What if dry socket packing comes out

As a result, the dentist no longer needs to debride the socket or apply medicament. The occlusal surface of a healing dry socket may be concave and collect food particles or plaque. If irrigation of bacterial material or food particles reveals a healthy layer of epithelium underneath, the bacteria or food particles are not preventing epithelialization of the socket.

Any discomfort can be managed with non-narcotic analgesics; strong narcotic analgesics are not required. A chlorhexidine gluconate mouth rinse helps disinfect the socket while healing continues.

A patient presenting with a healing dry socket may state that the socket had been uncomfortable in the past few days when the socket was in the dry socket stage , but now feels better and simply wants the dentist to check that the socket is healing. A dentist can use microscopes and co-axial illumination to verify that a previous dry socket lesion is fully covered by epithelium by probing the epithelium to determine the presence of tensile strength, indicating vital tissue, and that there is no exposed bone that elicits acute pain to probing.

Comprehensive reviews of the proposed causes of dry socket lesions and of the factors that correlate with increased dry socket incidence can be found in the literature 1 , 2 , 5 , 6 , 7 , 8 , 9. One hypothesis is that bacteria initiate dry socket lesions or prolong their duration 1 , 2 , 5 , 6 , 7 , 8 , 9 , However, there is little evidence that antibiotics given after an extraction reduce dry socket incidence 11 , 12 , An antiseptic Chlorhexidine gel, placed prophylactically in extraction sockets after the procedure, does not significantly reduce dry socket incidence 14 , However, one meta-analysis found that systemic antibiotics given before third molar surgery reduced dry socket incidence Overall, these findings suggest that reducing bacterial counts around extraction sockets may only result in an insignificant reduction in dry socket incidence.

A model of dry socket lesion pathogenesis can explain various facts about dry sockets including the findings that smoking 2 , 17 , 18 and use of oral contraceptives 2 , 18 increase the incidence of dry socket lesions. In addition, the model can also demonstrate that there can be a to hour delay after an extraction before dry socket lesions appear 2 , 5 ; that traumatic extractions, where heavy luxation or forceps forces are required to extract teeth particles, increase the incidence of dry socket lesions 19 ; that plasmin-induced fibrinolysis activity seems higher in dry socket lesions compared to non-dry-socket post-extraction sockets 2 , 6 , 9 ; and that bacteria do not seem to initiate dry socket lesions 11 , 12 , Such a model should explain whether or not inflammation causes dry socket lesions.

Birn observed high concentrations of plasmin and increased fibrinolytic activity in the alveolar bone lining dry socket lesions 6 , 9. Plasminogen, the precursor of plasmin, circulates in the blood and binds to clots at wound sites.

Various tissue activators, including tissue-type and urokase-type plasminogen activators 20 , 21 , convert plasminogen to plasmin 6 , 20 , 21 , Plasmin is experimentally identified as an important molecule for inducing inflammation 20 , 22 , 23 , 24 because it has been found to induce fibrinolysis to dissolve blood vessel clots, increase local capillary permeability, and attract inflammatory cells and its complements to wound sites.

Birn hypothesized that trauma during an extraction or the presence of a bacterial infection somehow facilitates the release of plasminogen tissue activators in the post-extraction socket, resulting in the plasmin induction of fibrinolysis that dislodges the blood clot that formed after the extraction and causing a dry socket lesion 6 , 9.

However, although Birn found a correlation between the presence of fibrinolytic activity in extraction sockets and dry socket lesion pathogenesis, fibrinolysis may not be the cause dry socket lesions.

Since fibrinolysis also increases capillary blood flow to the extraction socket, it might actually reduce the probability of dry socket lesion formation 25 , 26 , 27 , Dry socket lesions routinely exhibit an eventual stoppage of blood flow to the socket. This idiopathic ischemia counteracts the effect of fibrinolysis and is presumably a cause of dry socket lesion initiation and pathogenesis.

As an alternative to Birn's fibrinolytic theory, the author proposes a different model of dry socket lesion initiation and pathogenesis. In a high-stress extraction, that puts high compressive forces on alveolar bone surrounding the tooth, events are initiated that will cause, over a to hour period following the extraction, the necrosis of osteoblasts lining the intaglio surface of the socket.

The necrosis of the osteoblasts may initiate fibrinolytic activity that lyses any blood clot that may have formed after the extraction, or the blood clot may dislodge because the necrotic osteoblasts lose the ability to metabolically integrate with the blood clot.

Also, approximately at the time of osteoblast necrosis, the socket stops bleeding, even though the fibrinolytic activity should theoretically cause increased bleeding to the extraction socket to bring immune cells and complements to the socket to begin resorbing the necrotic osteoblasts.

This idiopathic socket ischemia event may prevent an initial blood clot to reform through additional bleeding and may prevent the immune system from accessing the site through local capillaries to initiate an inflammatory response to resorb the necrotic bone cells. The necrotic bone cells are then exposed and uncovered for several days, resulting in the major symptom or morbidity of dry socket lesions, acute pain of the exposed socket to mechanical stimulation that lingers for several days until the bone becomes completely covered by healing epithelium.

During a traumatic extraction, heavy luxation or forceps forces transfer to the jawbone surrounding the roots and may crush bone on the intaglio surface of the extraction socket 1 , 10 , This can induce necrosis or apoptosis of osteoblasts within the extraction socket 30 , 31 , Studies have shown that mechanical stress excess tensile or compression forces on osteoblasts can activate cellular signaling pathways that lead to osteoblast apoptosis 30 , 31 , 32 , Also, the percentage of apoptotic osteoblasts increases over 24 hours after the initial compressive force application 30 and increases in proportion to the compressive force 30 , The urokinase plasminogen tissue activator then converts plasminogen to plasmin.

The plasmin may directly result in the lysis of a blood clot that initially formed in the socket. However, a major function of plasmin is to initiate blood vessel perfusion to bring blood, immune system cells, and complements to the intaglio surface of the socket to begin resorbing the necrotic osteoblasts.

In dry socket lesions, however, an idiopathic blood vessel ischemia event is eventually observed that prematurely blocks this capillary perfusion-mediated immune system activation process. The cause of ischemia at a dry socket lesion site is unknown. Theoretically, the high forces of the extraction may crush and occlude blood vessels within the bone forming the intaglio surface of the socket although there is no experimental evidence for or against compression-induced blood vessel occlusion existing in dry socket lesions.

Some socket bone may be dense, with few blood vessels per unit of socket area, or a socket may be observed to only bleed from the apical aspect, making these sockets intrinsically incapable of significant bleeding. Smoking or oral contraceptive use may also reduce systemic blood circulation 17 , In addition, the pro-bleeding effect of plasminolysis may be counteracted chemically by pro-ischemia thrombin activity 34 at the dry socket wound site.

Due to the lack of blood flow to the intaglio surface of the socket, the immune system cells and their complement factors cannot be brought to the intaglio surface of the socket to resorb the necrotic bone cells lining the socket. Instead, clinical observation seems to show that the socket heals by a mechanism where vital epithelium, initially present at the outer perimeter of the socket, grows gradually from the outer perimeter of the socket inferiorly into the socket down to the apex of the socket.

As the vital epithelium gradually covers the surface area of the socket intaglio surface, the epithelium brings blood vessels, immune system cells, and their complements in direct contact with the necrotic bone cells of the socket to begin resorbing the necrotic bone cells. This process of epithelium growth may take several days; during this time, the uncovered bone is painful to the touch and is vulnerable to painful contact with bacterial biofilm or food impaction.

This model of dry socket pathogenesis and healing implies that inflammation does not fundamentally cause dry socket lesions and is not the cause of dry socket morbidity Fig. There is evidence that reduced post-extraction socket blood flow facilitates dry socket lesion formation. Smoking 17 , 18 and use of oral contraceptives 18 both facilitate blood clotting throughout the body 35 and may reduce blood circulation into the extraction socket.

Both smoking and use of oral contraceptives correlate with an increased incidence of dry socket lesions 2. Traumatic extractions correlate with dry socket lesion incidence The incidence of dry socket lesions is lower for non-surgical extractions that do not require tooth sectioning compared to surgical extractions 15 , 18 , 36 , This may be due to a correlation between the need to section a tooth and the need for heavy luxation forces to remove a tooth or individual roots.

The highest rate of dry socket incidence among all teeth types occurs with the extraction of mandibular third molars. Mandibular third molars are often deeply embedded in dense bone and have the highest incidence of root dilacerations among teeth 38 , 39 , Mandibular third molars may have roots that are not radially co-axial with the imaginary radial axis on which the dentist places luxation forces to remove the root, especially if difficult access limits the number of possible ways of positioning luxation instruments.

These factors may obligate a dentist to use heavy forceps or luxation forces, even after root sectioning, to extract mandibular third molars, and these heavy forces may transmit to the surrounding jawbone. The incidence of dry socket lesion formation is lower with maxillary third molar extractions compared to mandibular third molar extractions. Maxillary third molars often have conical roots embedded in cancellous bone bounded by thin buccal bone, requiring less force for removal.

Extracting teeth that are in cancellous bone may result in multiple sharp points of cancellous bone severing multiple blood vessels, which may ensure bleeding into the post-extraction socket and blood clot formation. One example of a low stress extraction is if the dentist sections teeth before attempting extraction using heavy luxation and forceps forces. Also, infected teeth where the periodontal ligament has been resorbed by an underlying abscess can often be extracted with minimal stresses on surrounding alveolar bone, even if the roots feature ellipsoid cross sections.

However, various situations can result in a tooth extraction where heavy stresses are placed on the surrounding jawbone:. A dentist may extract a multi-rooted tooth using heavy luxation and forceps forces, moving the tooth back and forth to expand the socket to facilitate tooth extraction without sectioning the tooth roots that may be interlocked in bone. A dentist may initially attempt to extract a multi-rooted tooth using heavy luxation and forceps forces, but after placing heavy forces on the tooth, decides to section the tooth Sectioning the tooth results in less force needed to extract the tooth, but the heavy forces placed on the tooth prior to sectioning stressed the jawbone.

A dentist sections a multi-rooted tooth prior to placing heavy luxation or forceps forces on the tooth. However, the sectioned individual roots still require heavy luxation forces to extract them. This often occurs when extracting endodontically treated roots that may be partially or fully ankylosed within the surrounding alveolar bone.

Teeth with ellipsoid cross sections particularly maxillary canines and two-rooted maxillary premolars often cannot be extracted by rotating in a superior direction inside the socket using forceps, unless heavy forces are used.

Dry socket is not very common. If symptoms do not appear within a few days of the extraction, it is unlikely that a person will develop a dry socket. Over-the-counter OTC or home remedies are not often enough to treat the pain of dry socket.

People with the condition must usually see their dentist for treatment. Sometimes multiple dental visits are necessary. The pain should begin to reduce following treatment and should go away within a few days.

If not, a dentist may do further investigations to rule out complications. The dentist will flush out the socket with a saline solution or other fluid that helps clean wounds. This will remove food particles or germs that may be causing pain or infection. It is essential to manage the pain until the dry socket heals. Many people will require prescription medication to provide enough pain relief. Sometimes multiple dental visits are necessary. The pain should begin to reduce following treatment and should go away within a few days.

If not, a dentist may do further investigations to rule out complications. The dentist will flush out the socket with a saline solution or other fluid that helps clean wounds.

This will remove food particles or germs that may be causing pain or infection. Depending on the severity of the symptoms, it may be necessary to change the dressing several times. It is essential to manage the pain until the dry socket heals. Many people will require prescription medication to provide enough pain relief. If symptoms are mild, OTC painkillers may work. Antibiotic medication may be necessary if an infection develops in the socket and begins to spread to other areas of the mouth.

In addition to dental treatment, home remedies can provide further relief. Self-care and home remedies include:. Certain steps can help people to reduce their risk of developing a dry socket.

Tips for prevention include:. Dentists recommend this before as well as after the extraction. Some OTC or prescription medications may reduce blood clotting. Others, such as oral contraceptives, can affect the healing process and increase the risk of dry socket. It can be helpful to drink plenty of water after a tooth extraction. Eating soft foods for the first 24 hours can also reduce the risk of irritating the extraction site. People should avoid alcohol, caffeine, or carbonated drinks.

They should also avoid using a straw, as these can dislodge a blood clot in the socket. Poor oral hygiene or failure to look after the wound after having an extraction can increase dry socket risk. Similarly, the development of a gum infection can increase the chances.

Proper dental hygiene reduces the likelihood of a gum infection. Some research suggests that antibiotics significantly reduce the risk of a dry socket in molar extractions.