SOFT TISSUE CALCIFICATIONS IN ORO-MAXILLO FACIAL REGION-with Radiographs

Pathologic calcification of soft tissues occurs when calcium and other mineral salts are deposited in a tissue or in a passage. There are three types of pathologic calcifications: 1) Dystrophic calcification is that which occurs in degenerating and dead tissues. Calcificationof the larval stage of tapeworm (cysticercus) is an example of dystrophic calcification. 2)Metastatic calcification is that in which calcium (and other) salts are deposited in previouslyundamaged tissue as a result of an excess of salts in the circulating blood.Hyperparathyroidism is an example of metastatic calcification which occurs in kidneys andblood vessels. 3) Calcinosis is calcification that occurs in or under the skin. Scleroderma,myositis ossificans, and multiple miliary osteomas are examples of calcinosis.

SIALOLITH

A sialolith is a stone (salivary calculus) within a salivary gland or duct. The formation of a sialolith is called sialolithiasis and occurs as a result of precipitation of calcium andphosphate salts around a nidus of mucous or bacterial debris. Sialoliths occur as single or multiple stones and can cause swelling and pain. The pain is experienced during salivary stimulation and is intensified at mealtimes. The accumulation of saliva in the gland produces swelling and the gland becomes enlarged and firm. The pain is produced as a result of the buildup of pressure due to the accumulation of saliva behind the stone. The pain gradually subsides and the swelling diminishes because the stone usually does not completely block the flow of saliva. If a sialolith is small or does not obstruct the flow of saliva, there may be an absence of pain and swelling. Most stones are found in the submandibular duct (Wharton's) and gland than in the parotid duct (Stensen's) and gland because of the viscous consistency and mineral content of the saliva from the submandibular gland and the long, irregular length of the Wharton's duct.

The best radiographic projection for visualizing sialoliths in the submandibular duct and gland is the standard mandibular occlusal view. Occasionally, sialoliths are seen incidentally on periapical radiographs, in which case they may be misdiagnosed as osteosclerosis. To differentiate a sialolith from an osteosclerosis, use the Clark's rule of tube-shift technique to localize objects, that is, to find the bucco-lingual relationship. Stones in the parotid duct and gland are best demonstrated by placing a periapical film in the buccal vestibule and x-radiating them with a reduced exposure time. Approximately 20% to 40% of all sialoliths are radiolucent. When this is suspected, sialography (injection of a radiopaque dye into the ductal opening and then x-radiating them) must be undertaken to visualize the stones. The duct or gland injected with the radiopaque dye shows the radiolucent sialolith as a non-filling defect. A sialolith must be differentiated from other soft tissue calcifications, especially from a calcified lymph node. The latter is usually asymptomatic and sialography may be required to distinguish the two lesions.

Fig 11-1 Mandibular occlusal projection shows a sialolith (salivary calculus) in the duct of the submandibular gland (Wharton's duct). The patient has a history of pain and swelling in the salivary gland which is intensified at mealtime when saliva flow is stimulated. The pain gradually subsides and swelling diminishes because the stone usually does not completely block the flow of saliva.

Fig. 11-2 On periapical radiographs, the radiopacity may be misdiagnosed as osteosclerosis. To differentiate an osteosclerosis from a sialolith, take two radiographs using different vertical (or horizontal) angulations of the x-ray beam. If the radiopacity changes its position in relation to the adjoining teeth, as shown here, the radiopacity is a sialolith in the floor of the oral cavity (Clark's rule: same lingual, opposite buccal). Another method to identify a submandibular sialolith is to take an occlusal projection.

Fig. 11-3 A sialolith on a panoramic radiograph may be misdiagnosed as a calcified lymph node. In the absence of clinical signs and symptoms it is difficult to differentiate the two types of calcifications unless a sialogram is made.

Fig. 11-4 Sialogram showing an obstruction in the Wharton's duct preventing the flow of the radiopaque dye into the submandibular salivary gland. The stone (arrow) is blended with the radiopaque dye.

CALCIFIED LYMPH NODE

A calcified lymph node is indicative of a prior chronic infection involving the node. A history of successfully treated tuberculosis is often associated with this calcification. The condition is asymptomatic. It may involve a single node or a chain of submandibular or cervical nodes. The calcified superficial lymph nodes are palpable as bony, hard, round or linear masses with variable mobility. They are often observed on a panoramic radiograph, where they may appear below the inferior border of the mandible and near the angle of the mandible. Calcified lymph nodes are often found incidentally on radiographic examinationsSome may be radiographically projected over the mandibular bone and may be misdiagnosed as osseous lesions.

A calcified submandibular lymph node may be difficult to distinguish from a sialolith. The former is invariably asymptomatic whereas the latter is frequently accompanied by pain and swelling at mealtimes. Sialography may be required to distinguish the two lesions.

Fig. 11-5 Calcified lymph nodes located inferior to the angle of the mandible. Priorchronic infection of the lymph nodes may result in calcification of the nodes. A history of successfully treated tuberculosis is often associated with this calcification. This asymptomatic condition may involve a single node or a chain of nodes.

Fig. 11-6 A lateral cervical radiograph shows a chain of calcified lymph nodes.

PHLEBOLITH

Phleboliths are calcified thrombi that occur in veins or sinusoidal vessels of hemangiomas involving the soft tissues adjacent to the jaws. On a radiograph they appear as round or oval bodies which may exhibit concentric calcific rings similar to the cross section of an onion. Phleboliths may occur singly or as multiple calcifications. On periapical radiographs, calcifications may be superimposed on the mandible and thus misdiagnosed as osseous lesions within the jaw or as sialoliths.

Fig. 11-7 Multiple phleboliths superimposed on the mandibular ramus. Phleboliths are calcified thrombi. These calcified masses in blood vessels are associated with hemangiomas found in the cheek.

Fig. 11-8 Multiple phleboliths of various sizes in cavernous hemangioma of the face. The radiograph is of the patient's cheek.

CALCIFICATION OF ARTERIES

Calcification of the walls of arteries occurs in arteriosclerosis and in secondary inflammatory conditions involving arteries. The calcium salts are deposited within the medial coat of the vessels. Calcification can occur in a number of arteries of the body (iliac, femoral, abdominal aorta, etc.), however, in the facial region the facial artery is the one that is often involved. Calcified arteries of the cheek and oral cavity may appear as faint images on periapical radiographs. In the Sturge-Weber syndrome (capillary hemangiomas of the face, oral mucosa, and cranium), the cranial hemangiomas often show marked calcification of the blood vessels.

Fig. 11-9 Calcification of the facial artery. It may occur in arteriosclerosis and represents an inflammatory process.

Fig. 11-10 Calcification of the facial artery. The radiopacity of the artery is the result of deposition of calcium salts within the medial coat of the vessel.

ANTROLITH

A calcified mass in the maxillary sinus is called an antrolith. It is produced by calcification of a nidus which may be a bone chip, root fragment, foreign object, or stagnant mucus in sites of previous inflammation. Most of the antroliths are asymptomatic and are detected incidentally on radiographic examinations. However, on rare occasions when an antrolith continues to grow and become very large, it may be associated with sinusitis. Antroliths must be differentiated from root fragments in the maxillary sinus. A root fragment will show the root anatomy such as the presence of a pulp canal in a cone-shaped (root-shaped) radiopacity. When calcification comparable to an antrolith occurs in the nasal fossa, it is called a rhinolith.

Fig. 11-11 Calcified mass in the maxillary sinus is called an antrolith. A foreign object, bone chip, root fragment or stagnant mucus acts as a nidus for calcific deposits. It is usually asymptomatic.

Fig. 11-12 Antrolith (stone in maxillary sinus) on the floor of the sinus. It is asymptomatic.

MULTIPLE MILLIARY OSTEOMAS OF SKIN

(Osteoma cutis, calcinosis cutis)

Multiple milliary osteomas of skin, also known as calcinosis cutis, are situated in the cutis and subcutis. Some of these calcifications are associated with acne or some other form of dermatosis. They are found incidentally on radiographic examinations. They appear as doughnut-shaped radiopacities with radiolucent centers which represent the central marrow cavities. Multiple miliary osteomas are imaged better by placing a dental film in the vestibules and against the inside surface of the cheek and using a reduced exposure time.

Fig. 11-13 Multiple miliary osteomas of skin are soft tissue calcifications of skin. Some are reported to be associated with acne or some other form of dermatosis.

Fig. 11-14 Calcinosis cutis showing doughnut-shaped radiopacities.

CALCIFIED STYLOHYOID LIGAMENT AND EAGLE'S SYNDROME

Calcification of the stylohyoid ligament may sometimes be found incidentally on a panoramic radiograph and located posterior to the ramus of the mandible. It may occur unilaterally or bilaterally. In about 50% of the cases, the individuals are asymptomatic. In those cases associated with pain and discomfort, the entity is called "Eagle's syndrome".

The syndrome includes vague pain on mandibular movements such as swallowing (dysphagia), turning the head or opening the mouth, sensation of foreign body in throat, and constant dull ache in the throat. Other symptoms include headache, earache (otalgia), dizziness, pain in temporomandibular joint area and also in the base of the tongue or transient syncope. The symptoms are probably caused by the elongated styloid process impinging on the glossopharyngeal nerve. When the jaws are closed, the pain subsides in some of the cases. It is important for the dentist to be aware that pain associated with calcified stylohyoid ligament may simulate pain associated with that of the temporomandibular joint.

On a radiograph, the calcified stylohyoid ligament appears as a thin, long, tapering radiopaque process extending downwards from the styloid process. Sometimes it may extend up to the lesser horn of the hyoid bone. The farther the mineralized ligament extends towards the hyoid bone, the more likely it is that it will be interrupted by radiolucent joint like junctions. Surgical resection is required in patients exhibiting symptoms.

Fig. 11-15A Patient with Eagle’s syndrome. The stylohyoid ligaments are bilaterally calcified. Patient complained of constant dull ache in the throat, pain on turning the head, and pain in the vicinity of the temporomandibular joints.

Fig. 11-15B Calcified stylohyoid ligament. Sometimes, this calcification may be associated with Eagle's syndrome. The syndrome produces cervical pain on turning the head, upon swallowing and on opening the mouth. The patient may have headaches, and dizziness.

Fig. 11-16 Calcified stylohyoid ligament in an asymptomatic patient.

Fig. 11-17 Bilateral calcified stylohyoid ligament in a case associated with Eagle's syndrome.

CALCIFIED THYROID CARTILAGE

Calcification of the thyroid cartilage is normal and increases with age. The thyroid and cricoid cartilages have been found to undergo a greater frequency of calcification in the female population, but a higher degree of ossification has been noted in male subjects. (In the hyaline cartilages of the larynx, calcification does not always precede ossification and there is little correlation between the two).

Fig. 11-18 Calcification of the thyroid cartilage. It is asymptomatic.

MYOSITIS OSSIFICANS

In myositis ossificans, bony structures such as lamellae, lacunae and marrow are deposited in soft tissue. The cause of this ossification in muscles, ligaments, tendons and fascia is unknown. It may be caused by trauma or heavy muscular strain that occurs in certain

occupations and sports. During the healing process, the blood in the traumatized region gets organized and later calcified. The calcification takes place in the connective tissues around the muscles. The digastric, masseter, temporal and sternomastoid are usually involved. The patient finds it difficult to open the jaws when the muscles of mastication are involved. The characteristic radiographic appearance is that of strand-like calcifications along the long axis of the muscle fibers.

CYSTICERCOSIS

Cysticercosis is a helminthic (parasitic worms) disease which completes the larval phase of its life cycle in the pig. When an individual ingests eggs of the (pork) tapeworms from contaminated water or food, the larval form of the tapeworms are hatched in the gastrointestinal tract, and enter the vascular and lymphatic systems. They are then deposited in various tissues and organs of the body. At this stage, there is no radiographic evidence of their presence. After their death, the larval spaces are filled with fibrous tissue which later becomes calcified. These calcifications in muscle and subcutaneous tissue are visible on a radiograph as multiple radiopaque ovoid or elliptical objects.

Fig. 11-19 Radiograph of patient with cysticercosis. The calcified encysted larvae are seen in the soft tissues at the back of the neck and a single one is seen in the area of Wharton’s duct.

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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