| Alveolar osteitis |
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Alveolar osteitis of a socket after tooth extraction. Note lack of blood clot in socket and exposed alveolar bone.
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| Classification and external resources |
| Specialty |
gastroenterology |
| ICD-10 |
K10.3 |
Alveolar osteitis is inflammation of the alveolar bone (i.e., the alveolar process of the maxilla or mandible). Classically, this occurs as a postoperative complication of tooth extraction.
Alveolar osteitis usually occurs where the blood clot fails to form or is lost from the socket (i.e., the defect left in the gum when a tooth is taken out). This leaves an empty socket where bone is exposed to the oral cavity, causing a localized alveolar osteitis limited to the lamina dura (i.e., the bone which lines the socket). This specific type of alveolar osteitis is also known as dry socket or, less commonly, fibrinolytic alveolitis, and is associated with increased pain and delayed healing time.[1]
Dry socket occurs in about 0.5–5% of routine dental extractions,[2][3][4] and in about 25–30% of extractions of impacted mandibular third molars (wisdom teeth which are buried in the bone).[1]
Contents
- 1 Classification
- 2 Signs and symptoms
- 3 Causes
- 3.1 Extraction site
- 3.2 Infection
- 3.3 Smoking
- 3.4 Surgical trauma
- 3.5 Vasoconstrictors
- 3.6 Radiotherapy
- 4 Diagnosis
- 5 Prevention
- 6 Treatment
- 7 Prognosis
- 8 Epidemiology
- 9 Etymology
- 10 References
Classification
Since dry socket occurs exclusively following a dental extraction, it could be considered both a complication and an iatrogenic condition, but this does not take into account both the reason why the tooth required extraction (i.e., extraction may have been unavoidable due to significant pain and infection) and also the fact that many dry sockets are the result of poor compliance with postoperative instructions, notably refraining from smoking in the days immediately after the procedure.
Signs and symptoms
The most common location of dry socket: in the socket of an extracted mandibular third molar (wisdom tooth).
Since alveolar osteitis is not primarily an infection, there is not usually any pyrexia (fever) and cervical lymphadenitis (swollen glands in the neck), and only minimal edema (swelling) and erythema (redness) is present in the soft tissues surrounding the socket.
Signs may include:
- An empty socket, which is partially or totally devoid of blood clot.[4] Exposed bone may be visible or the clot may be filled with food debris which reveals the exposed bone once it is removed.[2] The exposed bone is extremely painful and sensitive to touch.[5] Surrounding inflamed soft tissues may overlie the socket and hide the dry socket from casual examination.[1]
- Denuded (bare) bone walls.[6]
Symptoms may include:
- Dull, aching, throbbing pain in the area of the socket, which is moderate to severe and may radiate to other parts of the head such as the ear, eye, temple and neck.[2][4][6][7] The pain normally starts on the second to fourth day after the extraction,[4][7] and may last 10–40 days.[1] The pain may be so strong that even strong analgesics do not relieve it.[4]
- Intraoral halitosis (oral malodor).[6]
- Bad taste in the mouth.[6]
Causes
The cause(s) of dry socket are not completely understood.[2] Normally, following extraction of a tooth, blood is extravasated into the socket, and a blood clot (thrombus) forms.[3] This blood clot is replaced with granulation tissue which consists of proliferating fibroblasts and endothelial cells derived from remnants of the periodontal membrane, surrounding alveolar bone and gingival mucosa.[3] In time this in turn is replaced by coarse, fibrillar bone and finally by mature, woven bone.[1] The clot may fail to form because of poor blood supply (e.g., secondary to local factors such as smoking, anatomical site, bone density and conditions which cause sclerotic bone to form).[6] The clot may be lost because of excessive mouth rinsing, or disintegrate prematurely due to fibrinolysis.[3] Fibrinolysis is the degeneration of the clot and may be caused by the conversion of plasminogen to plasmin and formation of kinins.[1] Factors which promote fibrinolysis include local trauma, estrogens, and pyrogens from bacteria.[1]
Bacteria may secondarily colonize the socket, and lead to further dissolution of the clot.[4] Bacterial breakdown and fibrinolysis are widely accepted as a major contributing factors to the loss of the clot.[4] Bone tissue is exposed to the oral environment, and a localized inflammatory reaction takes place in the adjacent marrow spaces.[3] This localizes the inflammation to the walls of the socket, which become necrotic.[6] The necrotic bone in the socket walls is slowly separated by osteoclasts and fragmentary sequestra may form.[3] The bones of the jaws seem to have some evolutionary resistance to this process. When bone is exposed at other sites in the human body, this is a much more serious condition.
In a dry socket, healing is retarded because tissue must grow from the surrounding gingival mucosa, which takes longer than the normal organisation of a blood clot. Some patients may develop short term halitosis,[4] which is the result of food debris stagnating in the socket and the subsequent action of halitogenic bacteria.[8] The main factors involved in the development of dry socket are discussed below.
Dry sockets more commonly occur in the mandible than the maxilla, due to the relatively poor blood supply of the mandible and also because food debris tends to gather in lower sockets more readily than upper ones.[2] It more commonly occurs in posterior sockets (molar teeth) than anterior sockets (premolars and incisors),[3] possibly because the size of the created surgical defect is relatively larger, and because the blood supply is relatively poorer at these sites. Dry socket is especially associated with extraction of lower wisdom teeth.[3] Inadequate irrigation (washing) of the socket has been associated with increased likelihood of dry socket.[1]
Infection
Dry socket is more likely to occur where there is a pre-existing infection in the mouth,[1] such as necrotizing ulcerative gingivitis or chronic periodontitis. Wisdom teeth not associated with pericoronitis are less likely to cause a dry socket when extracted.[1] The oral microbiota has been demonstrated to have fibrinolytic action in some individuals, and these persons may be predisposed to developing dry sockets after tooth extraction.[2] Infection of the socket following tooth extraction is different from dry socket, although in dry socket secondary infection may occur in addition.
Smoking
Smoking and tobacco use of any kind are associated with increased risk of dry socket.[2] This may be partially due to the vasoconstrictive action of nicotine on small blood vessels.[2] Abstaining from smoking in the days immediately following a dental extraction reduces the risk of a dry socket occurring.
Surgical trauma
Dry socket is more likely to occur following a difficult tooth extraction.[2] It is thought that excessive force applied to the tooth, or excessive movement of the tooth burnishes the bony walls of the socket and crushes blood vessels, impairing the repair process.[2] It has also been shown that dry socket is more likely to occur when an inexperienced surgeon performed the extraction,[1] possibly because excessive force or excessive tooth movements are used.
Vasoconstrictors
Vasoconstrictors are present in most local anesthetics, and are intended to increase the length of analgesia by reducing blood supply to the region which reduces the amount of local anesthetic solution that is absorbed into the circulation and carried from the local tissues. Hence, use of local anesthetics with vasoconstrictors is associated with an increased risk of dry socket occurring.[2] However, frequently use of local anesthetic without vasoconstrictors would not provide sufficient analgesia, especially in the presence of acute pain and infection, meaning that the total dose of local anesthetic may need to be increased. Adequate pain control during the extraction is balanced against an increased risk of dry socket.
Radiotherapy
Radiotherapy directed at the bones of the jaws causes several changes to the tissue, resulting in decreased blood supply.[3]
Diagnosis
Dry socket typically causes pain on the second to fourth day following a dental extraction. Other causes of post extraction pain usually occur immediately after the anesthesia/analgesia has worn off, (e.g., normal pain from surgical trauma or mandibular fracture) or has a more delayed onset (e.g., osteomyelitis, which typically causes pain several weeks following an extraction).[8] Examination typically involves gentle irrigation with warm saline and probing of the socket to establish the diagnosis.[1] Sometimes part of the root of the tooth or a piece of bone fractures off and is retained in the socket. This can be another cause of pain in a socket, and causes delayed healing. A dental radiograph (x-ray) may be indicated to demonstrate such a suspected fragment.[8]
Prevention
A systematic review reported that there is some evidence that rinsing with chlorhexidine (0.12% or 0.2%) or placing chlorhexidine gel (0.2%) in the sockets of extracted teeth reduces the frequency of dry socket.[4] Another systematic review concluded that there is evidence that prophylactic antibiotics reduce the risk of dry socket (and infection and pain) following third molar extractions of wisdom teeth, however their use is associated with an increase in mild and transient adverse effects.[9] The authors questioned whether treating 12 patients with antibiotics to prevent one infection would do more harm overall than good,[9] in view of the potential side effects and also of antibiotic resistance. Nevertheless, there is evidence that in individuals who are at clear risk may benefit from antibiotics.[9] There is also evidence that antifibrinolytic agents applied to the socket after the extraction may reduce the risk of dry socket.[4]
Some dentists and oral surgeons routinely debride the bony walls of the socket to encourage hemorrhage (bleeding) in the belief that this reduces the incidence of dry socket, but there is no evidence to support this practice. It has been suggested that dental extractions in females taking oral contraceptives be scheduled on days without estrogen supplementation (typically days 23–28 of the menstrual cycle).[1] It has also been suggested that teeth to be extracted be scaled prior to the procedure.[2]
Prevention of alveolar osteitis can be exacted by following post-operative instructions, including:
- Taking any recommended medications
- Avoiding intake of hot fluids for one to two days. Hot fluids raise the local blood flow and thus interfere with organization of the clot. Therefore, cold fluids and foods are encouraged, which facilitate clot formation and prevent its disintegration.
- Avoiding smoking. It reduces the blood supply, leading to tissue ischemia, reduced tissue perfusion and eventually higher incidence of painful socket.
- Avoiding drinking through a straw or spit forcefully as this creates a negative pressure within the oral cavity leading to an increased chance of blood clot instability.[7]
Treatment
Treatment is usually symptomatic, (i.e., analgesic medications) and also the removal of debris from the socket by irrigation with saline or local anesthetic. Medicated dressings are also commonly placed in the socket, although these will act as a foreign body and prolong healing, they are usually needed due to the severe pain. Hence, the dressings are usually stopped once the pain is lessened. Examples of medicated dressings include antibacterials, topical anesthetics and obtundants, or combinations of all three, e.g., zinc oxide and eugenol impregnated cotton pellets, alvogyl (eugenol, iodoform and butamen), dentalone, bismuth subnitrate and iodoform paste (BIPP) on ribbon gauze and metronidazole and lidocaine ointment.[4] A systematic review of the efficacy of treatments for dry socket concluded that there was not enough evidence to discern the effectiveness of any treatments.[4] People who develop a dry socket typically seek medical/dental advice several times after the dental extraction, where the old dressing is removed, the socket irrigated and a new dressing placed. Curettage of the socket increases the pain and has been discouraged by some.[1]
Prognosis
If a dry socket occurs, the total healing time is increased. Postoperative pain is also worse than the normal discomfort which accompanies healing following any minor surgical procedure. The pain may last for seven to forty days.[1][2]
Epidemiology
Overall, the incidence of dry socket is about 0.5–5% for routine dental extractions,[2][3][4] and about 25–30% for impacted mandibular third molars (wisdom teeth which are buried in the bone).[1]
Females are more frequently affected than males, but this appears to be related to oral contraceptive use rather than any underlying gender predilection.[1][2] The majority of dry sockets occur in individuals aged between 20 and 40 which is when most dental extractions occur, although for any given individual it is more likely to occur in with increasing age.[1]
Other possible risk factors include periodontal disease, acute necrotizing ulcerative gingivitis, local bone disease, Paget's disease of bone, osteopetrosis, cemento-osseous dysplasia, a history of previously developing a dry socket with past extractions and inadequate oral hygiene.[3][4][8] Other factors in the postoperative period that may lead to loss of the blood clot include forceful spitting, sucking through a straw, and coughing or sneezing.[4]
Etymology
Alveolar refers to the alveolus, the alveolar processes of the mandible or maxilla; osteitis is derived from oste-, from Greek, osteon meaning "bone"; and -itis means a disease characterized by inflammation.
Osteitis generally refers to localized inflammation of bone with no progression through marrow spaces (compare with osteomyelitis).[3]
Often, the term alveolar osteitis is considered synonymous with "dry socket", but some specify that dry socket is a focal or localized alveolar osteitis.[2] An example of another type of osteitis is focal sclerosing/condensing osteitis.[3] The name dry socket is used because the socket has a dry appearance once the blood clot is lost and debris is washed away.
References
- ^ a b c d e f g h i j k l m n o p q r Neville, BW; Damm, DD; Allen, CM; Bouquot, JE (2002). Oral & Maxillofacial Pathology (2nd ed.). Philadelphia: W.B. Saunders. p. 133. ISBN 0721690033.
- ^ a b c d e f g h i j k l m n o p Wray, D; Stenhouse D; Lee D; Clark AJE (2003). Textbook of general and oral surgery. Edinburgh [etc.]: Churchill Livingstone. pp. 216–217. ISBN 0443070830.
- ^ a b c d e f g h i j k l m Soames JV; Southam JC (1999). Oral pathology (3. ed., [Nachdr.] ed.). Oxford [u.a.]: Oxford Univ. Press. pp. 296–298. ISBN 0192628941.
- ^ a b c d e f g h i j k l m n o Daly, B; Sharif, MO; Newton, T; Jones, K; Worthington, HV (Dec 12, 2012). "Local interventions for the management of alveolar osteitis (dry socket).". Cochrane database of systematic reviews (Online) 12: CD006968. doi:10.1002/14651858.CD006968.pub2. PMID 23235637.
- ^ Coulthard, P; Horner K; Sloan P; Theaker E (2008). Master dentistry. volume 1: Oral and maxillofacial surgery, radiology, pathology and oral medicine. (2nd ed.). Edinburgh: Churchill Livingstone/Elsevier. p. 90. ISBN 9780443068966.
- ^ a b c d e f Fragiskos, FD (2007). Oral surgery. Berlin: Springer. p. 199. ISBN 3-540-25184-7.
- ^ a b c Tucker, MR; Hupp JR; Ellis E (2008). Contemporary oral and maxillofacial surgery (5th ed.). St. Louis, Mo.: Mosby Elsevier. p. 198. ISBN 9780323049030.
- ^ a b c d Odell, edited by Edward W. (2010). Clinical problem solving in dentistry (3rd ed.). Edinburgh: Churchill Livingstone. pp. 67–69. ISBN 9780443067846.
- ^ a b c Lodi, G; Figini, L; Sardella, A; Carrassi, A; Del Fabbro, M; Furness, S (Nov 14, 2012). "Antibiotics to prevent complications following tooth extractions.". Cochrane database of systematic reviews (Online) 11: CD003811. doi:10.1002/14651858.CD003811.pub2. PMID 23152221.
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Oral and maxillofacial pathology (K00–K06, K11–K14, 520–525, 527–529)
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Lips
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- Cheilitis
- Actinic
- Angular
- Plasma cell
- Cleft lip
- Congenital lip pit
- Eclabium
- Herpes labialis
- Macrocheilia
- Microcheilia
- Nasolabial cyst
- Sun poisoning
- Trumpeter's wart
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Tongue
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- Ankyloglossia
- Black hairy tongue
- Caviar tongue
- Crenated tongue
- Cunnilingus tongue
- Fissured tongue
- Foliate papillitis
- Glossitis
- Geographic tongue
- Median rhomboid glossitis
- Transient lingual papillitis
- Glossoptosis
- Hypoglossia
- Lingual thyroid
- Macroglossia
- Microglossia
- Rhabdomyoma
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Palate
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- Bednar's aphthae
- Cleft palate
- High-arched palate
- Palatal cysts of the newborn
- Inflammatory papillary hyperplasia
- Stomatitis nicotina
- Torus palatinus
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Oral mucosa - Lining of mouth
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- Amalgam tattoo
- Angina bullosa haemorrhagica
- Behçet syndrome
- Bohn's nodules
- Burning mouth syndrome
- Candidiasis
- Condyloma acuminatum
- Darier's disease
- Epulis fissuratum
- Erythema multiforme
- Erythroplakia
- Fibroma
- Focal epithelial hyperplasia
- Fordyce spots
- Hairy leukoplakia
- Hand, foot and mouth disease
- Hereditary benign intraepithelial dyskeratosis
- Herpangina
- Herpes zoster
- Intraoral dental sinus
- Leukoedema
- Leukoplakia
- Lichen planus
- Linea alba
- Lupus erythematosus
- Melanocytic nevus
- Melanocytic oral lesion
- Molluscum contagiosum
- Morsicatio buccarum
- Oral cancer
- Benign: Squamous cell papilloma
- Keratoacanthoma
- Malignant: Adenosquamous carcinoma
- Basaloid squamous carcinoma
- Mucosal melanoma
- Spindle cell carcinoma
- Squamous cell carcinoma
- Verrucous carcinoma
- Oral florid papillomatosis
- Oral melanosis
- Pemphigoid
- Pemphigus
- Plasmoacanthoma
- Stomatitis
- Aphthous
- Denture-related
- Herpetic
- Smokeless tobacco keratosis
- Submucous fibrosis
- Ulceration
- Verruca vulgaris
- Verruciform xanthoma
- White sponge nevus
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Teeth (pulp, dentin, enamel)
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- Amelogenesis imperfecta
- Ankylosis
- Anodontia
- Caries
- Concrescence
- Delayed eruption
- Dens evaginatus
- Dentin dysplasia
- Dentin hypersensitivity
- Dentinogenesis imperfecta
- Dilaceration
- Ectopic enamel
- Enamel hypocalcification
- Enamel hypoplasia
- Enamel pearl
- Fluorosis
- Fusion
- Gemination
- Hyperdontia
- Hypodontia
- Impaction
- Macrodontia
- Meth mouth
- Microdontia
- Odontogenic tumors
- Keratocystic odontogenic tumour
- Odontoma
- Open contact
- Premature eruption
- Pulp calcification
- Pulp necrosis
- Pulp polyp
- Pulpitis
- Regional odontodysplasia
- Resorption
- Supernumerary root
- Taurodontism
- Trauma
- Avulsion
- Cracked tooth syndrome
- Vertical root fracture
- Occlusal
- Tooth loss
- Tooth wear
- Abrasion
- Abfraction
- Acid erosion
- Attrition
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Periodontium (gingiva, Periodontal ligament, cementum, alveolus) - Gums and tooth supporting structures
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- Cementoblastoma
- Cementoma
- Eruption cyst
- Epulis
- Pyogenic granuloma
- Congenital epulis
- Gingival enlargement
- Gingival cyst of the adult
- Gingival cyst of the newborn
- Gingivitis
- Desquamative
- Granulomatous
- Plasma cell
- Hereditary gingival fibromatosis
- Hypercementosis
- Hypocementosis
- Linear gingival erythema
- Necrotizing periodontal diseases
- Acute necrotizing ulcerative gingivitis
- Pericoronitis
- Peri-implantitis
- Periodontal abscess
- Periodontal trauma
- Periodontitis
- Aggressive
- As a manifestation of systemic disease
- Chronic
- Perio-endo lesion
- Teething
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Periapaical, mandibular and maxillary hard tissues - Bones of jaws
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- Agnathia
- Alveolar osteitis
- Cherubism
- Idiopathic osteosclerosis
- Mandibular fracture
- Microgenia
- Micrognathia
- Intraosseous cysts
- Odontogenic: periapical
- Dentigerous
- Buccal bifurcation
- Lateral periodontal
- Globulomaxillary
- Calcifying odontogenic
- Glandular odontogenic
- Non-odontogenic: Nasopalatine duct
- Median mandibular
- Median palatal
- Traumatic bone
- Osteomyelitis
- Osteonecrosis
- Bisphosphonate-associated
- Neuralgia-inducing cavitational osteonecrosis
- Osteoradionecrosis
- Osteoporotic bone marrow defect
- Paget's disease of bone
- Periapical abscess
- Periapical periodontitis
- Stafne defect
- Torus mandibularis
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Temporomandibular joints, muscles of mastication and malocclusions - Jaw joints, chewing muscles and bite abnormalities
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- Bruxism
- Condylar resorption
- Mandibular dislocation
- Malocclusion
- Crossbite
- Open bite
- Overbite
- Overjet
- Prognathia
- Retrognathia
- Temporomandibular joint dysfunction
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Salivary glands
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- Benign lymphoepithelial lesion
- Ectopic salivary gland tissue
- Frey's syndrome
- HIV salivary gland disease
- Necrotizing sialometaplasia
- Mucocele
- Pneumoparotitis
- Salivary duct stricture
- Salivary gland aplasia
- Salivary gland atresia
- Salivary gland diverticulum
- Salivary gland fistula
- Salivary gland hyperplasia
- Salivary gland hypoplasia
- Salivary gland neoplasms
- Benign: Basal cell adenoma
- Canalicular adenoma
- Ductal papilloma
- Monomorphic adenoma
- Myoepithelioma
- Oncocytoma
- Papillary cystadenoma lymphomatosum
- Pleomorphic adenoma
- Sebaceous adenoma
- Malignant: Acinic cell carcinoma
- Adenocarcinoma
- Adenoid cystic carcinoma
- Carcinoma ex pleomorphic adenoma
- Lymphoma
- Mucoepidermoid carcinoma
- Sclerosing polycystic adenosis
- Sialadenitis
- Parotitis
- Chronic sclerosing sialadenitis
- Sialectasis
- Sialocele
- Sialodochitis
- Sialosis
- Sialolithiasis
- Sjögren's syndrome
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Orofacial soft tissues - Soft tissues around the mouth
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- Actinomycosis
- Angioedema
- Basal cell carcinoma
- Cutaneous sinus of dental origin
- Cystic hygroma
- Gnathophyma
- Ludwig's angina
- Macrostomia
- Melkersson–Rosenthal syndrome
- Microstomia
- Noma
- Oral Crohn's disease
- Orofacial granulomatosis
- Perioral dermatitis
- Pyostomatitis vegetans
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Other
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- Eagle syndrome
- Hemifacial hypertrophy
- Facial hemiatrophy
- Oral manifestations of systemic disease
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Index of the mouth
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| Description |
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| Disease |
- Congenital
- face and neck
- cleft
- digestive system
- Neoplasms and cancer
- Other
- Symptoms and signs
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| Treatment |
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