question: How do wounds inside the mouth heal compared to the outside?
comment: Wounds in the oral cavity heal faster and with less scarring than wounds in other parts of the body. One of the factors implicated in this phenomenon is the presence of saliva, which promotes the healing of oral wounds in several ways. Saliva creates a humid environment, which improves the survival and functioning of inflammatory cells that are crucial for wound healing. Furthermore, saliva contains a variety of proteins that play a role in the various stages of the intraoral wound healing. Tissue factor, present in salivary exosomes, accelerates the clotting of blood dramatically. The subsequent proliferation of epithelial cells is promoted by growth factors in saliva, especially epidermal growth factor. The importance of secretory leucocyte protease inhibitor is demonstrated by the observation that in the absence of this salivary protein, oral wound healing is considerably delayed. Members of the salivary histatin family promote wound closure in vitro by enhancing cell spreading and cell migration. Cell proliferation is not enhanced by histatin. Cyclization of histatin increased its biological activity approximately 1,000-fold compared to linear histatin. These studies suggest that histatins could potentially be used for the development of new wound healing medications.
passages: The oral mucosa tends to heal faster and with less scar formation compared to the skin. The underlying mechanism remains unknown but research suggest that extracellular vesicles might be involved. 
  
  Section::::Classification.
  
  Oral mucosa can be divided into three main categories based on function and histology:
  
  BULLET::::- Masticatory mucosa, keratinized stratified squamous epithelium, found on the dorsum of the tongue, hard palate and attached gingiva.
  
  BULLET::::- Lining mucosa, nonkeratinized stratified squamous epithelium, found almost everywhere else in the oral cavity, including the:
   Oral mucosa heals faster than skin, suggesting that saliva may have properties that aid wound healing. Saliva contains cell-derived tissue factor, and many compounds that are antibacterial or promote healing. Salivary tissue factor, associated with microvesicles shed from cells in the mouth, promotes wound healing through the extrinsic blood coagulation cascade. The enzymes lysozyme and peroxidase, defensins, cystatins and an antibody, IgA, are all antibacterial. Thrombospondin and some other components are antiviral. A protease inhibitor, secretory leukocyte protease inhibitor, is present in saliva and is both antibacterial and antiviral, and a promoter of wound healing. Nitrates that are naturally found in saliva break down into nitric oxide on contact with skin, which will inhibit bacterial growth. Saliva contains growth factors such as epidermal growth factor, VEGF, TGF-β1, leptin, IGF-I, lysophosphatidic acid, hyaluronan and NGF, which all promote healing, although levels of EGF and NGF in humans are much lower than those in rats. In humans, histatins may play a larger role. As well as being growth factors, IGF-I and TGF-α induce antimicrobial peptides. Saliva also contains an analgesic, opiorphin. Licking will also tend to debride the wound and remove gross contamination from the affected area.
   When infections such as these occur elsewhere in the body, the host defense system, able to travel the body via the circulatory system, is, more often than not, capable of appropriately gaining access to the site of infection in order to mount a proper and successful retaliation. Dental pulp, which is a richly vascularized and innervated tissue, is enclosed by tissues, such as dentin, which are incapable of expanding. It has terminal blood flow and possesses only small-gauge circulatory access at the apical foramen. All of these characteristics severely constrain the defensive capacity of the pulp tissue when faced with the different aggressions to which it may be subjected. As a result, necrotic tissue located within the pulp chamber and canals provide nutrients for pathogenic bacteria to grow and form a periapical lesion; the infected tooth serves as a biochemically and physiologically ideal location for bacterial growth and maturation, and, in essence, acts as a refuge from which bacterial reinforcements can mobilize to the periapical lesion. It is this concept that serves as the basis for conventional endodontic therapy; both chemical and mechanical debridement procedures are essential in effectively disrupting and removing the microbial ecosystem that is associated with the disease process. Thus, whenever a pulp is removed and the canal treated and filled in a manner that is compatible with or favorable to a physiologic reaction, we may expect a satisfactory percentage of endodontic success.
   The mouth wounds recover in 7–10 days with precautions for fluid only diet for 5 days, and not to increase pressure in the nose or sinuses for 2–3 weeks. Evidence that the bone graft is forming will be seen on x-ray at about 8 weeks. Movement of teeth into the graft can begin at 3 months once bone graft consolidation is seen on xray. Recovery from the bone harvest will vary depending on the site (if harvested) with the anterior iliac crest being sore for 2–3 weeks.
   If the basement membrane is not breached, epithelial cells are replaced within three days by division and upward migration of cells in the stratum basale in the same fashion that occurs in uninjured skin. However, if the basement membrane is ruined at the wound site, reepithelization must occur from the wound margins and from skin appendages such as hair follicles and sweat and oil glands that enter the dermis that are lined with viable keratinocytes. If the wound is very deep, skin appendages may also be ruined and migration can only occur from wound edges.
   The body responds to postoperative wounds in the same manner as it does to tissue damage acquired in other circumstances. The inflammatory response is designed to create homeostasis. This first step is called the inflammatory stage. The next stage and wound healing is the infiltration of leukocytes and release of cytokines into the tissue. The inflammatory response and the infiltration of leukocytes occur simultaneously. The final stage of postoperative wound healing is called remodeling. Remodeling restores the structure of the tissue and that tissues ability to regain its function.
  
  Section::::Diagnosis.
   Section::::Proliferative phase.
  
  About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the proliferative phase even before the inflammatory phase has ended. As in the other phases of wound healing, steps in the proliferative phase do not occur in a series but rather partially overlap in time.
  
  Section::::Proliferative phase.:Angiogenesis.
   Keratinocytes continue migrating across the wound bed until cells from either side meet in the middle, at which point contact inhibition causes them to stop migrating. When they have finished migrating, the keratinocytes secrete the proteins that form the new basement membrane. Cells reverse the morphological changes they underwent in order to begin migrating; they reestablish desmosomes and hemidesmosomes and become anchored once again to the basement membrane. Basal cells begin to divide and differentiate in the same manner as they do in normal skin to reestablish the strata found in reepithelialized skin.
  
  Section::::Proliferative phase.:Contraction.
   For early lesions of inflammatory papillary hyperplasia, cessation of denture use for 2 to 4 weeks may allow the lesion to completely subside. This may be aided by use of topical antibiotic or antifungal therapies. Small lesions are also typically treated with mouthrinses such as chlorhexidine mouthrinse at 0.12% or antifungal mouthrinse/ gels.
  
  For more advanced and large lesions, excision of the hyperplastic tissue may be required before fabricating a new denture. Several surgical methods have been used, including:
  
  BULLET::::- Partial-thickness or full-thickness surgical blade excision
  
  BULLET::::- Electrosurgery
  
  BULLET::::- Curettage
  
  BULLET::::- Laser surgery
  
  BULLET::::- Cryosurgery
   In a recent study, scientists have confirmed through several experiments that the protein responsible for healing properties in human saliva is, in fact, histatin. Scientists are now looking for ways to make use of this information in ways that can lead to chronic wounds, burns, and injuries being healed by saliva, making this type of treatment as common as antibiotic creams and rubbing alcohol.
  
  Section::::In animals.
   Section::::Inflammatory phase.
  
  Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or stop blood loss by way of a fibrin clot. Thereafter, various soluble factors (including chemokines and cytokines) are released to attract cells that phagocytise debris, bacteria, and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing.
  
  Section::::Inflammatory phase.:Clotting cascade.
   Healing of a wound begins with clot formation to stop bleeding and to reduce infection by bacteria, viruses and fungi. Clotting is followed by neutrophil invasion three to 24 hours after the wound has been incurred, with mitoses beginning in epithelial cells after 24 to 48 hours .
  
  Section::::Wound healing.:Inflammation phase.
  
  In the inflammatory phase, macrophages and other phagocytic cells kill bacteria, debride damaged tissue and release chemical factors such as growth hormones that encourage fibroblasts, epithelial cells and endothelial cells which make new capillaries to migrate to the area and divide.
  
  Section::::Wound healing.:Proliferative phase.
   BULLET::::3. Degradation of endothelial basement membrane: The wound macrophages, mast cells and the endothelial cells themselves secrete proteases to break down existing vascular basal lamina.
   Section::::Technique.:Main surgical procedures.:One versus two-stage surgery.
  
  After an implant is placed, the internal components are covered with either a healing abutment, or a cover screw. A healing abutment passes through the mucosa, and the surrounding mucosa is adapted around it. A cover screw is flush with the surface of the dental implant, and is designed to be completely covered by mucosa. After an integration period, a second surgery is required to reflect the mucosa and place a healing abutment.
   Section::::Inflammatory phase.:Polymorphonuclear neutrophils.
   Gingivae lacerations that are small normally heals spontaneously and do not require any intervention. However, this can be one of the clinical presentation of an alveolar fracture. Gingivae bleeding especially around the margins may suggest injury to the periodontal ligament of the tooth.
  
  The facial nerve and parotid duct should be examined for any potential damage when the buccal mucosa is involved.
  
  Deep tissue wounds should be repaired in layers with sutures that are resorbable.
  
  Section::::Types.:Primary teeth.
   Section::::Anatomy of mouth.:Spread of oral infection.
  
  Mouth infections spread from the root of the infected tooth through the jaw bones and into potential spaces between the fascial planes of surrounding soft tissue, eventually forming an abscess. These potential spaces are usually empty, but can expand and form a pocket of pus when an infection drains into them. The potential spaces are categorized into primary and secondary spaces.
  
  Section::::Anatomy of mouth.:Spread of oral infection.:Primary space.
   Surrounding the oral cavity, there are many different muscles that facilitate chewing, opening the mouth, and swallowing. Each muscle, group of muscles, or separate anatomical compartment is encased in a thin fibrous layer of connective tissue called fascia. Normally, the fascia of adjacent structures are in direct contact with each other. However, air or pus can occupy the space between adjacent fascia, known as fascial planes, and collect over time. As the air pocket or pus enlarges within the fascial planes, the structures surrounding the abnormality can become compressed or shifted out of its normal place. These phenomena of compression and deviation due to a growing infection/air pocket drive the progression of disease into potentially life-threatening situations.
   Many genes play a role in healing. For instance, in wound healing, P21 has been found to allow mammals to heal spontaneously. It even allows some mammals (like mice) to heal wounds without scars. The LIN28 gene also plays a role in wound healing. It is dormant in most mammals. Also, the proteins MG53 and TGF beta 1 play important roles in wound healing.
  
  Section::::Wound healing.
  
  In response to an incision or wound, a wound healing cascade is unleashed. This cascade takes place in four phases: clot formation, inflammation, proliferation, and maturation.
  
  Section::::Wound healing.:Clotting phase.
   Thanks to progress in molecular biology techniques, scientific understanding of oral ecology is improving. Oral ecology is being more comprehensively mapped, including the tongue, the teeth, the gums, salivary glands, etc. which are home to these communities of different microorganisms.
  
  The host’s immune system controls the bacterial colonization of the mouth and prevents local infection of tissues. A dynamic equilibrium exists notably between the bacteria of dental plaque and the host’s immune system, enabling the plaque to stay behind in the mouth when other biofilms are washed away.
   Section::::Anatomy of mouth.
  
  The anatomy of the oral cavity affects the progression of infection and dictates the severity of disease. In other words, where the infection starts will determine the pattern of its spread and its catastrophic potential based on the surrounding anatomy.
  
  Section::::Anatomy of mouth.:Oral cavity.
   In the case of an infection breaching the dentin to or very near the pulp, or in the instance of odontoblast death due to other attack (e.g. chemical or physical), undifferentiated mesenchymal cells can differentiate into odontoblast-like cells which then secrete another type, reparative dentin, underneath the site of attack. This is not only to slow the progress of the attack, but also prevents the diffusion of bacteria and their metabolites into the pulp, reducing the probability of partial pulp necrosis.
   BULLET::::- Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris. This happens through the process of phagocytosis, where white blood cells "eat" debris by engulfing it. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase.
   BULLET::::1. Primary closure of the wound to promote undisturbed and uninterrupted healing
  
  BULLET::::2. Angiogenesis to provide necessary blood supply and undifferentiated mesenchymal cells
  
  BULLET::::3. Space creation and maintenance to facilitate space for bone in-growth
  
  BULLET::::4. Stability of the wound to induce blood clot formation and allow uneventful healing
  
  After tooth removal, it takes 40 days for the normal healing process to take place (clot formation to socket filled with bone, connective tissue and epithelium).
   Section::::Inflammatory phase.:Vasoconstriction and vasodilation.
  