Osteomyelitis-with Radiological features

OSTEOMYELITIS

• Suppurative osteomyelitis
• Garrés osteomyelitis (periostitis ossificans, proliferative osteomyelitis)
• Tuberculous osteomyelitis
• Syphilitic osteomyelitis
• Actinomycotic osteomyelitis
• Osteoradionecrosis

SUPPURATIVE OSTEOMYELITIS

Osteomyelitis is an inflammatory reaction of bone to infection which originates from either a tooth, fracture site, soft tissue wound or surgery site. The dental infection may be from a root canal, a periodontal ligament or an extraction site. Suppurative osteomyelitis can involve all three components of bone: periosteum, cortex, and marrow. Usually there is an underlying predisposing factor like malnutrition, alcoholism, diabetes, leukemia or anemia.

Other predisposing factors are those that are characterized by the formation of avascular bone for example, therapeutically irradiated bone, osteopetrosis, Paget's disease, and florid osseous dysplasia. Osteomyelitis is more commonly observed in the mandible because of its poor blood supply as compared to the maxilla, and also because the dense mandibular cortical bone is more prone to damage and, therefore, to infection at the time of tooth extraction.

Acute osteomyelitis is similar to an acute primary abscess in that the onset and course may be so rapid that bone resorption does not occur and, thus, a radiolucency may not be present on a radiograph. Clinical features include pain, pyrexia, painful lymphadenopathy, leukocytosis, and other signs and symptoms of acute infection. Later, after approximately two weeks, as the lesion progresses into the chronic stage, enough bone resorption takes place to show radiographic mottling and blurring of bone. A sclerosed border called an involucrum forms around the affected area. The involucrum prevents blood supply from reaching the affected part. This results in the formation of pieces of sequestra or necrotic bone surrounded by pus. A fistulous tract may develop by the suppuration perforating the cortical bone and periosteum. The fistulous tract discharges pus onto the overlying skin or mucosa.

The radiopacity of the sequestra and the radiolucency of the pus give rise to the characteristic "worm-eaten" radiographic appearance. Radiographs also aid in locating the original site of infection such as an infected tooth, a fracture, or infected sinus.

Fig. 13-1 Chronic suppurative osteomyelitis of dental origin. The lesion discharged pus into the oral cavity. Note the radiopaque sequestra (arrow) surrounded by the radiolucent suppuration.

Fig. 13-2 Chronic suppurative osteomyelitis demonstrating a worm-eaten appearance of the body of the mandible. Note the radiopaque sequestra surrounded by the radiolucent suppuration and a radiopaque involucrum. The patient had fetid breath.

Fig. 13-3 Chronic suppurative osteomyelitis of dental origin. The radiopaque sequestrum (arrow) is surrounded by the radiolucent suppuration.

Fig. 13-4 Sequestrum that has floated into the soft tissues. Patient gave a history of a problematic tooth extraction several years ago which resulted in clinical complications.

GARRÉS OSTEOMYELITIS

(Periostitis ossificans, Osteomyelitis with proliferative periostitis) Garrés osteomyelitis or proliferative periostitis is a type of chronic osteomyelitis which is nonsuppurative. It occurs almost exclusively in children and young adults who present symptoms related to a carious tooth. The process arises secondary to a low-grade chronic infection, usually from the apex of a carious mandibular first molar. The infection spreads towards the surface of the bone, resulting in inflammation of the periosteum and deposition of new bone underneath the periosteum. This peripheral formation of reactive bone results in localized periosteal thickening. The inferior border of the mandible below the carious first molar is the most frequent site for the hard nontender expansion of cortical bone. On an occlusal view radiograph, the deposition of new bone produces an "onion-skin" appearance.

Fig. 13-5 Garrés osteomyelitis (proliferative periostitis) demonstrating an expansion of the inferior border of the mandible (onion-skin appearance) caused by the periapical infection of the mandibular first molar.

Fig. 13-6 An occlusal radiograph of Garrés osteomyelitis showing the buccal expansion of the mandible caused by infection around the root tip of the extracted first molar.

Fig. 13-7 Garrés osteomyelitis (periostitis ossificans) exhibiting localized periosteal thickening. The source of infection is not known; it could have been from an exfoliated deciduous molar tooth.

TUBERCULOSIS OSTEOMYELITIS

Tuberculosis is a chronic granulomatous disease which may affect any organ, although in man the lung is the major seat of the disease and is the usual portal through which infection reaches other organs. The microorganisms may spread by either the bloodstream or the lymphatics. Oral manifestations of tuberculosis are extremely rare and are usually secondary to primary lesions in other parts of the body. Infection of the socket after tooth extraction can also be the mode of entry into the bone by Mycobacterium tuberculosis.

Mandible and maxilla are less commonly affected than long bones and vertebrae. On a radiograph, the appearance of bony lesions is similar to that of chronic suppurative osteomyelitis ("worm- eaten" appearance) with fistulae formation through which small sequestra are exuded. Periostitis ossificans (proliferative periostitis) can also occur and change the contour of bone. Calcification of lymph nodes is a characteristic sign of tuberculosis.

Fig. 13-8 Tuberculous osteomyelitis showing the "worm-eaten" appearance similar to that of a chronic suppurative osteomyelitis

Fig. 13-9 Calcified tuberculous lymph nodes

SYPHILITIC OSTEOMYELITIS

Syphilis is a chronic granulomatous disease which is caused by the spirochete Treponema pallidum. It is a contagious venereal disease which leads to many structural and cutaneous lesions. Acquired syphilis is transmitted by direct contact whereas congenital syphilis is transmitted in utero. In congenital syphilis, the teeth are hypoplastic, that is, the maxillary incisors have screwdriver-shaped crowns with notched incisal edges (Hutchinson's teeth) and the molars have irregular mass of globules instead of well-formed cusps ("mulberry molars"). Also, a depressed nasal bridge or saddleback nose occurs because of gummatous destruction of the nasal bones.

Acquired syphilis, if untreated, has three distinct stages. The primary stage develops after a couple of weeks of exposure and consists of chancres on the lips, tongue, palate, oral mucosa, penis, vagina, cervix or anus. These chancres are contagious on direct contact with them. The secondary stage begins 5 to 10 weeks after the occurrence of chancres and consists of diffuse eruptions on skin and mucous membrane. This rash may be accompanied by swollen lymph nodes throughout the body, a sore throat, weight loss, malaise, headache and loss of hair. The secondary stage can also damage the eyes, liver, kidneys and other organs. The tertiary-stage lesions may not appear for several years to decades after the onset of the disease. In this stage of osteomyelitis, the bone, skin, mucous membrane, and liver show gummatous destruction which is a soft, gummy tumor that resembles granulation tissue. Paralysis and dementia can also occur. In the oral cavity, the hard palate is frequently involved resulting in its perforation. The gummatous destruction is painless. Syphilitic osteomyelitis of the jaws is difficult to distinguish from chronic suppurative osteomyelitis since their radiographic appearances are similar.

Fig.13-10 Syphilitic osteomyelitis of the palate. The gummatous destruction has produced a palatal perforation.

Fig.13-11 Radiograph of syphilitic osteomyelitis of the palate. The perforation which is the site of gumma of the hard palate produces a radiolucency which may be mistaken for a median palatine cyst.

ACTINOMYCOTIC OSTEOMYELITIS

Like tuberculosis and syphilis, actinomycosis is a chronic granulomatous disease. It can occur anywhere in the body, but two-thirds of all cases occur in the cervicofacial region. The disease is caused by bacteria-like fungus called Actinomyces israeli. These microorganisms occur as normal flora of the oral cavity, and appear to become pathogenic only after entrance through previously seated defects. The portal of entry for the microorganisms is either through the socket of an extracted tooth, a traumatized mucous membrane, a periodontal pocket, the pulp of a carious tooth or a fracture. In cervicofacial actinomycosis, the patient exhibits swelling, pain, fever and trismus. The lesion may remain localized in the soft tissues or invade the jaw bones. If the lesion progresses slowly, little suppuration takes place; however, if it breaks down, abscesses are formed that discharge pus containing yellow granules ( (nicknamed sulfur granules) through multiple sinuses.

There is no characteristic radiographic appearance. In some cases the lesion resembles a periapical radiolucent lesion. The more aggressive lesion resembles chronic suppurative osteomyelitis. In chronic suppurative osteomyelitis there is usually a single sinus through which pus exudes; however, in actinomycotic osteomyelitis there are many sinuses through which pus and "sulfur granules" exude.

Fig.13-12 Actinomycotic lesion similar to radicular cyst. This is not a typical appearance.

OSTEORADIONECROSIS (and effects of irradiation on developing teeth)

In therapeutic radiation for carcinomas of the head and neck, the jaws are subjected to high exposure doses of ionizing radiation (average of 5000 R). This results in decreased vascularity of bone and makes them susceptible to infection and traumatic injury. Infection may occur in irradiated bone from poor oral hygiene, extraction wound, periodontitis, denture sores, pulpal infection or dental treatment. It is therefore advisable that a patient scheduled to undergo therapeutic radiation be given dental treatment prior to radiation therapy and that after radiation therapy the patient be taught to maintain good oral hygiene.

When infection occurs in irradiated bone, it results in a condition called osteoradionecrosis which is similar to chronic suppurative osteomyelitis. The mandible is affected more commonly than the more vascular maxilla. Therapeutic radiation may affect the salivary glands, producing decreased salivation. The resulting temporary or permanent xerostomia is responsible for radiation caries of teeth and erythema of the mucosa.

A radiograph of osteoradionecrosis, shows radiopaque sequestra and surrounding radiolucent purulency similar to that of chronic suppurative osteomyelitis. The two cannot be differentiated radiographically except by the history of therapeutic radiation. Effects of irradiation on developing teeth depends on the stage of development when irradiation occurs and on the dosage administered. The injured tooth germs may either fail to form teeth (anodontia), exhibit dwarf-teeth, produce agenesis of roots, shortening and tapering of roots, or develop into hypoplastic teeth. The eruption of teeth may be retarded and their sequencing may be disturbed. Other radiation induced effect may include maxillary and/or mandibular hypoplasia.

Fig.13-13 Occlusal projection of anterior region of mandible showing osteoradionecrosis. Notice the destruction of the trabecular pattern of bone.

Fig.13-14 Osteoradionecrosis of left mandible showing the radiopaque sequestra.

Fig.13-15 Osteoradionecrosis of left mandible has resulted in a pathologic fracture.

Fig.13-16 Dwarfing of teeth as a consequence of radiation therapy

Periapical periodontitis

Introduction
Inflammation in the periapical area of the periodontal ligament is similar to that occurring elsewhere in the body. It is often accompanied by resorption of bone, and occasionally the root apex, sufficient to be detected radiographically. However, the periapical vascular network has a rich collateral circulation, greatly enhancing the ability of the tissue to heal if the cause of the inflammation is removed. This potential for complete periapical healing, providing the source of irritation is removed, is the basis of endodontic treatment.

Whether the response to irritation in the periodontal ligament is principally an acute or chronic inflammation depends on factors such as the number and virulence of any microorganisms involved, the type and severity of any mechanical or chemical irritant, and the efficiency of the host defences. While it is convenient to describe acute and chronic periapical periodontitis as separate conditions, it must be realized that the tissue reaction to irritation is a dynamic response, often vacillating with time between acute and chronic inflammation. The sequelae are determined by the balance between the nature, severity, and duration of the irritant and the integrity of the defence mechanisms of the patient.

Aetiology

Introduction

The main causes of periapical periodontitis are detailed below.

Pulpitis and pulp necrosis

If pulpitis is untreated bacteria, bacterial toxins, or the products of inflammation will in time extend down the root canal and through the apical foramina to cause periodontitis. When pulp necrosis follows other causes, for example a blow to the tooth damaging the apical vessels, clinically significant periodontitis does not develop, unless bacteria gain access to the necrotic pulp or to the periapical tissues. The possible changes that may occur around the apex of an infected non-vital tooth and their inter-relationships are illustrated in

Changes that may occur around the apex of an infected non-vital tooth

Trauma

Occlusal trauma from, for example, a high restoration, undue pressure during orthodontic treatment, a direct blow on a tooth, and biting unexpectedly on a hard body in food may all cause minor damage to the periodontal ligament and localized inflammation. Traumatic periodontitis is often acute and transitory.

Key points - Periapical periodontitis
dynamic process; inflammation can vary with time
outcome reflects the balance between the nature, duration, and severity of the irritant and the effectiveness of the host defences
bacterial infection of the root canals is the major cause of clinically significant periodontitis
can follow acute traumatic injury to periapical tissues without pulp necrosis; usually transient

Key points - Mnemonic for differential diagnosis of pain of pulpal and periapical origin - LOCATE
Location
Other symptoms
Character
Associations
Timing
Evaluation of other investigations, e.g. pulp vitality tests
 

 Endodontic treatment

Mechanical instrumentation through the root apex during endodontic treatment, as well as chemical irritation from root-filling materials, may result in inflammation in the periapical periodontium. Instrumentation of an infected root canal may also be followed by periapical inflammation as a result of bacteria being forced inadvertently into the periapical tissues.

Acute periapical periodontitis

This is characterized by an acute inflammatory exudate in the periodontal ligament within the confined space between the root apex and the alveolar bone. Pain is elicited when external pressure is applied to the tooth because the pressure is transmitted through the fluid exudate to the sensory nerve endings. Even light touch may be sufficient to induce pain and, unlike pulpitis, this is generally well located by the patient to a particular tooth due to stimulation of proprioceptive nerve endings in the periodontal ligament. As the fluid is not compressible, the tooth feels elevated in its socket. Hot or cold stimulation of the tooth does not cause pain, as it would in pulpitis. The radiographic appearances are often normal as there is generally insufficient time for bone resorption to occur between the time of injury to the periodontal ligament and the onset of symptoms. If radiological changes are present, they consist of slight widening of the periodontal ligament and the lamina dura around the apex may be less well defined than normal.

The inflammation may be transient if it is due to acute trauma rather than infection and the condition soon resolves. If the irritant persists the inflammation becomes chronic and may be associated with resorption of the surrounding bone. Suppuration may occur if there is severe irritation and tissue necrosis associated with bacterial infection and the continued and massive exudation of neutrophil leucocytes leading to abscess formation. Such an abscess is called an acute periapical or alveolar abscess and, although such abscesses may develop directly from acute apical periodonitis, most arise because of acute exacerbation within a pre-existing periapical granuloma (see below and).

Periapical granuloma with central zone of suppurative inflammation

Chronic periapical periodontitis (periapical or apical granuloma)

Introduction

Persistent irritation, usually derived from bacteria and their products in the pulp chamber and root canals, leads to chronic periapical periodontitis. This is characterized by resorption of the periapical alveolar bone and its replacement by chronically inflamed granulation tissue to form a periapical granuloma. Around the periphery of the lesion the chronic inflammatory stimuli may lead to the formation of dense bundles of collagen fibres that separate the chronically inflamed granulation tissue from the surrounding bone. These collagen fibres, forming a sort of capsule around the lesion, are attached to the root surface and in some cases the granuloma may be removed attached to the extracted toot .

Histologically the lesion consists mainly of granulation tissue infiltrated by lymphocytes, plasma cells, and macrophages and, although the composition of the inflammatory infiltrate varies considerably, T-lymphocytes predominate. Immunological reactions, in response to persistent antigenic stimulation derived from the pulp chamber and root canals, are key factors in the development of the lesion. In addition to the inflammatory infiltrate, deposits of cholesterol and haemosiderin are often present in a periapical granuloma and both are probably derived from the breakdown of extravasated red blood cells. Cholesterol crystals in the granulation tissue are represented in routine histological sections as empty needle-like spaces or clefts, the crystals having dissolved out in the reagents used in section preparation. Multinucleate foreign-body giant cells are grouped around the cholesterol clefts. Foci of lipid-laden macrophages - foam cells - may also be seen . Epithelial cell rests of Malassez incorporated within the granuloma may begin to proliferate, probably as a result of stimulation by growth factors released by a variety of cells within the granuloma. The proliferated squamous epithelium forms anastomosing cords, often arranged in loops or arcades, throughout the granulation tissue. Neutrophil leucocytes in varying stages of degeneration are often seen infiltrating the oedematous intercellular spaces of the epithelium.

Periapical granulomas tend to be asymptomatic, but may be associated with occasional tenderness of the tooth to palpation and percussion. Percussion may produce a dull note because of the lack of resonance caused by the granulation tissue around the apex. Radiological examination at first shows a widening of the periodonal ligament space around the apex and later a definite periapical radiolucency may develop. In some instances this radiolucency is well circumscribed and clearly demarcated from the surrounding bone by a corticated margin, while in others the border is poorly defined. These appearances are related to differences in cellular activity around the margins of the lesion. Where there is active bone resorption and expansion of the lesion the margin is ill-defined. Where the lesion is static and a balance is established between the level of irritation and the host defences, the chronic inflammatory stimulus may lead to bone apposition and the formation of a zone of sclerosis around the lesion (see osteosclerosis (point 5) below). Histological evidence of external resorption of the apical cementum and dentine is frequent and is occasionally sufficient to be detected radiographically.

The importance of the root canal as a continued source of infection and antigenic challenge in an apical granuloma is shown by the fact that most periapical lesions heal once the canal is sealed by satisfactory endodontic treatment. The predominant organisms are obligate anaerobes (70 per cent or more) with smaller numbers of facultative anaerobes. Microorganisms surviving in the root canals or dentinal tubules after endodontic treatment may be important in teeth with persistent apical radiolucencies.

	Periapical granuloma attached to extracted root. 0
	Histological section of root and attached periapical granuloma from.Note the more heavily inflamed central area of the periapical granuloma (blue/purple stained), compared to the less inflamed, more collagenous peripheral zone.   0

	Cholesterol clefts with associated foreign-body giant cells   0
	0

	Periapical granuloma containing proliferating strands of squamous epithelium. 0
	Periapical radiolucency and apical resorption associated with a periapical granuloma. 0

Sequelae

1. If the level of antigenic challenge is in equilibrium with the host's immunological response, the granuloma can remain quiescent for long periods. However, if the equilibrium is disturbed in favour of the microbial flora in the root canal, the granuloma will continue to enlarge and be associated with continued resorption of bone, the process being symptomless, until equilibrium is restored.

2. When organisms invade the granuloma from the root canal acute exacerbation is likely and the patient may present with acute symptoms. Acute exacerbation can cause rapid enlargement of the lesion and may progress to abscess formation (see below). Alternatively, the inflammatory response may overcome the infection and a new equilibrium can be established.

3. Suppuration may occur in the granuloma. This may continue to enlarge to form an acute periapical (alveolar) abscess. Clinically this may present with rapid onset of pain, followed by redness and swelling of the adjacent soft tissues as the abscess tracks and points. The affected tooth is tender to percussion, and there may be slight mobility on palpation. Alternatively, the area of suppuration may be contained by the host's defences to form a chronic abscess that shows little tendency to enlarge or spread and which causes few, if any, clinical signs or symptoms until a further acute exacerbation.

4. Proliferation of the epithelial cell rests of Malassez associated with the inflammation may lead to the development of an inflammatory radicular cyst.

5. Low-grade irritation to the apical tissues may result in bone apposition (osteosclerosis) rather than resorption, histologically a mild chronic inflammatory infiltrate being seen in the rather scanty, fibrous marrow. The process is clinically asymptomatic and shows as an opaque area of bone on radiographs. On occasions, the opacity is well circumscribed while on others it shows no clear line of demarcation from the normal surrounding bone.

6. Low-grade irritation to the apical tissues may also result in the apposition of cementum on the adjacent root surface to produce hypercementosis.

Key points - Periapical granuloma
chronically inflamed granulation tissue around apex of a non-vital tooth
infection and antigenic challenge from endodontic flora
apical radiolucency; margins reflect dynamics of the lesion
host response may be in equilibrium with level of irritation
may be symptomless and remain quiescent for long periods
stimulation and proliferation of rests of Malassez within the lesion

Osteosclerosis around the roots of a mandibular molar.

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Information on Dry mouth (Xerostomia)

 Causes of Dry Mouth: 

• Certain prescription drugs
• Certain over-the-counter medications
• Tobacco
• Mouth breathing
• Anxiety
• Depression
• Alcohol
• Caffeine
• Spicy or salty foods
• Breathing unusually dry, cold, dusty, or dirty air
• Stress
• Vitamin deficiencies
• Simply not drinking enough water
• Radiation and chemotherapy
• Arthritis
• Diabetes
• Menopause
• Sjogren's Syndrome
• Lupus
• Parkinson’s disease
  
  
  

What drugs and medications can cause dry mouth? 

• High blood pressure medicines
• Antidepressants
• Tranquilizers
• Antihistamines
• Anti-Parkinson agents
• Antipsychotics
• Decongestants
• Narcotic pain relievers
• Chemotherapy
• Antidiarrheals
• Bronchodilators

What problems may develop because of dry mouth

• Rapid development of tooth decay
• Sore tissues
• Worsening periodontal disease
• Sore spots and ulcers under dentures
• Difficulty wearing dentures
• Mouth sores in non-denture wearers
• Breath doesn’t feel as fresh
• Difficulty chewing and swallowing  normal foods
• Difficulty tasting normal foods
• Difficulty speaking
• Burning sensation in the mouth
• Dry or painful tongue

How can I avoid destruction from rapid tooth decay?

• Avoid hidden sugars, such as cough drops, lemon drops, hard candy, breath mints, chewing gum, soda pop, etc.  People with dry mouths can get literally dozens of cavities in a matter of a few months.
• Use a prescription fluoride preparation.  These get more fluoride to the teeth than regular fluoride toothpaste.  They are available as a mouthrinse, brush-on gel, or a gel applied in a custom-made mouth tray.  Ask your dentist for prescriptions, or construction of a custom fluoride tray.  Prevident and Gel-Kam are examples.
• Maintain superior oral hygiene habits:  brush at least twice a day for two minutes per brushing, floss every day, and have your teeth cleaned/checked twice a year.

What will help relieve my dry mouth?

• Increase water intake throughout the day, and take frequent small sips
• Add moisture to the air with a humidifier.
• Protect lips with a balm.
• In cold weather keep mouth and nose covered with a scarf when outdoors.
• Don’t use tobacco or alcohol.
• Avoid strong toothpastes.
• Avoid mouthwashes containing alcohol.
• Use only toothpastes and mouthwashes that don’t contain sodium laurel sulfate.
• Avoid spicy and salty foods, and products containing cinnamon, peppermint, or wintergreen.
• Take a daily multi-vitamin.
• Use oral products that contains Xylitol.
• Be sure your doctors and pharmacist are aware of all the medications you are taking.
• Ask your doctor if your medications can be adjusted or changed.
• Use a saliva substitute or mouth moisturizers.
• Use sugarless hard candies to stimulate saliva flow.

What products  are available?

Mouthwashes

Oasis

BetaCell Oral Rinse

Biotene Mouthwash

TheraBrite Oral Rinse

Tom’s of Maine Natural Mouthwash, Oral Moistening

Sprays

Moi-Stir Mouth Moistener spray (carboxymethylcellulose)

Mouth Kote mouth spray

Salivart Oral Moisturizer spray (carboxymethylcellulose)

Stoppers 4 Dry Mouth Spray (glycerin)

Thayers Dry Mouth Spray (glycerin)

                Toothpastes

Biotene Dry Mouth Toothpaste

Rembrandt Toothpaste for Canker Sore Sufferers

TheraBreath Oxygenating Toothpaste

Tom’s of Maine Natural Anticavity & Dry Mouth Toothpaste

                Gums, 

                                Mints

Biotene Dry Mouth Gum

XyliChew mints

                Gels

Orajel Dry Mouth Moisturizing Gel

Oral Balance Mouth Moisturizing Gel, by Biotene

Saliva Substitute, by Roxane

Spry Dry Mouth Tooth Gel

                Other

Biotene Dry Mouth Denture Grip

Moi-Stir Oral Swabsticks (carboxymethylcellulose)

Salagen Tablets, 5mg (pilocarpine HCl); by prescription only

Where can I find these products?

• Stores carry a variety of products, but there is no one store that has them all.  Keep trying different stores.
• The pharmacist can help you locate some of these products.