Pathobiology—The Most Important Forms of Periodontitis

The pathobiological nomenclature for the various forms of periodontitis is not a rigid, definitive classification. Today, one differentiates between chronic and aggressive forms of the disease, which may be localized or generalized (pp. 327–330). The chronic form of the disease may transform into an aggressive form, e.g., in the elderly, where the immune system is less effective. Most types of periodontitis progress in a step-wise fashion (random burst theory). Stages of exacerbation alternate with stages of remission.

Type II (Chronic Periodontitis; formerly AP)

This most common form of periodontitis begins between the ages of 30 and 40 years, generally from a pre-existing gingivitis. The entire dentition may be equally affected (generalized, Type II B). More often, however, the distribution of the disease is irregular, with more severe destruction primarily in molar areas but secondarily also in anterior segments (localized; Type II A). The gingivae exhibit varying degrees of inflammation, with “shrinkage” in some areas and fibrotic manifestations elsewhere.

Exacerbations occur at rather lengthy intervals. Risk factors (e.g., heavy smoking, IL-1-positive genotype) can accentuate the clinical course. In the elderly, the disease can lead to tooth loss, which may also be due to a decrease in host immune response and more frequent acute stages.

Therapy: Chronic periodontitis can be successfully treated by means of purely mechanical therapy, even if the patient’s cooperation/compliance is not optimum.

As science continually provides new knowledge concerning microbiology as well as pathogenesis—especially the host response to the infection—the diagnosis and the nomenclature can no longer simply be defined according to the clinical course of the disease; it is now possible to characterize periodontitis as an Aa– or a Pg-associated disease (etc.). In the future, it may become even more important to characterize the diverse parameters of the host immune response, the mediators and the risk factors; these are ultimately responsible for the existence of the disease and the speed of its progression.

Type III B (Aggressive Periodontitis; formerly EOP/RPP)

Aggressive forms of periodontitis are relatively rare (Page et al. 1983a, Miyazaki et al. 1993, Lindhe et al. 1997, Armitage 1999). They are usually diagnosed between the ages of 20 and 30 years. Females appear to be more frequently affected than males. The severity and distribution of attachment loss vary considerably. One observes infrequent acute stages, which may transition into chronic disease. The cause of the active stages is specific microorganisms (Aa, Pg etc.), which may actually invade the ulcerated tissues. Risk factors (smoking, systemic disease such as diabetes, conditions of psychic tension and stress) and pro-inflammatory mediators that reduce the immune response can amplify the disease picture.

Therapy: The majority of aggressive cases can be successfully treated by means of purely mechanical therapy. In severe cases, a supportive systemic antibiotic regimen may be indicated.

Type III A (Aggressive Periodontitis, formerly EOP/LJP)

This rare disorder occurs early and attacks the permanent dentition. It begins in puberty, but is usually not diagnosed until several years later, often when lesions are discovered serendipitously (e.g., on bitewing radiographs taken for caries assessment). In the initial stages, incisors and/or first molars are affected in both maxilla and mandible; later, other teeth may also be affected. Hereditary factors (genetics, ethnic origin) have been demonstrated. Girls are affected more frequently than boys. In the early stages of aggressive periodontitis, one seldom observes pronounced gingivitis. The gingival pockets almost always (90%) harbor Aa. The patient’s serum contains immunoglobulins against Aa leukotoxins, which damage PMNs.

Therapy: With early diagnosis and therapy consisting of vigorous mechanical debridement and supportive systemic administration of medicaments, the destructive process can be halted rather easily. Osseous defects may eventually regenerate.

Type IV B (Aggressive Periodontitis; formerly EOP/PP)

This extraordinarily rare form of periodontitis may be detected even upon eruption of the deciduous teeth and is usually associated with genetic aberrations and systemic disorders (Page et al. 1983b, Tonetti & Mombelli 1999, Armitage 1999; cf. p.118). The disease progresses rapidly and is usually generalized:

Therapy: The localized form can be halted by a combination of mechanical therapy and systemic antibiotics. The generalized form appears to be refractory to therapy.

Pathomorphology—Clinical Degree of Severity

Periodontitis is a general term. As already described, it subsumes pathobiologically dynamic forms of disease progressing at varying rates, and exhibits differing microbial etiologies and varying influences by the host immune response (p.21). It may sound trite, but one must understand that all forms of periodontitis begin at some point in time. They develop at various times during a patient’s life, usually from a pre-existing plaque-elicited gingivitis. In the absence of treatment, the disease progresses, albeit at varying rates. It is therefore clear that during clinical data collection, which leads to the diagnosis for an individual case, not only must the type of disease be ascertained, it is also necessary to determine in what pathomorphologic stage the disease process currently exists or, in other words, how far attachment loss has progressed. From these diagnostic criteria, clinical course, expanse (localized, e.g., less than 30% of all sites, or generalized) and clinical degree of severity, the practitioner can derive a prognosis and estimate the degree of difficulty of the necessary treatment, which will naturally be higher for aggressive periodontitis (Type III) than for a similarly advanced chronic periodontitis (Type II).

Case Diagnosis—Single-Tooth Diagnosis—“Sites”

While it is usually possible to diagnosis the type of periodontitis for the entire dentition, it is rather a more difficult matter to precisely define the clinical degree of severity. Periodontitis almost always progresses at different rates in different areas of the mouth, on different teeth, and even at different sites on individual teeth. Therefore, any statement about “average” disease severity is usually meaningless.

The following pathomorphologic classification (degree of severity) cannot be understood as pertinent to the individual case (patient); it relates more to single tooth diagnosis as well as single tooth prognosis. The reasons for the often quite irregular localized destruction are not always clear (oral hygiene, plaque-retentive niches, localized specific bacteria, tooth type, function?). In addition to describing gingivitis, practitioners will continue to use the terms mild, moderate and severe to differentiate the stages of periodontitis. It is perhaps important to remember that different authors, “schools,” and periodontologic societies use various synonyms for these different clinical manifestations of disease.

Clinical Degrees of Severity

Most recently, the AAP (1996c) has defined the degree of severity of periodontitis not exclusively according to probing depths and terms such as mild, moderate or severe; rather, more consideration is given also to gingival inflammation, bone loss, attachment loss, furcation invasion and tooth mobility.

Conclusions

All of the pathomorphologic classifications of periodontitis presented on this page (cf. AAP Glossary 2001) attempt to describe the severity of the disease as it exists immediately after clinical examination; these descriptors say very little about the pathobiology, the dynamics or the speed of progression of periodontitis (prognosis).

Pockets and Loss of Attachment

Pocket formation without any loss of connective tissue attachment is seen in gingivitis in the form of the gingival pocket and the pseudopocket (p.79). A true periodontal pocket will exhibit attachment loss, apical migration of the junctional epithelium, and transformation of the junctional epithelium into a pocket epithelium (Müller-Glauser & Schroeder 1982). The true periodontal pocket may assume two forms (Papapanou & Tonetti 2000):

• Suprabony pockets, resulting from horizontal loss of bone

• Infrabony pockets, resulting from vertical, angular bone loss. In such cases the deepest portion of the pocket is located apical to the alveolar crest.

Whether pocket development is horizontal or vertical appears to be due to the thickness of the interdental septum or the facial and oral bony plates.

True loss of attachment results from microbial plaque and the metabolic products of plaque microorganisms. The range and effective radius of destruction is ca. 1.5–2.5 mm (Tal 1984; Fig. 195).

Intra-alveolar Defects, Infrabony Pockets

The infrabony pocket (infra-alveolar vertical bone loss) may exhibit various forms in relation to the affected teeth (Goldman & Cohen 1980, Papapanou & Tonetti 2000).

Classification of Bony Pockets

• Three-wall bony pockets are bordered by one tooth surface and three osseous surfaces

• Two-wall bony pockets (interdental craters) are bordered by two tooth surfaces and two osseous surfaces (one facial and one oral)

• One-wall bony pockets are bordered by two tooth surfaces, one osseous surface (facial or oral) and soft tissue

• Combined bony pockets (cup-shaped defects) may be bordered by several surfaces of a tooth and several of bone. The defect surrounds the tooth.

The causes for this wide variation in pocket morphology and resorption of bone are myriad and cannot always be wholly elucidated in each individual case.

Mention was already made of the significance of bone thickness (Fig. 195). Since the bony septa between the roots become thinner coronally, the initial stage of periodontitis generally presents as horizontal resorption. The greater the distance between the roots of two teeth, the thicker will be the intervening septum, and the development of a vertical defect is more likely.

In addition to such simple osseous morphology, other factors almost certainly play some role in the type of resorption:

• local acute exacerbation elicited by specific bacteria in the pocket

• local inadequate oral hygiene (plaque)

• crowding and tipping of teeth (plaque-retentive areas)

• tooth morphology (root irregularities, furcations)

• improper loading due to functional disturbances (?).

The morphology of the bony pocket is of importance in both prognosis and treatment planning (defect selection). The amount of bone remaining will affect the chances of osseous regeneration after treatment.