sugery 5. If patient chronically receives corticosteroid 1. Terminate all dental procedures therapy, manage patient for adrenal 2. Position patient in fully sitting posture insufficiency. Administer bronchodilator by spray 6. Avoid placing patient in supine position until 4.

Administer oxygen confident that patient can tolerate it. Keep a bronchodilator- containing inhaler accessible. Closely monitor respiratory and heart rates. Schedule afternoon appointments to allow for clearing of secretions.

Terminate all dental treatment. Position patient in supine position, with legs Management of Patient Suffering raised above level of head. Have someone summon medical assistance. Administer corticosteroid mg of 1. Terminate all dental treatment hydrocortisone or its equivalent I. V For Mild Hypoglycemia: Administer oxygen 2. Administer glucose source such as sugar or 6.

Monitor vital signs. Start I. V line and drip of crystalloid solution. Start basic life support, if necessary. Before further dental care, consult physician, 9. Transport to emergency care facility. Orally administer glucose source, such as 1. Defer surgery until thyroid dysfunction is well sugar or fruit juice controlled.

Monitor pulse and blood pressure before, 4. If symptoms do not rapidly improve, during and after surgery. Limit amount of epinephrine used. V or intramuscularly I. Management of Patient Suffering 5. Consult physician before further dental care. Insulin Dependent Diabetes 2. Administer 50 ml, 50 percent glucose IV or IM or 1mg glucagon. Defer surgery until diabetes is well 3. Have someone summon medical assistance controlled; consult physician.

Monitor vital signs 2. Schedule an early morning appointment; 5. Use anxiety reduction protocol, but avoid deep sedation techniques in outpatients. Features Confirming Acute 4. Monitor pulse, respiration and blood Adrenal Insufficiency pressure before, during and after surgery. Pharmacologic means of anxiety control Watch for signs of hypoglycemia.

Treat infections aggressively. Defer surgery until diabetes is well controlled. After surgery 2. If patient can eat before and after surgery, instruct patient to eat a normal breakfast and IV. Avoid the use of drugs that depend on renal metabolism or excretion.

Modify the dose if Management of Patients with Anxiety such drugs are necessary. Anxiety Protocol 2. Avoid the use of nephrotoxic drugs, such as non-steroidal anti inflammatory drugs.

Before Appointment 3. Monitor blood pressure and heart rate. Look for signs of secondary hyper- reception room time is minimized. Consider hepatitis B screening before dental 6. Take some extra measures during and after treatment. Take hepatitis precautions if surgery, to help promote clot formation and unable to screen for hepatitis. Restart warfarin on the day of surgery.

Attempt to learn the cause of the liver the safety of stopping heparin for the problem; if the cause is hepatitis B, take usual perioperative period. Defer surgery until at least 6 hours after the 2.

Avoid drugs requiring hepatic metabolism or heparin is stopped or reverse heparin with excretion; if there use is necessary, modify protamine. Restart heparin once a good clot has formed. Screen patients with severe liver disease for bleeding disorders with platelet count, Management of Patient with prothrombin time, partial thromboplastin a Seizure Disorder time and bleeding time 1. Defer surgery until the seizures are well 4. Attempt to avoid situations in which the controlled patient might swallow large amount of blood.

Consider having serum levels of anti seizure Management of Patient with medications measured if patient compliance Anticoagulant Therapy is questionable. Patient receiving aspirin or other platelet 3. Avoid hypoglycemia and fatigue. Consult physician to determine the safety of Manifestation and Management of stopping the anticoagulant drug for several Hypersensitivity Allergic Reactions days.

Defer surgery until the platelet inhibiting drugs Manifestations Management have been stopped for 5 days. Skin signs 3. Take extra measures during and after surgery a. Delayed onset i. Stop administration of all skin signs: Benadryl 50 mg 4.

Restart drug therapy on the day after surgery iii. Benadryl 50 mg q6h 1. Immediate onset i. Obtain the baseline prothrombin time. IM or IV. Stop warfarin approximately 2 days before vi. Check the PT daily and proceed with surgery vii.

Wheezing, mild dyspnea i. V access v. Stridorous breathing i. Anaphylaxis with or i. Terminate all dental treatment and remove without skin signs: Position patient in chair in almost fully upright dyspnea, stridor, have someone summon position cyanosis, total assistance.

Attempt to verbally calm patient airway obstruction, iii. Have patient breathe CO2 — enriched air, nausea, and vomiting, iv. If symptoms persist or worsen, administer tachycardia, trained in use and if diazepam, 10 mg I. M or titrate slowly I. V until hypotension, laryngospasm is not quickly anxiety is relieved, or administer midazolam cardiac dysrythmias, relieved with epinephrine. V access. Monitor vital signs IV or IM 7.

Perform all further dental surgery using ix. Loosen tight clothing. Maintain airway Remove any obstruction in It is transient loss of consciousness due to cerebral path anoxia reduced cerebral perfusion thus inable 4. Inhalation of aromatic spirit of ammonia to maintain posture. Oxygen administration 6. Maintain vital signs 1. Cardiac syncope 7. If unconsciousness for longer time than treat 2. Vasovagal syncope cause. Postural syncope 4. Drug induced syncope 5.

Cerebrovascular syncope Prodrome 1. Terminate all dental treatment Pathophysiology and Manifestation of 2. Position patient in supine position with legs Vasovagal Syncope raised above level of head. Attempt to calm patient 4. Monitor vital signs Syncopal Episode 1. Terminate all dental treatment 2. Position patient in supine position with legs raised 3. Management Shock 1. Maintain supine position with legs lifted above It is hemodynamic disturbance where there is head, therefore increased blood to brain.

Irreversible stage — — Decrease in blood pressure Type Cause Mechanism — Decrease in cardiac output 1. Hypovolaemic -Haemorrhage, -Decrease in blood — Tachypnea shock trauma volume — Decrease blood to vital organ and - fluid loss, specific features burns 2.

Cardiogenic - Myocardial -Decrease in — Can lead to death. Anaphylactic shock - Anaphylaxis -Peripheral vasodilatation and It can be easily prevented than treated: Supine position with head below the feet periphery should be positioned. Oxygen inhalation 3. Maintain airway, and it may need tracheostomy. Monitor vital signs 5. Maintain body heat by covering with blanket and hot packs. Restore lost body fluid. Treat cause and symptomatic relief should be provided.

Injection hydrocortisone and atropine sulphate, antibiotics, adrenaline. Tachyphylaxis It is the falling off in the effect produced by a drug during continuous use or constantly repeated administration. Features It is mainly seen in drugs of nervous Three stages in shock are: Progressive stage: Mild toxicity: Moderate toxicity: V nystagmus, tremors, — Place in supine position — administer diazepam headache, dizziness, — Monitor all vital signs.

Severe toxicity: Seizure, cardiac — if seizure occurs, protect — Transport to emergency dysrhythmia or arrest patient from nearby care facility. Position patient in sitting posture. Bone wax on bone bleeding point. Postoperative Hemorrhage Causes Six reasons and difficulty to stop bleeding from extracted socket: In normal patients: The tissues of mouth and jaw are highly i. Intraoperative vascular — Incision 2.

Extraction leads a open wound in soft tissue — Damage caused while using various and bone hemostatic techniques 3. Difficult to apply dressing material and proper ii. Postoperative pressure and sealing to the intraoral sites. Patient tends to play with the surgical area, — reactionary therefore dislodges clot. Small negative pressure is created repeatedly 2. In diseased patients: Salivary enzymes lyse clot. This occurs generally due to infection varnish present in the area of surgery.

Defer surgery after delivery if possible 2. Avoid dental radiographs unless information about tooth roots or bone is necessary for proper dental care. If radiographs must be taken, use proper shielding. Avoid the use of drugs with teratogenic potential. Use local anesthetics when anesthesia is necessary. Use at least 50 percent oxygen if nitrous oxide sedation is used Fig.

Hemorrhage management 6. Avoid keeping the patient in the supine on applying pressure position for long periods, to prevent vena cava compression 7. Allow the patient to take frequent trips to the rest room. CPR can be administered outside hospital or in hospital. If it is done outside hospital, then cardio- pulmonary resuscitation is providing basic life support, but if it is done in hospital, then basic life support BLS as well as advanced care life support ACLS is also given.

Objectives The ABCs of life is maintained. Mouth to mouth breathing They are: Place the patient is supine position with head higher than the legs. Patency of the airway is checked iii. Any obstruction in the airway by any foreign body is removed.

Patients airway is opened by a head tilt-chin lift position. Administer mouth to mouth breathing Fig. Mouth to nose breathing or mouth to airway breathing, can also be given if mouth is seriously Fig. Chest compression injured or cannot be opened. External cardiac compressions are given to restore blood circulation.

Antibiotics These are substances produced by micro Compression Method organisms that either retard the growth of or 1. In case of 1 operator, 15 compressions with kill other micro-organisms at high dilution. If the pulse is absent, then CPR These are similar to antibiotics, except that they should be resumed Fig. In case of 2 operators, 5 compressions with 1 ventilation is administered. Drugs inhibiting cell wall synthesis: The improvement of the patient during administ- — Penicillin ration of basic life support is evaluated by the — Cephalosporins colour of the skin and mucosa, chest size, pulse — Vancomycin rate, respiratory movements, and pupil of the — Cyclosporine eyes.

Drugs inhibiting protein synthesis: Extended spectrum penicillin — Drug binds to 30s ribosomal subunit: Drugs affecting cell permeability — Salbactam — Aminoglycoside — Tazobactum 4. Drugs affecting DNA Gyrase: Cephalosporin 5. Drugs interfering with DNA function: First generation against gram positive cocci — Rifampicin and gram negative aerobes — E. Coli, proteus — Metronidazole i. Oral 6. Drugs interfering with DNA synthesis: Drugs interfering with intermediate ii.

Parenteral metabolism: Second generation against first generation — Pyrimethamine organism and H. Parenteral — cefuroxime A. Penicillin — cefatetan 1. Natural penicillin — cefoxitin i. Benzyl penicillin 3. Third generation Neisseria, E. Sodium penicillin H. Depot penicillin procaine pen i.

Oral 2. Semisynthetic penicillin — cefixine i. Acid resistant penicillin — cefprodoxine — phenoxy ethyl penicillin ii. Parenteral — phenoxy methyl penicillin — ceftriaxone ii. Fourth generation gram positive, gram — cloxacillin negative, Pseudomonos iii. Broad spectrum penicillin Parenteral — Amoxycillin — cefipime — Ampicillin — cefpirome http: Short acting and thus preventing cell wall formation of i.

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Thus are bacteriocidal. Intermediate acting succeptible than gram negative. Thus inhibits are: Use of Opoid analgesic 3. Acupuncture patients. Morphine ii. Hydroxodone 3. Naltrexone iii. Sodium salicylate http: Ibuprofen ii. Ketoprofen Contraindications 4. Phenylbutazone ii. Oxicams i. Piroxicam Classification ii. Meloxicam 1. Short acting Natural 8. Fenamate i. Hydrocortisone i.

Mefanamic acid ii. Cortisone 9. Furanones 2. Intermediate acting Synthetic i. Rofecoxib i. Prednisolone ii. Celecoxib ii. Methylprednisolone Sulfoanilide 3. Long acting Synthetic i. Nimesulide i. Beclamethasone Acetic acid ii. Betamethasone i. Diclofenac iii. Dexamethasone Alkanone 4. Inhaled i. Nabumetone i. Benzoxazocine ii.

Budesonide i. Nefopan iii. Fluticasone 5. Topical Mechanism of Action i. Betamethasone iv. Fluticasone Effects v. Pharmacological therapy Adverse Reactions i. Mineralocorticosteroid ii. Collagen disorder i. Sodium and water retention — Systemic lupus erythromatosis SLE ii. Edema — Discoid lupus erythromatosis DLE iii.

Hypokalemic alkalosis — Nephritis syndrome iv. Progressive rise in blood pressure iii. Allergic disorders 2. Hyperglycemia — Angioneuretic edema iii. Muscles weakness — Serum sickness iv. Susceptibility to infection iv.

Autoimmune disorders v. Delayed wound healing — Pemphigus vi. Osteoporosis — Hepatitis vii. Peptic ulceration v. Bronchial asthma viii. Psychiatric disturbance vi. Pulmonary edema ix. Growth retardation vii. Skin disease x. Suspension of hypothalamopitiutary axis. Shock and septicemia. Apthous ulcer ii. Desquamative gingivitis iv. Oral lichen planus Classification v. Oral pemphigus 1.

Centrally acting vi. Postextraction edema. Pulp capping 2. Peripherally acting viii. Pulpotomy i. Competitive blockers. TMJ arthritis a. Intracanal medicament — Pancuronium. Persistent depolarisers 5. Oxidized cellulose Oxycel: These are surgical — Scoline. Directly acting to control bleeding from extracted socket. Oxidized regenerated cellulose: These are Indications modified oxygel which does not retard epithelization.

Microfibrillar collagen hemostat: I disturbances. Iron substances These are locally applied agents which causes Antibiotics Prophylaxis Regimens control in bleeding. Standard oral Amoxicillin 2 gm 1 hour vasoconstriction action.

It causes cardiac regimen before procedure abnormalities if absorbed systemically. Alternative regimen Clindamycin mg 1 hour 2. Prepared from human or bovine for patients allergic or before plasma, is used as a freeze — dried powder to amoxicillin, Azithromycin mg penicillin or both or 1 hour before or freshly prepared solution. Used in cephalexin 2 g 1 hour before hemophilia, skin grafting and neurosurgery 3. Patients unable Ampicillin 2 g I. V but never given by injection as can cause to take oral within 30 min.

Patients unable Clindamycin mg I. V within 3. He was a teacher who, when honored, thanked his students for teaching him. Although surrounded by personal success, he found the greatest satisfaction in the success of others.

He was our boss but was more comfortable as our partner in a raft on the New River. He would argue with you, not to get you to agree, but to get you to disagree and defend. He trained many to reach great financial success but placed the reward gained by teaching higher than any financial reward. He had much of which to boast and be proud, but instead practiced humility.

He was perhaps the smartest man I have ever known but was always first to admit when you had a good idea, and was gracious enough not to point out that he had thought of it himself, perhaps even years prior.

I never heard him speak on a topic when I was not totally impressed with the insight and knowledge he seemed to have, but he was often more content listening to what others had to say. He was more interested in finding the truth than about being right himself. He was 15 years older than me but looked younger.

He would often tell residents, much to their dismay, I might add, that it is not the answer that is important, but the question. He knew more than many of the speakers at the lectures he attended, but he always took notes. He was a man most deserving of a long and wonderful life, yet we are here today because this wonderful life has been tragically cut short. For, as I look around, I see scores of us who owe so much of what we are to this one life well spent.

Pete died too young, and he will be missed, but through this textbook his teachings will continue. Bertolami, DDS, D. Mark C. Richard H. Stephen B. Vincent J. Michael S. Suzanne U. Scott D. Joel M. The healing wound is an overt expression of an intricate and tightly choreographed sequence of cellular and biochemical responses directed toward restoring tissue integrity and functional capacity following injury.

Although healing culminates uneventfully in most instances, a variety of intrinsic and extrinsic factors can impede or facilitate the process.

Understanding wound healing at multiple levels—biochemical, physiologic, cellular, and molecular—provides the surgeon with a framework for basing clinical decisions aimed at optimizing the healing response.

Equally important it allows the surgeon to critically appraise and selectively use the growing array of biologic approaches that seek to assist healing by favorably modulating the wound microenvironment.

The Healing Process The restoration of tissue integrity, whether initiated by trauma or surgery, is a phylogenetically primitive but essential defense response. Injured organisms survive only if they can repair themselves quickly and effectively. The healing response depends primarily on the type of tissue involved and the nature of the tissue disruption. When restitution occurs by means of tissue that is structurally and functionally indistinguishable from native tissue, regeneration has taken place.

However, if tissue integrity is reestablished primarily through the formation of fibrotic scar tis-. With the exception of bone and liver, tissue disruption invariably results in repair rather than regeneration. At the cellular level the rate and quality of tissue healing depends on whether the constitutive cells are labile, stable, or permanent.

Labile cells, including the keratinocytes of the epidermis and epithelial cells of the oral mucosa, divide throughout their life span. Stable cells such as fibroblasts exhibit a low rate of duplication but can undergo rapid proliferation in response to injury. For example, bone injury causes pluripotential mesenchymal cells to speedily differentiate into osteoblasts and osteoclasts.

On the other hand permanent cells such as specialized nerve and cardiac muscle cells do not divide in postnatal life. Whereas a fibrous scar is normal for skin wounds, it is suboptimal in the context of bone healing.

At a more macro level the quality of the healing response is influenced by the nature of the tissue disruption and the circumstances surrounding wound closure.

Healing by first intention occurs when a clean laceration or surgical incision is. If conditions are less favorable, wound healing is more complicated and occurs through a protracted filling of the tissue defect with granulation and connective tissue. This process is called healing by second intention and is commonly associated with avulsive injury, local infection, or inadequate closure of the wound.

For more complex wounds, the surgeon may attempt healing by third intention through a staged procedure that combines secondary healing with delayed primary closure. Once adequate granulation tissue has formed and the risk of infection appears minimal, the wound is sutured close to heal by first intention. Wound Healing Response Injury of any kind sets into motion a complex series of closely orchestrated and temporally overlapping processes directed toward restoring the integrity of the involved tissue.

The reparative processes are most commonly modeled in skin1; however, similar patterns of biochemical and cellular events occur in virtually every other tissue.

Vasoconstriction of the injured vasculature is the spontaneous tissue reaction to staunch bleeding. Tissue trauma and local bleeding activate factor XII Hageman factor , which initiates the various effectors of the healing cascade including the complement, plasminogen, kinin, and clotting systems.

Circulating platelets thrombocytes rapidly aggregate at the injury site and adhere to each other and the exposed vascular subendothelial collagen to form a primary platelet plug organized within a fibrin matrix. 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 Figure Increasing vascular permeability allows blood plasma and other cellular mediators of healing to pass through the vessel walls by diapedesis and populate the extravascular space.

Corresponding clinical manifestations include swelling, redness, heat, and pain. Cytokines released into the wound provide the chemotactic cues that sequentially recruit the neutrophils and monocytes to the site of injury. Neutrophils normally. Migrating through the scaffolding provided by the fibrin-enriched clot, the shortlived leukocytes flood the site with proteases and cytokines to help cleanse the wound of contaminating bacteria, devitalized tissue, and degraded matrix components.

Neutrophil activity is accentuated by opsonic antibodies leaking into the wound from the altered vasculature. Unless a wound is grossly infected, neutrophil infiltration ceases after a few days. Activated monocytes, now termed macrophages,. They secrete collagenases and elastases to break down injured tissue and phagocytose bacteria and cell debris.

Beyond their scavenging role the macrophages also serve as the primary source of healing mediators. The centrality of. Immediately following wounding, platelets facilitate the formation of a blood clot that secures hemostasis and provides a temporary matrix for cell migration.

Cytokines released by activated macrophages and fibroblasts initiate the formation of granulation tissue by degrading extracellular matrix and promoting development of new blood vessels. Although the numbers and activity of the macrophages taper off by the fifth post injury day, they continue to modulate the wound healing process until repair is complete. Proliferative Phase The cytokines and growth factors secreted during the inflammatory phase stimulate the succeeding proliferative phase Figure An essential first step is the establishment of a local microcirculation to supply the oxygen and nutrients necessary for the elevated metabolic needs of regenerating tissues.

Around the same time, matrix-generating fibroblasts migrate into the wound in response to the cytokines and growth factors released by inflammatory cells and wounded tissue.

The scaffold of collagen fibers serves to support the newly formed blood vessels supplying the wound. Stimulated fibroblasts also secrete a range of growth factors, thereby producing a feedback loop and sustaining the repair process.

Collagen deposition rapidly increases the tensile strength of the wound and decreases the reliance on closure material to hold the wound edges together. Once adequate collagen and ECM have been generated,. This phase is distinguished by the establishment of local microcirculation and formation of extracellular matrix and immature collagen. Epidermal cells migrate laterally below the fibrin clot, and granulation tissue begins to organize below the epithelium.

At the surface of the dermal wound new epithelium forms to seal off the denuded wound surface. Epidermal cells originating from the wound margins undergo a proliferative burst and begin to resurface the wound above the basement membrane.

The process of reepithelialization progresses more rapidly in oral mucosal wounds in contrast to the skin. In a mucosal wound the epithelial cells migrate directly onto the moist exposed surface of the fibrin clot instead of under the dry exudate scab of the dermis. Once the epithelial edges meet, contact inhibition halts further lateral proliferation. Reepithelialization is facilitated by underlying contractile connective tissue, which shrinks in size to draw the wound margins toward one another.

Wound contraction is driven by a proportion of the fibroblasts that transform into myofibroblasts and generate strong contractile forces. The extent of wound contraction. In some instances the forces of wound contracture are capable of deforming osseous structures. Remodeling Phase The proliferative phase is progressively replaced by an extended period of progressive remodeling and strengthening of the immature scar tissue.

As the metabolic demands of the healing wound decrease, the rich network of capillaries begins to regress. Under the general direction of the cytokines and growth factors, the collagenous matrix is continually degraded, resynthesized, reorganized, and stabilized by molecular crosslinking into a scar.

The fibroblasts start to disappear and the collagen Type III deposited during the granulation phase is gradually replaced by stronger Type I collagen. Correspondingly the tensile strength of the scar tissue. Homeostasis of scar collagen and ECM is regulated to a large extent by serine proteases and matrix metalloproteinases MMPs under the control of the regulatory cytokines.

Tissue inhibitors of the MMPS afford a natural counterbalance to the MMPs and provide tight control of proteolytic activity within the scar.

Any disruption of this orderly balance can lead to excess or inadequate matrix degradation and result in either an exuberant scar or wound dehiscence. Specialized Healing Nerve Injury to the nerves innervating the orofacial region may range from simple contusion to complete interruption of the nerve. The healing response depends on injury severity and extent of the injury.

The continuity of the epineural sheath and the axons is maintained and morphologic alterations are minor. Recovery of the functional deficit is spontaneous and usually complete within 3 to 4 weeks. If there is a physical disruption of one or more axons without injury to stromal tissue, the injury is described as axonotmesis. Whereas individual axons are severed, the investing Schwann cells and connective tissue elements remain intact. The nature and extent of the ensuing sensory or motor deficit relates to the number and type of injured axons.

Morphologic changes are manifest as degeneration of the axoplasm and associated structures distal to the site of injury and partly proximal to the injury. Recovery of the functional deficit depends on the degree of the damage. Complete transection of the nerve trunk is referred to as neurotmesis and spontaneous recovery from this type of. Histologically, changes of degeneration are evident in all axons adjacent to the site of injury. The degeneration is evident in all axons of the distal nerve segment and in a few nodes of the proximal segment.

Within 78 hours injured axons start breaking up and are phagocytosed by adjacent Schwann cells and by macrophages that migrate into the zone of injury. Once the axonal debris has been cleared, Schwann cell outgrowths attempt to connect the proximal stump with the distal nerve stump.

The proliferating Schwann cells also promote nerve regeneration by secreting numerous neurotrophic factors that coordinate cellular repair as well as cell adhesion molecules that direct axonal growth. In the absence of surgical realignment or approximation of the nerve stumps, proliferating Schwann cells and outgrowing axonal sprouts may align within the randomly organized fibrin clot to form a disorganized mass termed neuroma.

The rate and extent of nerve regeneration depend on several factors including type of injury, age, state of tissue nutrition, and the nerves involved. The regeneration phase lasts up to 3 months and ends on contact with the end-organ by a thin myelinated axon.

In the concluding maturation phase both the diameter and performance of the regenerating nerve fiber increase. Bone The process of bone healing after a fracture has many features similar to that of skin healing except that it also involves calcifica-.

Bone is a biologically privileged tissue in that it heals by regeneration rather than repair. Left alone, fractured bone is capable of restoring itself spontaneously through sequential tissue formation and differentiation, a process also referred to as indirect healing.

As in skin the interfragmentary thrombus that forms shortly after injury staunches bleeding from ruptured vessels in the haversian canals, marrow, and periosteum. Necrotic material at the fracture site elicits an immediate and intense acute inflammatory response which attracts the polymorphonuclear leukocytes and subsequently macrophages to the fracture site. The organizing hematoma serves as a fibrin scaffold over which reparative cells can migrate and perform their function.

Invading inflammatory cells and the succeeding pluripotential mesenchymal cells begin to rapidly produce a soft fracture callus that fills up interfragmentary gaps.

Comprised of fibrous tissue, cartilage, and young immature fiber bone, the soft compliant callus acts as a biologic splint by binding the severed bone segments and damping interfragmentary motion. An orderly progression of tissue differentiation and maturation eventually leads to fracture consolidation and restoration of bone continuity.

More commonly the surgeon chooses to facilitate an abbreviated callus-free bone healing termed direct healing Figure The displaced bone segments are surgically manipulated into an acceptable alignment and rigidly stabilized through the use of internal fixation devices.

The resulting anatomic reduction is usually a combination of small interfragmentary gaps separated by contact areas. Ingrowth of mesenchymal cells and blood vessels starts shortly thereafter, and activated osteoblasts start depositing osteoid on the surface of the fragment ends.

In contact zones where the fracture ends are closely apposed, the fracture line is filled concentrically by lamellar bone. Larger gaps are filled through a succession of fibrous. The fracture site shows both gap healing and contact healing. The internal architecture of bone is restored eventually by the action of basic multicellular units. In the absence of any microinstability at the fracture site, direct healing takes place without any callus formation.

Subsequent bone remodeling eventually restores the original shape and internal architecture of the fractured bone. Functional sculpting and remodeling of the primitive bone tissue is carried out by a temporary team of juxtaposed osteoclasts and osteoblasts called the basic multicellular unit BMU.

As osteoclasts at the leading edge of the BMUs excavate bone through proteolytic digestion, active osteoblasts move in, secreting layers of osteoid and slowly refilling the cavity. Osteoclasts reaching the end of their lifespan of 2 weeks die and are removed by phagocytes. While the primitive bone mineralizes, remodeling BMUs cut their way through the reparative tissue and replace it with mature bone.

Consequently the shape and strength of the reparative bone tissue changes to accommodate greater functional loading.

Tissue-level strains produced by functional loading play an important role in the remodeling of the regenerate bone.

Text book of Oral and Maxillofacial Surgery

In contrast osseous healing across stabilized fracture segments occurs primarily through intramembranous ossification. Major fac-. If a fracture fixation device is incapable of stabilizing the fracture, the interfragmentary microinstability provokes osteoclastic resorption of the fracture surfaces and results in a widening of the fracture gap.

Although bone union may be ultimately achieved through secondary healing by callus production and endochondral ossification, the healing is protracted. Fibrous healing and nonunions are clinical manifestations of excessive microstrains interfering with the cellular healing process.

Extraction Wounds The healing of an extraction socket is a specialized example of healing by second intention. Both intrinsic and extrinsic pathways of the clotting cascade are activated. The resultant fibrin meshwork containing entrapped red blood cells seals off the. Organization of the clot begins within the first 24 to 48 hours with engorgement and dilation of blood vessels within the periodontal ligament remnants, followed by 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 setting the stage for active crestal resorption. Angiogenesis proceeds in the remnants of the periodontal ligaments.

In the second week the clot continues to get organized through fibroplasia and new blood vessels that begin to penetrate towards the center of the clot. 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.

By the third week the extraction socket is filled with granulation tissue and poorly calcified bone forms at the wound perimeter. The surface of the wound is completely reepithelialized with minimal or no scar formation.

Active bone remodeling by deposition and resorption continues for several more weeks. Radiographic evidence of bone formation does not become apparent until the sixth to eighth weeks following tooth extraction. Due to the ongoing process of bone remodeling the final healing product of the extraction site may not be discernible on radiographs after 4 to 6 months. Occasionally the blood clot fails to form or may disintegrate, causing a localized alveolar osteitis.

In such instances healing is delayed considerably and the socket fills gradually. 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. Skin Grafts Skin grafts may be either full thickness or split thickness.

Depending on the amount of underlying dermis included, split-thickness grafts are described as thin, intermediate, or thick.

A fibrin clot forms at the graft-host interface, fixing the graft to the host bed. Host leukocytes infiltrate into the graft through the lower layers of the graft. Graft survival depends on the ingrowth of blood vessels from the host into the graft neovascularization and direct anastomoses between the graft and the host vasculature inosculation.

Endothelial capillary buds from the host site invade the graft, reaching the dermoepidermal junction by 48 hours. Concomitantly vascular connections are established between host and graft vessels.

However, only a few of the ingrowing capillaries succeed in developing a functional anastomosis. Formation of vascular connections between the recipient bed and transplant is signaled by the pink appearance of the graft, which appears between the third and fifth day postgrafting.

Fibroblasts from the recipient bed begin to invade the layer of fibrin and leukocytes by the fourth day after transplantation. The fibrin clot is slowly resorbed and organized as fibroblastic infiltration continues.

By the ninth day the new blood vessels and fibroblasts have achieved a firm union, anchoring the deep layers of the graft to the host bed. Reinnervation of the skin graft occurs by nerve fibers entering the graft through its base and sides.

The fibers follow the vacated neurilemmal cell sheaths to reconstruct the innervation pattern of the donor skin. Recovery of sensation usually begins within 2 months after transplanta-. Grafts rarely attain the sensory qualities of normal skin, because the extent of re-innervation depends on how accessible the neurilemmal sheaths are to the entering nerve fibers.

The clinical performance of the grafts depends on their relative thickness. As split-thickness grafts are thinner than full-thickness grafts, they are susceptible to trauma and undergo considerable contraction; however, they have greater survival rates clinically.

Nevertheless full-thickness grafts are less susceptible to trauma and undergo minimal shrinkage. However, this changes when complications arise and encumber the wound healing continuum.

Most wound healing complications manifest in the early postsurgical period although some may manifest much later. The two problems most commonly encountered by the surgeon are wound infection and dehiscence; proliferative healing is less typical.

Wound Infection Infections complicating surgical outcomes usually result from gross bacterial contamination of susceptible wounds. All wounds are intrinsically contaminated by bacteria; however, this must be distinguished from true wound infection where the bacterial burden of replicating microorganisms actually impairs healing.

The continual presence of a bacterial infection stimulates the host immune defenses leading to the production of inflammatory mediators, such as prostaglandins and thromboxane. Neutrophils migrating into the wound release cytotoxic enzymes and free oxygen radicals.

Thrombosis and vasoconstrictive metabolites cause wound hypoxia, leading to enhanced bacterial proliferation and continued tissue damage. Bacteria destroyed by host defense mechanisms provoke varying degrees of inflammation by releasing neutrophil proteases and endotoxins. Newly formed cells and their collagen matrix are vulnerable to these breakdown products of wound infection, and the resulting cell and collagen lysis contribute to impaired healing.

Clinical manifestations of wound infection include the classic signs and symptoms of local infection: Inadequate tissue perfusion and oxygenation of the wound further compromise healing by allowing bacteria to proliferate and establish infection.

Failure to follow aseptic technique is a frequent reason for the introduction of virulent microorganisms into the wound. Transformation of contaminated wounds into infected wounds is also facilitated by excessive tissue trauma, remnant necrotic tissue, foreign bodies, or compromised host defenses. Careful technique must be augmented by proper postoperative care, with an emphasis on keeping the wound site clean and protecting it from trauma. Proliferative Scarring Some patients may go on to develop aberrant scar tissue at the site of their skin injury.

The two common forms of hyperproliferative healing, hypertrophic scars and keloids, are characterized by hypervascularity and hypercellularity. Distinctive features include excessive scarring, persistent inflammation, and an overproduction of extracellular matrix components, including glycosaminoglycans and collagen Type I. In general, hypertrophic scars arise shortly after the injury, tend to be circumscribed within the boundaries of the wound, and eventually recede.

Keloids, on the other hand, manifest months after the injury, grow beyond the wound boundaries, and rarely subside. There is a clear familial and racial predilection for keloid formation, and susceptible individuals usually develop keloids on their face, ear lobes, and anterior chest.

Although processes leading to hypertrophic scar and keloid formation are not yet clarified, altered apoptotic behavior is believed to be a significant factor. Ordinarily, apoptosis or programmed cell death is responsible for the removal of inflammatory cells as healing proceeds and for the evolution of granulation tissue into scar. Dysregulation in apoptosis results in excessive scarring, inflammation, and an overproduction of extracellular matrix components.

Additionally, proliferative scar tissue exhibits increased numbers of neoangiogenesis-promoting vasoactive mediators as well as histamine-secreting mast cells capable of stimulating fibrous tissue growth. Although there is no effective therapy for keloids, the more common methods for preventing or treating these lesions focus on inhibiting protein synthesis.

These agents, primarily corticosteroids, are injected into the scar to decrease fibroblast proliferation, decrease angiogenesis, and inhibit collagen synthesis and extracellular matrix protein synthesis. Optimizing Wound Healing At its very essence the wound represents an extreme disruption of the cellular microenvironment. Restoration of constant internal conditions or homeostasis at the cellular level is a constant undertow of the healing response.

A variety of local and systemic factors can impede healing, and the informed surgeon can anticipate and, where possible, proactively address these barriers to healing so that wound repair can progress normally. Tissue Trauma Minimizing surgical trauma to the tissues helps promote faster healing and should be a central consideration at every stage of the surgical procedure, from placement of the incision to suturing of the wound.

Properly planned, the surgical incision is just long enough to allow optimum exposure and adequate operating space. The incision should be made with one clean consistent stroke of evenly applied pressure.

Sharp tissue dissection and carefully placed retractors further minimize tissue injury. Sutures are useful for holding the severed tissues in apposition until the wound has healed enough. However, sutures should be used judiciously as they have the ability to add to the risk of infection and are capable of strangulating the tissues if applied too tightly. Wound Dehiscence Partial or total separation of the wound margins may manifest within the first week after surgery.

Most instances of wound dehiscence result from tissue fail-. Achieving complete hemostasis before wound closure helps prevent the formation of a hematoma postoperatively. The collection of blood or serum at the wound site provides an ideal medium for the growth of microorganisms that cause infection. Additionally, hematomas can result in necrosis of overlying flaps. However, hemostatic techniques must not be used too aggressively during surgery as the resulting tissue damage can prolong healing time.

Postoperatively the surgeon may insert a drain or apply a pressure dressing to help eliminate dead space in the wound.

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A necrotic burden allowed to persist in the wound can prolong the inflammatory response, mechanically obstruct the process of wound healing, and impede reepithelialization. The surgeon should also keep in mind that prosthetic grafts and implants, despite refinements in biocompatibility, can incite varying degrees of foreign body reaction and adversely impact the healing process. Tissue Perfusion Poor tissue perfusion is one of the main barriers to healing inasmuch as tissue.

Relative hypoxia in the region of injury stimulates a fibroblastic response and helps mobilize other cellular elements of repair. Cell lysis follows, with releases of proteases and glycosidases and subsequent digestion of extracellular matrix.

Neutrophils are affected because they require a minimal level of oxygen tension to exert their bactericidal effect. Delayed movement of neutrophils, opsonins, and the other mediators of inflammation to the wound site further diminishes the effectiveness of the phagocytic defense system and allows colonizing bacteria to proliferate.

Collagen synthesis is dependent on oxygen delivery to the site, which in turn affects wound tensile strength. Most healing problems associated with diabetes mellitus, irradiation, small vessel atherosclerosis, chronic infection, and altered cardiopulmonary status can be attributed to local tissue ischemia.

Similarly, tissue ischemia produced by tight or improperly placed sutures, poorly designed flaps, hypovolemia, anemia, and peripheral vascular disease, all adversely affect wound healing. Smoking is a common contributor to decreased tissue oxygenation. Smoking also increases carboxyhemoglobin, increases platelet aggregation, increases blood viscosity, decreases collagen deposition, and decreases prostacyclin formation, all of which negatively affect wound healing.

Patient optimization, in the case of smokers, may require that the patient abstain from smoking for a minimum of 1 week before and after surgical procedures. Another way of improving tissue oxygenation is the use of systemic hyperbaric oxygen HBO therapy to induce the growth of new blood vessels and facilitate increased flow of oxygenated blood to the wound. Diabetes Numerous studies have demonstrated that the higher incidence of wound infection associated with diabetes has less to do with the patient having diabetes and more to do with hyperglycemia.

Simply put, a patient with well-controlled diabetes may not be at a greater risk for wound healing problems than a nondiabetic patient. Tissue hyperglycemia impacts every aspect of wound healing by adversely affecting the immune system including neutrophil and lymphocyte function, chemotaxis, and phagocytosis.

The hemoglobin release of oxygen is impaired, resulting in oxygen and nutrient deficiency in the healing wound. The wound ischemia and impaired recruitment of cells resulting from the small vessel occlusive disease renders the wound vulnerable to bacterial and fungal infections.

Immunocompromise The immune response directs the healing response and protects the wound from infection. In the absence of an adequate immune response, surgical outcomes are. An important assessment parameter is total lymphocyte count. A mild deficit is a lymphocytic level between 1, and 1,, and levels below are considered severe total lymphocyte deficits. Patients with debilitated immune response include human immunodeficiency virus HIV -infected patients in advanced stages of the disease, patients on immunosuppressive therapy, and those taking high-dose steroids for extended periods.

The use of steroids, such as prednisone, is a typical example of how suppression of the innate inflammatory process also increases wound healing complications.

Exogenous corticosteroids diminish prolyl hydroxylase and lysyl oxidase activity, depressing fibroplasias, collagen formation, and neovascularity. Epithelialization and wound contraction are also impaired. The inhibitory effects of glucocorticosteriods can be attenuated to some extent by vitamin A given concurrently. The reduction in protein synthesis or cell division reveals itself as impaired proliferation of fibroblasts and collagen formation.

Attendant neutropenia also predisposes to wound infection by prolonging the inflammatory phase of wound healing. Because of their deleterious effect on wound healing, administration of antineoplastic drugs should be restricted, when possible, until such time that the potential for healing complications has passed. Radiation Injury Therapeutic radiation for head and neck tumors inevitably produces collateral damage in adjacent tissue and reduces its capacity for regeneration and repair.

The pathologic processes of radiation injury start right away; however, the clinical and histologic features may not become apparent for weeks, months, or even years after treatment. Early acute changes are observed within a few weeks of treatment and primarily involve cells with a high turnover rate. The common symptoms of oral mucositis and dermatitis result from loss of functional cells and temporary lack of replacement from the pools of rapidly proliferating cells.

The inflammatory response is largely mediated by cytokines activated by the radiation injury. Overall the response has the features of wound healing; waves of cytokines are produced in an attempt to heal the radiation injury.

The cytokines lead to an adaptive response in the surrounding tissue, cause cellular infiltration, and promote collagen deposition. Damage to local vasculature is exacerbated by leukocyte adhesion to endothelial cells and the formation of thrombi that block the vascular lumen, further depriving the cells that depend on the vessels. The acute symptoms eventually start to subside as the constitutive cells gradually recover their proliferative abilities. However, these early symptoms may not be apparent in some tissues such as bone, where cumulative progressive effects of radiation can precipitate acute breakdown of tissue many years after therapy.

The late effects of radiation are permanent and directly related to higher doses. Once these changes occur they are irreversible and do not change with time. Hence, the surgeon must always anticipate the possibility of a complicated healing following surgery or traumatic injury in irradiated tissue. Wound dehiscence is common and the wound heals slowly or incompletely. Even minor trauma may result in ulceration and colonization by opportunistic bacteria.

If the patient cannot mount an effective inflammatory response, progressive necrosis of the tissues may follow. Healing can be achieved only by excising all nonvital tissue and covering the bed with a well-vascularized graft. Due to the relative hypoxia at the irradiated site, tissue with intact blood supply needs to be brought in to provide both oxygen and the cells necessary for inflammation and healing. The progressive obliteration of blood vessels makes bone particularly vulnerable.

Following trauma or disintegration of the soft tissue cover due to inflammatory reaction, healing does not occur because irradiated marrow cannot form granulation tissue. In such instances the avascular bone needs to be removed down to the healthy portion to allow healing to proceed.

Hyperbaric Oxygen Therapy HBO therapy is based on the concept that low tissue oxygen tension, typically a partial pressure of oxygen PO2 of 5 to 20 mm Hg, leads to anaerobic cellular metabolism, increase in tissue lactate, and a decrease in pH, all of which inhibit wound healing.

The HBO therapy is repeated daily for 3 to 10 weeks. HBO increases the quantity of dissolved oxygen and the driving pressure for oxygen diffusion into the tissue. Correspondingly the oxygen diffusion distance. The therapy stimulates the growth of fibroblasts and vascular endothelial cells, increases tissue vascularization, enhances the killing ability of leukocytes, and is lethal for anaerobic bacteria.

Clinical studies suggest that HBO therapy can be an effective adjunct in the management of diabetic wounds. However, in the absence of controlled scientific studies with well-defined end points, HBO therapy remains a controversial aspect of surgical practice.

Age In general wound healing is faster in the young and protracted in the elderly. The decline in healing response results from the gradual reduction of tissue metabolism as one ages, which may itself be a manifestation of decreased circulatory efficiency.

The major components of the healing response in aging skin or mucosa are deficient or damaged with progressive injuries. In addition the regional vascular support may be subjected to extrinsic deterioration and systemic disease decompensation, resulting in poor perfusion capability. Nutrition Adequate nutrition is important for normal repair. Dietary protein has.

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Amino acids are critical for wound healing with methionine, histidine, and arginine playing important roles. As long as a state of protein catabolism exists, the wound will be very slow to heal. Methionine appears to be the key amino acid in wound healing. It is metabolized to cysteine, which plays a vital role in the inflammatory, proliferative, and remodeling phases of wound healing. Serum prealbumin is commonly used as an assessment parameter for protein.

As such it provides a more rapid assessment ability. Normal serum prealbumin is about As part of the perioperative optimization process, malnourished patients may be provided with solutions that have been supplemented with amino acids such as glutamine to promote improved mucosal structure and function and to enhance whole-body nitrogen kinetics.

An absence of essential building blocks obviously thwarts normal repair, but the reverse is not necessarily true. Whereas a minimum protein intake is important for healing, a high protein diet does not shorten the time required for healing.

Several vitamins and trace minerals play a significant role in wound healing. Healing wounds appear to be more sensitive to ascorbate deficiency than uninjured tissue. Increased rates of collagen turnover persist for a long time, and healed wounds may rupture when the individual becomes scorbutic. Local antibacterial defenses are also impaired because ascorbic acid is also necessary for neutrophil superoxide production.

The B-complex vitamins and cobalt are essential cofactors in antibody formation, white blood cell function, and bacterial resistance. Depleted serum levels of micronutrients, including magnesium, copper, calcium, iron, and zinc, affect collagen synthesis.

Zinc deficiency retards both fibroplasia and reepithelialization; cells migrate normally but do not undergo mitosis. On the other hand, exceeding the zinc levels can exert a distinctly harmful effect on healing by inhibiting macrophage migration and interfering with collagen cross-linking.

Advances in Wound Care An increased understanding of the wound healing processes has generated heightened interest in manipulating the wound microenvironment to facilitate healing. Traditional passive ways of treating surgical wounds are rapidly giving way to approaches that actively modulate wound healing. Therapeutic interventions range from treatments that selectively jumpstart the wound into the healing cascade, to methods that mechanically protect the wound or increase oxygenation and perfusion of the local tissues.

Growth Factors Through their central ability to orchestrate the various cellular activities that underscore inflammation and healing,. However, the potential of these extrinsic agents has not yet been realized clinically and may relate to figuring out which growth factors to put into the wound, and when and at what dose. To date only a single growth factor, recombinant human platelet-derived growth factor-BB PDGF-BB , has been approved by the United States Food and Drug Administration for the treatment of cutaneous ulcers, specifically diabetic foot ulcers.

Results from several controlled clinical trials show that PDGF-BB gel was effective in healing diabetic ulcers in lower extremities and significantly decreased healing time when compared to the placebo group. It enhanced both the formation of granulation tissue in rabbits and wound closure of the human meshed skin graft explanted on athymic nude rats.

Several growth factors belonging to the neurotrophin family have been implicated in the maintenance and repair of nerves. Nerve growth factor NGF , synthesized by Schwann cells distal to the site of injury, aids in the survival and development of sensory nerves.

This finding has led some investigators to suggest that exogenous NGF application may assist in peripheral nerve regeneration following injury. Osteoinductive growth factors hold special appeal to surgeons for their ability to promote the formation of new bone.

Advances in recombinant DNA techniques now allow the production of these biomolecules in quantities large enough for routine clinical applications. In particular, recombinant human bone morphogenetic protein-2 rhBMP-2 and rhBMP-7 have been studied extensively for their ability to induce undifferentiated mesenchymal cells to differentiate into osteoblasts osteoinduction.

Similarly, Toriumi and colleagues showed that rhBMP-2 could heal mandibular defects with bone formed by the intramembranous pathway. Genes encoding for select growth factors are delivered to the site of injury using a variety of viral, chemical, electrical, or mechanical methods. The more popular methods for transfecting wounds involve the in vivo use of adenoviral vectors. Existing gene therapy technology is capable of expressing a number of modulatory proteins at the physiologic or supraphysiologic range for up to 2 weeks.

Numerous experimental studies have demonstrated the use of gene therapy in stimulating bone formation and regeneration. Mesenchymal cells transfected with adenovirus-hBMP-2 cDNA have been shown to be capable of forming bone when injected intramuscularly in the thighs of rodents.

These early studies suggest that advances in gene therapy technology can be used to facilitate healing of bone and other tissues and may lead to better and less invasive reconstructive procedures in the near future. Dermal and Mucosal Substitutes Immediate wound coverage is critical for accelerated wound healing. The coverage protects the wound from water loss, drying, and mechanical injury. Although autologous grafts remain the standard for replacing dermal mucosal surfaces, a number of bioengineered substitutes are finding their.

Gene Therapy The application of gene therapy to wound healing has been driven by the desire to selectively express a growth factor for controlled periods of time at the site of tissue injury. The human skin substitutes available are grouped into three major types and serve as excellent alternatives to autografts. The first type consists of grafts of cultured epidermal cells with no dermal components.

The requirement of basic general surgical training, assessed by a surgical Fellowship examination, was developed in conjunction with the Royal Surgical Colleges. The specialty, while retaining its dental base, was formally established as one of the nine surgical specialties in and has membership of the Senate of Surgery and its Committees [ 20 ].

However, it has been stated that apart from a training period lasting 18 long years, postgraduate training in both dentistry and surgery has led to a suffocating schedule of examinations and an intellectually stultifying syllabus for trainees [ 41 ]. In Europe, disparate systems of training exist with dual qualifications being the norm in certain countries while some have only medical or only dental degrees as the requirement for higher training in OMFS. In , the Dental Education Consultative Committee approved the teaching programs in Oral Surgery run by many dental schools throughout Europe and the UK, which are generally of 1- to 2-year duration [ 29 ].

The rotation in allied medical subjects during second year of training is grossly inadequate bordering on being farcical.

Stand-alone dental colleges with attached bedded hospitals usually have very poor infrastructure and manpower to provide general surgical training. Also, the spectrum of maxillofacial surgeries being performed in such centers is limited in scope for the same reasons. However, the curriculum has not yet been modified to include an extended surgical training. It is an unfortunate fact that while on the one hand, OMFS in India has taken ownership of several procedures that were traditionally with other surgical specialties such as cleft and craniofacial surgery, oral oncology and microvascular reconstruction; a majority of young OMFS are narrowing their scopes of work, staying within their offices and clinics, and performing lesser and lesser major procedures either due to economic reasons or due to a sense of inadequacy instilled by a faulty training system [ 42 , 44 ].

It is generally agreed that dual qualifications followed by five plus long years of higher surgical training before one is independently allowed to practice are a luxury we can simply not afford in our country [ 45 ].

The economic costs involved in undergraduate education and inadequate financial compensations received during training preclude such a notion. However, for several years the Association Of Oral and Maxillofacial Surgeons Of India AOMSI has desperately tried to restructure the curriculum including the addition of another year to accommodate the extra needs [ 45 ].

These proposals have yet to see the light of the day. The suggestion to start an abbreviated MBBS course for dental graduates has also not been appreciated by the concerned authorities.

In , an attempt was made to start M. This higher degree was supposedly aimed to address the demands of the specialty for enhanced general surgical training [ 46 ]. However, this move was opposed by members of AOMSI as there was a fear that the new degree would undermine the existing one. A few opportunities are available to interested maxillofacial surgeons in India to enhance their skills.

Candidates may apply for a limited number of structured post-qualification fellowships through AOMSI as well as through University and Institutional support [ 44 ]. Most of these are not formally recognized by the DCI but they maintain credible training records to certify a higher level of proficiency.

Board certification in OMFS is important as the specialty yearns for formal recognition and credibility as providers of surgical care [ 47 ]. This process not only assesses the quality of the candidate but also plays an important role in channeling education and training [ 47 ]. Hopefully, if more and more youngsters become Board certified and opt for a future in academics, it would have a positive effect on the overall training standards in our country.

References 1. Are people aware of oral and maxillofacial surgery in India? J Maxillofac Oral Surg. Laskin DM. The past, present, and future of oral and maxillofacial surgery. J Oral Maxillofac Surg. Dental Council Of India. Revised MDS course regulations , No. New Delhi: Controller of Publications; Amin M, Ahmed B. Dental education in Pakistan: current trends and practice. J Coll Physicians Surg Pak. Dental degree Mawatha NK Prospectus, MD oral and maxillofacial surgery and board certification.

Postgraduate Institute of Medicine, University of Colombo 8. Utama Lau SL. Do you think they know about us? Oral and maxillofacial surgery in Hong Kong. Fiehn N-E. Perspectives on dental education in the Nordic Countries. J Dent Educ. Finland, 1st edn. EU manual of dental practice Cardiff: Cardiff University; Yuce E, Komerik N.Lancet Oncol ;4: To Beth and Macy, my two reasons for being, for your love and support.

The extent of wound contraction. Care must be taken when using afterload reducers to not allow aortic diastolic pressure to drop so low as to compromise coronary perfusion. Bertolami, DDS; D. The process of reepithelialization progresses more rapidly in oral mucosal wounds in contrast to the skin. Gene therapy: Smith PD. The authors and publisher have made every effort to ensure that the patient care recommended herein, including choice of drugs and drug dosages, is in accord with the accepted standard and practice at the time of publication.

ROSEMARY from Pembroke Pines
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