Periodontitis

10.1055/b-0034-56506

Periodontitis

Periodontitis maintains its position as one of the most widespread diseases of mankind, but fortunately only ca. 5–10% of all cases are aggressive, rapidly-progressing forms (Ahrens & Bublitz 1987, Miller et al. 1987, Miyazaki et al. 1991, Brown & Löe 1993, Papapanou 1996).

Periodontitis is a multifactorial disease of the tooth-supporting structures, elicited by a microbial biofilm (dental plaque). It usually develops from a pre-existing gingivitis; however, not every case of gingivitis develops into periodontitis. The quantity and virulence of microorganisms on the one hand, and host resistance factors (immune status, genetics and therefore heredity, as well as the presence of risk factors) on the other hand are the primary determinants for the initiation and progression of periodontal destruction (p.21).

The classification of periodontitis evolves from dynamic, pathobiologic criteria, as recommended by the AAP (Armitage 1999; more extensive listing on p. 78; complete classification on p.327):

  • Chronic Periodontitis    (Type II, formerly AP)

  • Aggressive Periodontitis   (Type III, formerly EOP/RPP)

  • Necrotizing Periodontitis  (Type V B/NUP, formerly ANUP)

The two main forms (Types II and III) are further subclassified according to their expansion into localized (A: ≤. 30% of all sites involved) or generalized (B: > 30% of all sites involved).

Similarly, the degree of severity—as determined by clinical attachment loss—is divided into mild (1–2 mm), moderate (3—4 mm) and severe (≥ 5 mm).

An entire group of periodontal diseases comprise the aggressive forms (Type III), which were previously referred to as PP (prepubertal periodontitis), LJP (localized juvenile periodontitis), and RPP (rapidly progressive periodontitis).

The pathobiologic nomenclature, i.e., the description of the clinical course of periodontitis, is presented on pages 98 and 99. One must, of course, keep in mind that a “practical” diagnosis for every patient, for every tooth, and for every site must be performed clinically and radiographically to assess the severity, i.e., the pathomorphology of the disease process.

In this chapter, the following aspects of periodontitis will be presented:

  • Severity of periodontitis

  • Types of pockets

  • Morphology of bone loss

  • Furcation invasion

  • Histopathology

  • Clinical and radiographic symptoms

  • Clinical cases depicting the various forms of periodontitis

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.

188 Characteristics of Type II—formerly AP
189 Characteristics of Type III B—formerly EOP/RPP
190 Forms of Periodontitis 1 Chronic, slowly progressive periodontitis in adults—Type II 2 Aggressive, rapidly progressing periodontitis—Type III B 3 Aggressive, localized (juvenile) periodontitis—Type III A 4 Aggressive, generalized, prepubertal, rapidly progressing periodontitis—Type IV B

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:

  • A localized form begins at ca. age 4 and exhibits only mild gingival inflammation with relatively little plaque.

  • The generalized form (Type IV B) begins immediately after eruption of the deciduous teeth. It is associated with severe gingivitis and gingival shrinkage. The microbiology remains unclear.

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.

191 Characteristics of Type III A (formerly EOP/LJP)
192 Characteristics of Type IV B (formerly EOP/PP)

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

• mild/slight

levis

superficialis

• moderate

media

media

• severe/advanced

gravis

profunda

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).

193 Types of Periodontal Pockets A Normal Sulcus The apical termination of the junctional epithelium (JE) is at the cementoenamel junction (open arrow). B Suprabony Pocket (red) Attachment loss; proliferation of pocket epithelium. A remnant of junctional epithelium (pink) persists at the base of the pocket. C Infrabony Pocket Bony pocket
194 Types of Bone Loss No Attachment Loss (left) Normal alveolar septa. Lamina dura and alveolar crest remain intact. Horizontal Bone Loss (middle) Up to 50% loss of interdental septal bone. Vertical Bone Loss, Furcation Involvement (right) Severe bone loss distal to the first molar. The furcation of this tooth is also involved.
195 “Range” of Destruction = Contour of Bone Resorption The destructive process radiating from the plaque measures ca. 1.5–2.5 mm (red circle). The expanse (width) of the interdental septa therefore determines for the most part the type (morphology) of bone loss. A Narrow: horizontal resorption B Average: horizontal resorption, incipient vertical resorption C Wide: vertical resorption, bony pocket

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.

196 Schematic Representation of Pocket Morphology A Three-Wall bony defect B Two-Wall bony defect C One-Wall bony defect D Combined bony defect, crater-like resorption (“cup”) The walls of each pocket are shown in red (1–3).
197 Small Three-Wall Defect Early pocket formation on the mesial aspect of the second premolar. The color-coded probe (CP12) measures a depth of ca. 3 mm. If gingiva were present, the total probing depth would be ca. 5 mm.
198 Deep Three-Wall Bony Pocket The periodontal probe descends almost 6 mm (measured from the alveolar crest) to the base of this three-wall defect.

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.

199 Two-Wall Bony Pocket, Interdental Crater The coronal portion of this defect is bordered by only two bony walls (and two tooth surfaces). In the apical areas the two-wall defect becomes a three-wall defect (see left probe tip in the radiograph, left).
200 One-Wall Bony Pocket on the Mesial of Tooth 45 Advanced bone loss in premolar/molar area. On tooth 45, the facial wall of bone is reduced almost to the level of the mesial pocket (*). A portion of the lingual plate of bone remains intact. The facial root surface and the interdental spaces could be covered with soft tissue to the cementoenamel junction, masking the defect clinically.
201 Combined Pocket, Cup-shaped Defect In the region of tooth 45, the apical portion of the osseous defect courses around the tooth, creating a “moat” or “cup” (Goldman probe in situ). The bony pocket is therefore bordered by several osseous and several tooth surface walls.
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Jul 2, 2020 | Posted by in Dental Hygiene | Comments Off on Periodontitis
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