Apical periodontitis
Apical periodontitis is an inflammatory lesion in theperiodontal tissues that is caused mostly by bacterialelements derived from the infected root canal system of teeth (Core concept 7.1). Ion-treated teeth apical periodontitisrepresents a defensive response to a primaryinfection in a necrotic pulp. Apical periodontitis may alsodevelop due to a secondary infection subsequent toendodontic treatment procedures. Post-treatment apicalperiodontitis is most commonly due to either unsuccessfulcontrol of primary root canal infection by endodontictreatment measures, or infection or reinfection of theroot canal system due to inadequate obturation and/orinadequate coronal seal that allowed bacterial leakage totake place.
In advertent extrusion of certain medicamentsand root filling materials into the periapical tissue compartment may also cause tissue toxic effects as well as precipitate foreign body reactions. In this chapter the focus will be on apical periodontitis associated with non-endodontically treated teeth affected by root canal infection. It will be described in terms of biological function, pathogenesis and clinical as well as histologicalpresentation.
The nature of apical periodontitis
Apical periodontitis serves an important protective function, aimed at confining bacteria discharged from theroot canal space and preventing them from spreading into adjacent bone marrow spaces and other remotesites. The process is unique in the sense that it cannot eradicate the source of infection. The reason is that oncea pulp has become necrotic, defense mechanisms cannot operate far into the root canal owing to the lack of vascular support. Although these mechanisms can act at the apical margins of the necrotic tissue, they are unable to penetrate it in a fully developed tooth. Consequently,without proper endodontic treatment apical periodontitis may prevail chronically. Bone resorption is a most conspicuous feature of apical periodontitis and is an unavoidable side-effect of the defensive process. Some may view it as a “price” paid bythe host to provide the necessary, effective, immuneresponse to the root canal infection. Bone loss that appearsin radiographs serves as the main clinical indicator fothe presence of apical periodontitis , as many ofthese lesions are silent and prevail without overt clinical symptoms. Such lesions will be referred to in this textas asymptomatic apical periodontitis. Asymptomatic apical periodontitis is mostly biofilm derived. Yet,acute forms do occur and may develop during the expanding phase of the initial lesion. Lesions of symptomatic apical periodontitis may also emerge as a result of adisturbed equilibrium between the host defense and the bacterial infection in an already established lesion. Symptomatic apical periodontitis results mostly from theaction of planktonic bacteria. Hence, single lesions of apical periodontitis can be symptomatic or asymptomatic at different stages of their development and progress ion. By far, most cases of apical periodontitis are asymptomatic. Pain, tenderness to biting pressure, percussion orpalpation as well as swellings are typical clinical expressions of symptomatic apical periodontitis .The symptoms may vary from mild to severe. More dramatic clinical symptoms of apical periodontitis may appear and dominate when the local immune defense has failed to detain the infection resulting in an apical abscess. Although very rare, acute apical periodontitismay develop into a very serious and even life- threatening condition. Phlegmonous spread of the infection into theconnective tissue around the upper respiratory tract,orbit, neck or even to the brain is alarming. Infectiouselements released in conjunction with symptomaticapical periodontits may also be distributed via the bloodstream and cause heart valve and myocardial infections. Even though apical periodontitis may beassociated with such severe clinical manifestations, itneeds to be stressed that its basic function is to containroot canal bacteria and not allow their dissimenation todistant sites (Core concept 7.2). Identification of apicalperiodontitis is directly related to the resolution of ourexamination tools; many apical periodontitis lesions thaton CBCT (cone beam computed tomography) andmany more may be identified only upon histologicalexamination.On a microscopic level, different structural frameworksof apical periodontitis can be identified. Theseforms include apical granuloma, apical abscess and apicalcyst. These lesions will be described here in terms of theirgeneral histological features while their clinical presentationwill be detailed later in the chapter. Clinically andradiographically these histopathological entities cannotbe distinguished from each other or recognized, with theexception of abscesses with a sinus tract.Apical granuloma is the most common form of apicalperiodontitis and consists of an inflammatory lesiondominated by lymphocytes, macrophages and plasmacells (see also Key literature 7.1 and Advanced concept7.1) (Fig. 7.3). Numerous fibroblasts and connective tissuefibers are usually present with abundant capillaries. Atits periphery an encapsulation attempt may often befound but great structural heterogeneity is the norm forapical periodontitis (31, 34).Epithelial cell proliferation is a common finding in long standing apical granulomas and may occur in up to50% of the lesions . The epithelium is believed to originate from the epithelial cell rests of Mallasez. Under the influence of cytokines and growth factors released in the inflammatory process, the normallyresting cells divide and migrate. They may formmore or less continuous strands that seem to take a random course (Fig. 7.4). They may also become attached to the rootsurface
Apical abscess denotes the presence of pus within thelesion. Abscess formation may reflect a shift in cellulardynamics within a pre-existing apical granuloma or be adirect outcome of an acute primary infection. The influxof PMNs is now dramatically increased. Upon the intense phagocytic activity of these cells and upon their death, tissue-destructive elements (e.g. hydrolytic enzymes andreactive oxygen species) are released to the extent that macrophages are no longer able to keep up with clearing and repairing the cell and tissue damage induced. Connective tissue constituents such as collagen and hyaluronic acid are degraded and the tissue in the centerof the lesion is liquefied. In the periphery, granulomatous tissue may persist. Consequently, a continuum exists between apical abscesses and apical granulomas. While in some case sapical granulomas may contain only small numbers ofinfiltrating PMNs, other cases present with a massive influx of PMNs, leading to tissue liquefaction and pusformation.An apical cyst is an epithelium-lined cavity that contains fluid or semi-solid material and is commonly surrounded by dense connective tissue variably infiltrated by mononuclear leukocytes and PMNs.. The cyst cavity is most commonly lined with stratified squamous epithelium of varying thickness that originates from the epithelial rest cells of Malassez. Rarely, the lining may be ciliary epithelium originating from the adjacent maxillary sinus. The epithelial lining may be continuous, but may also be disrupted oreven completely missing in certain areas of the cavity. It should be noted that apical cysts may also become abscessed. In contrast to periapical granulomas, some apical cysts appear never to arrive at a steady state. They may slowly expand over time and eventually, if left untreated, may consume a considerable portion of the surrounding bone . Apical cysts are divided into pocket cysts (bay cyst) andtrue cysts. A pocket cyst is an apical inflammatory cyst that contains a sac-like, epitheliumlinedcavity that is open to and continuous with the rootcanal space.
True apical cysts, on the other hand, arelocated within the periapical granuloma with no apparentconnection between their cavity and that of the rootcanal space.The mechanism by which cysts are formed, grow andexpand is not well understood, but is most likely toinvolve inflammatory mediators that are present in thetissue lession.Given the presumed mechanisms of pathogenesis(Advanced concept 7.2), epithelial growth in some apicalcysts ceases when the stimulating factors are eliminated,for example after proper endodontic treatment.Subsequently the epithelium lining may become thinand even disappear and thus provide conditions forhealing.In some cases both the cyst capsule and the cyst cavitymay contain cholesterol, which forms oblong needle-likecrystals (Fig. 7.7). In tissue sections the crystals are notseen but appear as typical tissue clefts resulting from thedissolution of the cholesterol during histological tissueprocessing. The crystals are formed in the connectivetissue of the cyst capsule and are gradually movedtowards and into the cyst cavity. They attract multinucleargiant cells of the foreign body type and, thus, elicita foreign body response in the connective tissue (28). The crystals are thought to derive from disintegrating redblood cells in stagnant vessels of the lesion. Inflammatorycells and circulating plasma lipids are other proposedsources
Clinical manifestations and diagnostic terminology
Diagnostic terminology discussed here includes normalperiapical conditions, asymptomatic apical periodontitis (syn.;chronic apical/periradicular periodontitis), symptomaticapical periodontitis (syn.: acute apical/periradicular periodontitis),acute apical abscess (syn.: acute periradicularabscess), chronic apical abscess (syn.: chronic periradicularabscess, suppurative apical/periradicular periodontitis),cellulitis, condensing osteitis (syn.: focal sclerosing osteomyelitis,periradicular osteosclerosis, sclerosing osteitis,sclerotic bone). It needs be recognized that these entitiesreflect clinical conditions and may not directly define thehistopathological character of the lesion. Indeed thereis a rather limited potential, under clinical conditions, totell a granuloma from a cyst or even from an abscess.This applies in particular to asymptomatic lesionsincluding abscesses with no evident sinus tract.
Normal periapical conditions.
Recognition of “normality” is essential to estimatechanges that may occur with disease, as well as theirgradual disappearance with healing. It is thereforenecessary to recognize what is a normal healthy condition.A healthy tooth is comfortable to the patient, it isnot tender to percussion or occlusal pressure neither is itsensitive to palpation of the mucosa overlying the periapicalregion. There should furthermore be no sinustract, or swelling or complaint of painful symptoms.Pocket-probing should not be deep: while indicatingperiodontal disease, pocketing may also imply a sinustract from a chronic periapical abscess draining along theperiodontal ligament space. Normal periapical conditionsare also recognized in periapical radiographs byunbroken lamina dura and a distinct periodontal ligamentspace of normal width, comparable to adjacent andcontralateral teeth.
Asymptomatic apical periodontitis.
Asymptomatic apical periodontitis is a longstandingperiapical inflammatory process with radiographicallyvisible periapical bone resorption but with no clinicalsigns and symptoms. The designation of this diagnosticterm should only be done in association with a toothwith a non-vital pulp (untreated or treated). It needs berecognized that progressive pulpitis, e.g. in response to acarious exposure, can also manifest itself radiographicallyby loss of lamina dura, and a small periapical radiolucentarea. Such a periapical tissue response may emergebefore major breakdown of the pulp tissue.The development of asymptomatic apical periodontitismay go unnoticed by the patient and is often discoveredonly by routine radiographic examination. It may also besurmised from a carefully taken disease history in caseswhen patient has experienced a prior painful event.The radiological appearance may take a wide rangeof forms. This has tempted clinicians to search for acorrelation between size and morphology of the lesionwith its histological nature, but there are no diagnosticmeans currently available to distinguish a granulomafrom a cyst.Symptomatic apical periodontitisSymptomatic apical periodontitis may develop as a directc on sequence of the breakdown and infection of the pulpwithin a previously healthy periapical region. It then reflects a response to an initial exposure of the periapical periodontium to bacteria or their products emerging from the infected root canal. Symptomatic apical periodontitis may also appear in atooth with previous asymptomatic apical periodontitis. This may either reflect a natural shift in the balance previously established between the bacteria and the hostor occur in response to endodontic treatment (endodontic flare-up).The typical symptoms include pain of an aching nature that may become severe or even unbearable to the patientand which brings the patient to the dentist. The toothwill usually be tender to percussion, with the mucosaand bone overlying the apical area sensitive to palpation.The tooth may occlude prematurely, owing to occlusaldisplacement caused by the edema in the periapicalarea.
Acute apical abscess
An acute apical abscess is characterized by rapid onset, spontaneous pain, tenderness of the tooth to pressure,pus formation and eventual swelling of associated tissues. At the initial stages of its formation, the processmay be extremely painful, as pressure builds up in the restricted periapical bony crypt or periodontal space. The overlying cortical plate may eventually perforateand pus will accumulate under the periosteum producinga most severe painful condition. Only with the perforation of the periosteum will the pus be able to drain and allow pain to subside. At this stage, a tender local swelling will appear. In some cases, natural drainage will be established within a few days by perforation of thecovering tissue. In other cases, the swelling will remainfor some time before it gradually subsides. Drainage of an apical abscess will take the “path ofleast resistance” which is usually defined by the thicknessof overlying bone (Fig. 7.15). Following penetrationof the bone and periosteum, drainage will often be visiblein the oral cavity but it may also occur into perioraltissues or into the maxillary sinus.
Chronic apical abscess.
A sinus tract is the typical feature of the chronic apical abscess. The inflammatory process has perforated one ofthe cortical plates and a draining sinus tract is established which allows continuous discharge of pus forming in theperiapical lesion through an opening in the oral mucosa.In rare cases, a sinus tract may drain extraorally throughthe skin (Fig. 7.16). Typically, a stoma of a parulis can bedetected that, from time to time, will discard pus. A sinustract may establish exit with drainage into the gingivalsulcus, in a periodontal pocket (Fig. 7.17) or in a furcationarea and must be differentiated from periodontal diseaseand from a pocket associated with a vertical root fracture.A sinus tract may also lead into the maxillary sinus andcause unilateral chronic sinusitis.A chronic apical abscess is most commonly, but notalways, associated with an apical radiolucency. It isasymptomatic or only slightly symptomatic and thepatient may often be unaware of its presence. This maylast as long as the sinus tract is not obstructed. Evenwhen such an obstruction occurs, it is most likely thatany swelling will be of limited duration and will be limitedto the local area of the sinus tract, as both the boneand the periosteum are already perforated.
