Osteitis.

Osteitis.

1. Definition

These are localized or diffuse inflammatory lesions of bone tissue. They can be of local or general cause.

The manifestations of bone infection, its development and especially its spread depend on the anatomical and physiological conditions of the infected sites (maxillae).

2. Anatomical reminders

Bone is a supportive connective tissue with a “lamellar” structure. Its surface is covered by the periosteum , a whitish connective membrane that allows bone growth in thickness, and the production of calluses in the event of a fracture.

Below this is a dense, particularly resistant layer of bone: compact bone or cortical bone . 

Under this blade, the bone is much less dense: it is the spongy bone , or trabecular  ; it contains the red bone marrow, which produces blood cells.

Bone tissue is made up of: 

– a protein framework, mainly composed of collagen;

– by a mineral fraction consisting of calcium and phosphorus and 

– by three families of cells: Osteoblasts and osteocytes, which develop the bone matrix. Osteoclasts, which destroy it.

The maxilla 

It is suitable for withstanding the stresses of vertical mandibular forces, it has a double structure:

Spongy at the level of the palatine vault, alveolar edges and tuberosity.

Compact at the level of its ascending apophysis and its anterior region. 

Its arterial vascularization is provided by the internal maxillary artery which divides into: suborbital artery, sphenopalatine artery, and alveolodental artery.

Osteitis.

Osteitis.

The mandible 

In a cross-section, this bone appears as a groove of compact bone, open at the top over the teeth and covered by two internal and external cortices which join to form the basilar edge. This sleeve of compact bone of the Haversian type encases a core of spongy bone; the distribution of the latter predominates at the level of the horizontal branch and the symphysis. It is much rarer at the level of the ascending branch.  

Its vascularization is ensured by a double network:

– Centrally provided by the inferior alveolar artery.

– Peripheral, periosteum affecting all bony surfaces of the mandible except the dental implantation area.

The central system is predominant. Anastomoses between the two systems exist but are of low flow.

3. Histopathology

During osteoarthritis, bone remodeling intensifies and results in:

• To bone destruction by rarefaction or necrosis.
• A bony construction: condensation.

1. Bone destruction can occur in two ways   

• Rarefaction: ( at the level of the spongy bone )

A progressive process that results in a decrease in the density or quantity of bone. There are two mechanisms of rarefaction:

• When the bone is infected, the inflamed connective tissue is hypervascularized and frees itself of its mineral deposit: This is OSTEOLYSIS .
• The second mechanism is of cellular origin, it is OSTEOCLASIA which is a real phagocytosis of bone tissue by specialized cells, OSTEOCLASTS.
• Necrosis: ( at the level of the cortical bone ).

 Sudden phenomenon which occurs following devascularization either by thrombophlebitis of the nourishing vessels; or by periosteal detachment. 

 The compact bone will eventually release a “sequestrum”: which is a detached bone fragment, of which the calcium framework is the only one to remain, the protein framework being completely destroyed by the microbial toxins.

2. Construction or condensation

It can follow bone destruction or occur at the same time as it. The periosteum reacts to the infection with irregular thickening and more or less anarchic periosteal appositions. 

4. Etiologies

• Local causes
• Alveolar dental causes:

All complications of tooth decay

Post-extraction complications (alveolitis)

• Traumatic causes:

Open fracture

• Tumor causes:

Superinfection of tumor focus 

In case of skin infection (boil, carbuncle on the chin), or mucous membrane (ulceration, stomatitis, tonsillitis, etc.).

• Peri-implant pathology.
• Sinus pathology (chronic sinusitis). 
• General causes:

Septic inoculation by hematogenous route

• Exogenous causes:

• Radiotherapy
• Poisoning (arsenic, phosphorus, lead poisoning, etc.)
• Bisphosphonates

5. Favoring factors:
   1. The terrain: plays a predisposing role when:

• Defenses are reduced (Diabetes, Neutropenia, AIDS).
• Some harmful habits (alcoholism). 
• Certain treatments which reduce the body’s resistance (prolonged corticosteroid therapy, antimitotics).

2. Age: certain age groups are particularly exposed:

• The highest frequency is in young people, when successive dental eruptions lead to bone remodeling.
• Likewise, elderly people are exposed due to the restructuring of the bone structure added to a slowed metabolism and reduced defenses.

6. The germs involved: 

Any germ can cause a bone infection. 

•  Staphylococcus +++ , 
•  Streptococcus, 
•  Pneumococcus,
•  Gram negative bacillus. 
•  A certain number of germs that are usually not very pathogenic (candida, aspergillus) can become so, when there is a deficiency in the immune defense processes.

7. Clinical study

7.1. Osteitis of local causes

7.1.1. Localized osteitis

      7.1.1.1.Osteoperiostitis and osteoperiostosis:

7.1.1.1.1. Osteoperiostitis or hyperostotic osteitis of Garré:

Observed mainly in children (10 – 12 years old, sometimes rather often in relation to the 6 year tooth).

 Usually follows a pulp infection that extends to the apex.

Seated exclusively in the mandible.

Clinic: 

• Signs of desmodontitis (mobility and pain).
• The pus migrates from the apex to the periosteum which rises.
• Severe, throbbing pain.
• Swollen gum opposite the causative tooth.
• More or less significant edema, which can deform the face.
• Thickening of one or both bony tables (especially the outer table).
• Very rarely a fistula is present.

X-ray: 

Dental panoramic scan reveals the etiology: tooth with apical infection; sometimes presence of underlying osteolytic image.

Evolution :

The course of treatment is generally long, over several months, with regression of the swelling and normalization of the bone appearance. A sequelae of swelling may sometimes persist.

7.1.1.1.2. Osteoperiostosis:

Occurs most often in young children, during chronic arthritis of the first lower molar.

Clinic:

• A hard, chronic swelling, adhering to the bone, deforming the face, not painful.
• Lockjaw.
• Absence of suppuration or sequestration.
• We often find an untreated dental starting point (cyst, apical granuloma, chronic arthritis)

Evolution: Usually disappears slowly after extraction or medical treatment of the causative tooth. 

Treatment of Garré’s osteoperiostitis and osteoperiostosis: Dental etiological treatment is necessary and sufficient, leading in several months to a partial or more often complete regression of the symptoms.

7.1.1.2. Subperiosteal abscess: Occurs only where the gum adheres to the periosteum (palate and attached gingiva). 

Clinic:

• At the palace level: 

 Fluctuating and painful curvature (swelling with watch glass deformation).

 Edematous and congested mucosa.

 Related to the palatal roots of the premolars and molars and the lateral incisor.

• At the level of the attached gum:

 Small congestive red abscess, located at the level of the necks of the teeth (Parulie).

 Relapsing rapidly without treatment.

 Often involving periodontal pockets and dead baby teeth.

7.1.1.3. Circumscribed osteitis
Depending on its location, it manifests itself in 3 ways:

7.1.1.3.1. Osteitis of the alveolar rim or alveolitis

Main infectious complication post extraction. There are 2 types:

• Dry socket:

The physiological clot that should normally fill the alveolus after tooth extraction does not form or is absorbed too quickly.

Dry socket is characterized by: 

Acute, violent pain, resistant to analgesics, occurring in the hours following tooth extraction.

The endooral examination found an empty alveolus, the alveolar bone was exposed and surrounded by a grayish mucosa.

• Suppurative alveolitis:

Related to superinfection of the alveolar clot after extraction.

It manifests itself by:

      Less intense pain than dry socket appearing 2 to 3 days after extraction.

Endo buccal: the alveolus is filled with a more or less purulent brownish growth, with a fetid odor.

Etiologies of alveolitis: the following are blamed:
– Anatomical conditions.

• Ischemic effect of a vasoconstrictor.
• Crushing of the alveolar bone by the tooth during extraction maneuvers with reduction of alveolar bleeding or even formation of a thrombus in the local vessels supposed to bring blood into the alveolus.
•  Smoking (formation of small vascular thrombi), or taking oral contraceptives (increased plasma fibrinolytic activity).

Treatment : 

A) Dry alveolitis:

• Curettage of the alveolus, under anesthesia without vasoconstrictor until bleeding.
• Irrigation and asepsis of the alveolus.
• Placement of a cotton wick, soaked and wrung out with eugenol, placed superficially on the roof of the cell.
• Prescription of NSAIDs (antiplatelet agents for vasodilation) and analgesics, antibiotics are not systematic except in the case of infection of the alveolus.

B) Suppurative alveolitis:

Same treatment as the previous form except that antibiotics are systematic (Amoxicillin® + Flagyl® or Orogyl®).

7.1.1.3.2. Septum syndrome

It is the irritation of the interdental bone by:

• a bad point of contact,
• an overflowing filling
• irritating prosthesis…

**Manifests itself by

• Pain similar to periodontitis in the 2 adjacent teeth. 
• The gingival papilla is inflamed and sometimes ulcerated.
• The septum is exposed.

Radio: blurred or amputated spearhead (panoramic and retro alveolar).

Treatment of septal syndrome 

• Elimination of the cause (foreign bodies, hook, overflowing filling).
• Interdental curettage.
• Wash with hydrogen peroxide, or with eugenol.

7.1.1.3.3. Central circumscribed osteitis (centromedullary)

Often following superinfection of a granuloma or a suppurative cyst, it can progress outwards (cortical osteitis). Occurs mainly in the mandible (compact structure)

Preferred location: Premolar and symphysis areas.

Clinically we find:

• Local signs of apical monoarthritis (dental signs) 
• Very marked general signs (fever, asthenia)
• Significant bone swelling 
• Clear dental mobility, in view of this swelling. The pulp vitality test is negative 
• Radiating shooting pains.

 The evolution is towards fistulization with sometimes perimaxillary cellular reaction. The elimination of a bone sequestrum is possible.

Radiography: possibly shows the initial cause and significant and irregular decalcification (rarefaction) at the apical level.

Differential diagnosis
Perimaxillary phlegmon must be eliminated where the general signs are more moderate.

7.1.1.3.4.Cortical osteitis 

It is a frequent complication of central osteitis, poorly treated perimaxillary phlegmon or chronic progression.

      Characterized by necrosis of the cortex and periosteum in contact with cellulite (Dechaume).

Clinic: we find 

 * facial deformation (sign of swelling)

 * painful bone swelling 

 * the presence of a fistula 

Evolution: is happening 

• Either in an acute mode with purulent collection and sometimes sequestration; Vincent’s sign (labiomental hypoesthesia) is negative except during infectious manifestations localized to the mental hole.
• Either in a subacute mode towards the periosteum, without suppuration 
• Either towards diffusion: this is then the appearance of diffuse osteitis with marked general and functional signs, but the symptoms remain localized to the region concerned. Vincent’s sign is late positive. 
• Radiologically: the interpretation is sometimes delicate:

We find an image of decalcification with or without sequestrum formation.

Treatment of circumscribed osteitis (centromedullary and cortical):

• Antibiotic therapy, often dual therapy.
• Etiological treatment.
• Collection of the sequestration and curettage.
• Draining the collection.

7.1.1.4. Diffused osteitis
Corresponds to the extension of a process that was initially circumscribed (which has become rare since the advent of antibiotics)

Evolves in 04 phases:

1. Beginning phase

-Signs of acute desmodontitis

– With trismus and filling of the vestibule by a hard mass fixed to the bone

2 – State phase

Worsening of the previous signs and appearance of general signs (fever, asthenia), mobility of the causal tooth and even of adjacent teeth

Rx: bone rarefaction around the causal tooth

3 – Sequestration phase: 

The pain subsides, the stylus examination shows a rough bone which becomes mobile to finally be eliminated by the fistula.

Rx: opaque or flaky radio image (sequestrum).

4- Repair phase

Corresponds to re-ossification and repair of bone loss.

7.1.1.5. Diffuse osteitis

It is mainly manifested by:

• a serious impairment of the general condition
• severe pain 
• extensive dental mobility (an entire sector) 
• swelling of both bony tables
• the formation of sequestrations 

7.1.1.5.1. Acute diffuse osteitis (ADO):
7.1.1.5.1.1. ADO of the mandible: 

– Occurs after a periapical infectious episode

– Evolves according to the same pattern as diffuse osteitis with the addition of

* Tight pink skin, tight trismus, sign of early Vincent

* Skin fistulization relieves the patient and exploration of the fistula path leads to a bone of “wet sugar” consistency  

– Rx: demineralization zone with blurred limits. Later, sequestration gives opaque radio images.

7.1.1.5.1.2. ODA of the upper jaw:

• Severe pain under the orbit and in the upper jaw on the side of the causative tooth 
• Impressive picture of vestibular, palatine or antral cellulitis, accompanied by multiple abscesses 
• Infraorbital hypoesthesia
• Mobility of several teeth
• Presence of one or more fistulas 
• Sequestrations are eliminated through the mouth, sometimes accompanied by the teeth, or through the nasal passages. 

7.1.1.5.2. Subacute diffuse osteitis:

• Often found in children in the region of the mandibular angle.
• Onset: slow, insidious, without clear signs of infection but the swelling of the bony tables attracts attention. The trismus is mild, and no Vincent’s sign.

X-ray: shows central bone rarefaction with periosteal reaction.

It is imperative to perform a biopsy and bacteriological sample to make the differential diagnosis with an osteosarcoma in order to eliminate it.

Treatment of diffuse and widespread osteitis:

• Hospitalization as a rule.
• Intense and prolonged intravenous (IV) antibiotic therapy as soon as the vital prognosis is lifted.

– Limited intervention excising necrotic tissues (soft parts and bones) and drainage under antibiotics, while avoiding dental extractions.

– Surgical excision, passing through healthy tissue, with immediate grafting.

7.1.1.5.3. Chronic diffuse osteitis

It follows previous forms that were insufficiently or poorly treated by too brief antibiotic therapy. 

It mainly concerns the lower jaw with absence of functional and general signs 

This is called “cold osteitis”

* Clinically there are:

– Painless swelling of both tables 

– Vincent’s sign +  and multiple fistulas, the exploration of which leads to a bone with a “wet sugar” consistency 

* Radio: hyperostosis or clear radio geodes or images of sequestra in the center of these geodes. 

* The biopsy will allow an anapathological examination which will confirm the positive diagnosis.

7.1.1.5.4.Hyperplastic osteitis fibrosa

It manifests itself by bone hypertrophies for which a dental origin is suspected when they are opposite dead teeth. 

Functional signs are absent. The evolution is very slow.

X-ray: shows a flaky image with densification of the bone matrix 

It is sometimes difficult to distinguish them from fibrous dysplasia (biopsy).

7.2. Osteitis of general cause

7.2.1. Hematogenous osteitis

7.2.1.1. Acute hematogenous osteitis (acute hematogenous osteomyelitis)

     – Maxillary localization is rare, it follows a dissemination of pathogenic germs through the blood.

     – It is more common in children

     – The phases of development are reminiscent of those described for diffuse osteitis except that the onset phase in hematogenous osteitis corresponds to the septicemia phase characterized by intense general signs.

Treatment of acute osteomyelitis:

•  Directed antibiotic treatment must be initiated quickly (this is an emergency).
• Surgical treatment will be indicated after cleaning the site.
•  Etiological treatment is the rule.

7.2.1.2. Chronic hematogenous osteitis (chronic hematogenous osteomyelitis):

It is very rare. It is distinguished from the first forms by its manifestation one month after the onset of symptoms (a completely arbitrary basis). Characterized by its high tendency to recurrence.

Osteitis.

Treatment of chronic osteomyelitis: 

• Medical :

•  Antibiotics are useful at the beginning of the course, and are prescribed for several months, in a directed manner, or by application of gentamicin beads.
• Corticosteroids prescribed in the absence of etiological germs would be useful for their anti-inflammatory action, for at least 10 days.
• Hyperbaric oxygen therapy has been recommended because of its effectiveness on anaerobic germs and in hypoxic lesions.
• Surgical:

•  Decortication, in case of failure of medical treatments.
• Dental extractions in osteomyelitis areas must be carried out under antibiotic cover, otherwise they accelerate and aggravate the development of infectious phenomena.

7.2.1.2. Specific osteitis

• Actinomycotic osteitis: classically begins with actinomycotic cellulitis. The diagnosis is based mainly on bacteriological data (actinomyces).
• Syphilitic osteitis: related to tertiary or congenital syphilis (Treponema pallidum). Specific serologies allow the diagnosis to be made: Treponema Pallidium Hemagglutination Assay (TPHA) – Venereal Disease Research Laboratory  (VDRL) – Fluorescent treponemal antibody absorption (FTA abs) .
• Tuberculous osteitis: produces a picture of chronic osteitis. The intradermal reaction (IDR) to tuberculin, the isolation of Koch’s bacillus (BK), the anatomopathological examination (tuberculoid granuloma with caseous necrosis) and the notion of contagion allow the diagnosis.

Treatment of specific osteitis 

• Actinomycotic: ßlactams, cyclins or macrolides or the combination Tetracycline – erythromycin.
• Tuberculosis: triple therapy: Rifampicin 10mg/Kg + Isoniazid 4 to 5mg/Kg + Pyrazinamide 25mg/Kg to which Ethambutol 15mg/Kg can be added.
• Syphilitic: penicillin therapy; if allergic: tetracyclines. Macrolides (pregnant women).

7.3. Osteitis of exogenous cause

1. Post-radiation osteitis (osteoradionecrosis: ORN)

It is an osteitis observed in patients who have undergone radiotherapy of the orofacial sphere.

The occurrence of ORN is linked to tissue modifications produced by radiation (hypovascularization, hypocellularity, hypoxia) in interaction with the determining occurrence of local accidents (infection, ischemia).

ORN can occur even years after radiation therapy ends.

2. Arsenical necrosis

These are necroses that follow the leakage of arsenic used as an escharotic agent in necropulpectomy. These necroses can become secondarily infected and give rise to osteitis.

3. Osteitis under antiresorptive drugs (bisphosphonates, antiangiogenics, etc.)

Bisphosphonates are osteoclasis inhibitors indicated in the treatment of certain osteolytic conditions (bone metastases, osteoporosis, Paget’s disease, etc.).

Forms of chronic non-bacterial osteomyelitis secondary to this type of treatment have been described. 

8. Differential diagnosis: will be done with:

• Primary or secondary malignant bone disorders:

• Osteogenic sarcoma, 
• Ewing’s sarcoma, 
• Hodgkin’s sarcoma, 
• Lymphomas, 
• Bone metastases from cancer (especially glandular)  

• Benign tumors of the jaws
• Cellular accidents.

9. Treatment 

9.1. Preventive treatment

• Motivation for oral hygiene and caries prophylaxis;
• Resumption of defective dental treatments (overflowing filling, periapical lesion, etc.)
• Treatment of periodontal diseases
• Early treatment of perimaxillary cellulitis and phlegmon
• Antibiotic therapy for open fracture
• Antibiotic prophylaxis in case of risk ( irradiated patient , taking bisphosphonates, etc.)
• Strict asepsis in all surgical procedures.

9.2. Curative treatment 

9.2.1. Medical treatment

• Antibiotics (prefer bone-disseminating ATBs: amoxicillin, lincosamides), antibiotic therapy is particularly long in osteitis, especially in the chronic form where antibiotic therapy must be continued for several months even after the physical signs have disappeared.
• Anti-inflammatories
• Painkillers
• Hyperbaric oxygen therapy

9.2.2. Surgical treatment

• Extraction of the causal tooth
• Incision and drainage in case of purulent collection
• Sequestrectomy: consists of going to “pick” the sequestrum if it does not eliminate itself spontaneously without too much stress. Must be done under antibiotic therapy.

Osteitis.

CONCLUSION

Facial osteitis should always be considered potentially serious, requiring early medical or surgical treatment.

We cannot stress enough the importance of preventive treatment, which is of the utmost importance here.

Osteitis.

  Cracked teeth can be healed with modern techniques.
Gum disease can be prevented with proper brushing.
Dental implants integrate with the bone for a long-lasting solution.
Yellowed teeth can be brightened with professional whitening.
Dental X-rays reveal problems that are invisible to the naked eye.
Sensitive teeth benefit from specific toothpastes.
A diet low in sugar protects against cavities.
 

Osteitis.