The general term “periodontal diseases” encompasses inflammatory as well as recessive alterations within the gingiva and the periodontium (Page & Schroeder 1982; AAP 1989, 1996; Ranney 1992, 1993; Lindhe et al. 1997; Armitage 1999).
While gingival recession may have various etiologies, including morphologic, mechanical (improper oral hygiene) and even functional (p. 155), gingivitis and periodontitis are plaque-associated diseases. Today it is becoming more and more clear that bacteria alone, including even the so-called periodontopathic bacteria, can always elicit gingivitis, but not periodontitis in every case. The initiation of periodontitis, its speed of progress and the expression of its clinical picture also involve the responsibility of negative host factors and additional so-called risk factors (Clark & Hirsch 1995). One of the most important are defects of the acute host response resulting from functional disturbances of polymorphonuclear granulocytes (PMN), other insufficient immunologic reactions, and the predominance of pro-inflammatory mediators, many of which are genetically determined. The now well established alterable risk factors include, particularly, “unhealthy” habits such as smoking, alcohol consumption and a less than well-rounded diet (p. 22).
Furthermore, systemic disorders and syndromes are usually un alterable, obligate or facultative risk factors for periodontitis. In this regard, especially Diabetes mellitus is viewed as prejudicial (p. 132). Finally, the entire social environment of an individual can play an important role for the initiation and propagation of periodontitis (pp. 22, 51).
All of the factors discussed in the chapter “Etiology and Pathogenesis” (p. 21) enhance the occurrence of all diseases, including periodontitis. Thus, periodontitis is considered to be of multifactorial etiology. It remains difficult in the face of a manifest disease process to differentiate the “etiologic weight” of bacteria on the one hand and the host response and risk factors on the other hand, or to differentiate between and among such etiologic factors. The contemporary, on-going search for responsible “risk markers” is therefore very important.
Today, clinicians can use additional clinical parameters such as bleeding on probing, the severity of the disease in relation to patient age, as well as microbiologic and genetic tests in order to establish some semblance of a proper diagnosis and prognosis (p. 165).
In the future, more precise research into the reduced host defense occasioned by immunologic defects, as well as the type and quantity of participating cytokines and inflammatory mediators (e. g., in sulcus fluid, blood or saliva) will simplify diagnosis and permit more definitive predictions about the probable course of the disease, as well as indicating more targeted therapy.
Most recent research results and clinical knowledge have led the nomenclature of the periodontal diseases into a state of constant change. Indeed, because of varying interpretations of scientific results, it has often led to conflict between authors and scientific societies.
Relatively recently, the new nomenclature from the American Academy of Periodontology (AAP, 1989) was generally accepted. This classification distinguished between gingivitis (G) and adult periodontitis (AP) of the following types: Early-onset periodontitis (EOP) with further subclassifications (PP, JP, RPP), periodontitis associated with systemic diseases (PSD), the acute necrotizing, ulcerative gingivoperiodontitis (ANUG/P), and the therapy-resistant, refractory periodontitis (RP).
After only a few years, however, this “new” classification was no longer satisfactory! The European Federation of Periodontology (EFP) proposed in 1993 a new classification, and even this was modified in 1999/2000 during an international workshop in collaboration with the AAP (Armitage 1999).
The “old” classification from 1989 was criticized because it placed too much weight upon the age of the patient vis-àvis the initiation of the disease process. For example “adult periodontitis” (AP) as a chronic disease could also be observed in adolescents; rapidly-progressing periodontitis (RPP) was observed not only in young individuals (EOP) but also could appear “suddenly” in older patients; the localized, juvenile form (LJP) was not observed only in young patients. Furthermore, “refractory periodontitis” (RP) cannot be viewed as a specific disease entity, because following treatment for periodontitis the disease might recur or the disease might simply not respond to the therapy.
This third edition of the Color Atlas of Periodontology consistently utilizes the most recent nomenclature (1999/2000), but several “old” and well-known terms are used for occasional clarification, e. g., LJP, which is now classified as “Type III, aggressive periodontitis A, localized.”
The table below is a brief summary of the new nomenclature to assist the dentist. The complete and extremely comprehensive “Classification of Periodontal Diseases and Conditions” can be found in the appendix (“Classifications,” p. 519). Some view the new classification as too expansive and comprehensive, while others criticize it as incomplete!
Classification of Periodontal Diseases (International Workshop of the AAP/EFP, 1999)
|Type I||Gingival Diseases
A Plaque-Induced Gingival Diseases
B Non-Plaque-Induced Gingival Lesions
|Type II||Chronic Periodontitis
|Type III||Aggressive Periodontitis
|Type IV||Periodontitis as a Manifestation of Systemic Disease A Associated with Hematological Disorders
B Associated with Genetic Disorders
C Not Otherwise Specified (NOS)
|Type V||Necrotizing Periodontal Disease
A Necrotizing Ulcerative Gingivitis (NUG)
B Necrotizing Ulcerative Periodontitis (NUP)
|Types VI-VIII||Further forms as well as transitions and “status pictures” of the diseases described, as well as the strengths and weaknesses of the new classifications are described in details (pp. 519–522) and in the original publications.|
Plaque-induced Gingivitis, Gingivitis Simplex, Type I A 1
Gingivitis is ubiquitous. It is a bacterially-elicited inflammation (non-specific mixed infection) of the marginal gingiva (Löe et al. 1965).
In the chapter “Etiology and Pathogenesis,” the development and progression of gingivitis from healthy tissue to an early lesion and on to established gingivitis was described (pp. 56–59; Page & Schroeder 1976, Kornman et al. 1997). In children, the early lesion (gingivitis) with T-cell dominance can persist for many years; on the other hand, in adults, the persistent lesion is almost exclusively established gingivitis (with plasma cell dominance), which can assume quite variable clinical severity. It is possible, clinically and pathomorphologically, to differentiate gingivitis into mild, moderate and severe, although this classification is relatively subjective.
For a more precise diagnosis of gingival inflammation, it is prudent to employ accepted indices that quantitate bleeding upon probing of the gingival sulcus.
The borderline between healthy gingiva and gingivitis is difficult to ascertain. Gingiva that appears to be clinically healthy will nevertheless almost always exhibit histologically a mild inflammatory infiltrate. If there is an increase in clinical and histologic inflammation, one observes lateral proliferation of the junctional epithelium. The JE becomes detached from the tooth at its marginal aspect, as the bacterial front progresses between the tooth surface and the epithelium. The result is a gingival pocket.
In cases of severe gingivitis with edematous swelling and hyperplasia of the tissues, a clinical pseudopocket often forms.
Gingival pockets and pseudopockets are not true periodontal pockets because no connective tissue attachment loss has occurred, nor has there been apical proliferation of the junctional epithelium. However, because the milieu of pseudopockets is an oxygen-poor environment, periodontopathic anaerobic microorganisms can thrive.
It is true that gingivitis may develop into periodontitis. However, even without treatment, gingivitis can persist over many years in a stationary manner, exhibiting only minor variations in intensity (Listgarten et al. 1985). With treatment, gingivitis is fully reversible.
The clinical and histopathologic pictures of established gingivitis are well correlated (Engelberger et al. 1983).
The mild infiltration that occurs even in clinically healthy gingiva may be explained as a host response to the small amount of plaque that is present even in a clean dentition. Such plaque is composed of non-pathogenic or mildly pathogenic microorganisms, primarily gram-positive cocci and rods.
As plaque accumulation increases, so does the severity of clinically detectable inflammation, as evidenced by the quantity and expanse of inflammatory infiltrate. The subepithelial infiltrate consists primarily of differentiated Blymphocytes (plasma cells), with a smaller number of other types of leukocytes.
With increasing inflammation, more and more PMN granulocytes transmigrate the junctional epithelium. As a consequence, the junctional epithelium takes on the characteristics of a pocket epithelium (p. 104, Fig. 209; Müller-Glauser & Schroeder 1982), but without any significant apical proliferation.
• Edematous and hyperplastic swelling
The earliest clinical symptom of an established lesion is bleeding subsequent to careful sulcus probing. This hemorrhage is elicited by the penetration of the probe tip through the disintegrating junctional epithelium and into the highly vascular sub-epithelial connective tissue. At this stage of the inflammatory process (PBI = 1), no gingival erythema may be visible clinically. Clinical symptoms of advanced (established) gingivitis include profuse bleeding after sulcus probing, obvious erythema and simultaneous edematous swelling. In the most severe cases, spontaneous bleeding and eventually ulceration may occur. The chronic types (and severities) do not elicit pain; pain occurs only in acute gingivitis (e. g., NUG, p. 85).
Even severe gingivitis may never progress to periodontitis. With proper treatment, gingivitis is reversible.
A 23-year-old female came to the dentist for a routine check-up. She had no complaints and was not aware of any gingival problems, although in her medical history she indicated that her gingiva bled occasionally during tooth brushing. Her oral hygiene was relatively good. She had received tooth brushing instructions from a dentist once, but no subsequent OHI. The patient was not on a regular recall schedule. Calculus removal had been performed sporadically in the past during routine dental check-ups, and several restorations placed.
|API||(Approximal Plaque Index): 30%|
|PBI||(Papilla Bleeding Index): 1.5|
|PD||(Probing depths): ca. 1.5 mm maxilla, ca. 3 mm mandible|
|TM||(tooth mobility): 0|
Diagnosis: Gingivitis in initial stage
Therapy: Motivation, OHI, plaque and calculus removal
Recall: Prophylaxis at 6-month intervals
Prognosis: Very good
A 28-year-old female presented with a chief complaint of gingival bleeding. She “brushes her teeth,” but had never received any oral hygiene instruction from a dentist or hygienist. Calculus had been removed only infrequently, and a professional debridement had never been systematically performed. Generalized crowding of the teeth in both arches is evident, combined with an anterior open bite. These anomalies reduced any self-cleansing effects and made oral hygiene difficult. This also likely increased the severity of gingivitis.
|API: 50%||PD: ca. 3 mm maxilla, ca. 4 mm mandible|
|PBI: maxilla 2.6, mandible 3.4. TM: 0 maxilla, 1 mandible|
Diagnosis: Maxilla, moderate gingivitis; mandibular anterior region, severe gingivitis with pseudopockets.
Therapy: Motivation, oral hygiene, plaque and calculus removal; after re-evaluation, possible gingivoplasty.
Recall: Every six months initially.
Prognosis: With patient cooperation and compliance, very good.
A 15-year-old male was referred for evaluation and treatment of suspected juvenile periodontitis (LJP/Type III A). The extremely pronounced gingivitis was, however, inconsistent with this diagnosis. Sulcus probing and radiographic examination revealed no attachment loss on anterior teeth or molars.
The patient practiced virtually no oral hygiene, stating that it was impossible to brush his teeth because the gingiva bled at the slightest touch. He had never received adequate motivation, nor any oral hygiene instruction, nor any treatment for his gingivitis.
|API: 88%||PD: pseudopockets to 5 mm|
|PBI: 3.5||TM: 0|
Diagnosis: Severe gingivitis with edematous hyperplastic enlargement of the facial aspect of the anterior area; mouth breathing as possible etiologic co-factor (?).
Therapy: Motivation, oral hygiene instruction, definitive debridement. After re-evaluation, possible gingivoplasty.
Recall: Initially every three months.
Prognosis: With patient cooperation and compliance, good.
NUG/P = Necrotizing Ulcerative Gingivitis/Periodontitis, Type V A (NUG) and V B (NUP)
Ulcerative gingivitis is usually an acute, painful, rapidly progressing inflammation of the gingiva, which may enter a sub-acute or chronic stage. Without treatment, this disease usually develops quickly into localized ulcerative periodontitis. It seldom occurs as a generalized process, nor is its severity always identical. It may be quite advanced in anterior segments, while the premolars or molars are not affected at all, or only mildly so. The reasons for this remain unknown (oral hygiene? ischemia? locally predominating pathogenic bacteria? plaque-retentive areas? tooth type?). Probing depths are usually shallow because gingival tissue is lost to necrosis as attachment loss proceeds. Secondary ulceration of other oral mucosal surfaces is rarely observed, and only in severe cases (AAP 1996e). Caution: Ulceration can represent an early oral symptom in HIV-positive patients and AIDS victims (p. 151).
Ulcerative gingivitis/periodontitis has become less common in recent decades than earlier (exception: HIV-positive and AIDS patients). In the younger population, the morbidity has been variously reported between 0.1–1 %.
The etiology of NUG is not completely understood. In addition to plaque and a previously existing gingivitis, the following local and systemic predisposing factors are suspected:
• Poor oral hygiene
• Predominance of spirochetes, fusiforms and P. intermedia, and occasionally Selenomonas and Porphyromonas in the plaque
• Smoking (local irritation by tar products)
• Poor general health, psychic stress, alcohol
• Smoking: nicotine as a sympatheticomimetic, and carbon monoxide (CO) as a chemotaxin (p. 216)
• Age (15–30 years)
• Season of the year (September/October and December/January; Skâch et al. 1970)
NUG/P patients usually exhibit similar life styles and habits: The teeth do not occupy a high position in the patient’s consciousness. They are usually young adults, heavy smokers (tobacco: high content of tar and nicotine), exercise poor oral hygiene, and become interested in treatment only during acute, painful exacerbations.
The clinical course is acute, but fever occurs only seldom. Within only a few days, interdental papillae may be lost to ulceration. The acute phase may gravitate into a chronic interval stage if host resistance improves (see pre-disposing factors) or through self-treatment (rinsing with a disinfectant mouthwash). Untreated ulcerative gingivitis exhibits a high recurrence rate, and may develop rapidly into ulcerative periodontitis (attachment loss with shallow pockets!).
Therapy: In addition to local debridement, the early stages of treatment should be supported with medicaments. Topical application of ointments containing cortisone or antibiotics, or metronidazol may be effective. In severe cases, systemic metronidazol (e. g., Flagyl) may be prescribed (see Medicaments, p. 287). After reduction of the acute symptoms in advanced cases, surgery to correct gingival contours may be indicated.
The clinical and histopathologic pictures in NUG are correlated. The histopathology of NUG is, however, significantly different from that of simple gingivitis.
As a consequence of the acute reaction, an enormous number of PMNs transmigrate the junctional epithelium in the direction of the sulcus and the col. In contrast to the situation in simple gingivitis, PMNs also migrate toward the oral epithelium and the tips of papillae, which undergo necrotic destruction. The ulcerated wound is covered by a clinically visible, whitish pseudomembrane that consists of bacteria, dead leukocytes and epithelial cells as well as fibrin. The tissue subjacent to the ulcerated areas is edematous, hyperemic and heavily infiltrated by PMNs. In long-standing disease, the deeper tissue regions will also contain lymphocytes and plasma cells. Within the infiltrated area, collagen destruction progress rapidly.
Spirochetes and other bacteria often penetrate into the damaged tissues (Listgarten 1965, Listgarten & Lewis 1967).
• Necrotic destruction of the gingiva, ulceration
• Specific bacteria
Beginning in the tissues of the interdental col, there is necrotic destruction of papilla tips, followed by destruction of entire papillae and even portions of the marginal gingiva. It is not clear whether gingival destruction is caused primarily by vascular infarction or by invasion of bacteria into the tissues. In rare instances, depressed ulcerations may also be seen on the cheeks, lips or tongue. In the absence of treatment, the osseous portion of the periodontal supporting apparatus can also become involved. The earliest clinical symptom of ulcerative gingivitis is localized pain.
The patient with NUG is characterized by a typical, insipid, sweetish halitosis.
Generalized ulcerative gingivitis must be differentiated from acute herpetic gingivostomatitis (p. 131), which is generally accompanied by fever.
A 19-year-old female experienced gingival pain and hemorrhage for three days.
|PBI:||Anterior segments, 3.2
Premolar and molar regions, 2.6
|PD:||2–3 mm proximal|
Diagnosis: Acute ulcerative gingivitis, early stage; NUG, Type V A.
Therapy: At the first appointment, careful mechanical debridement; topical medicaments: antibiotic or cortisone-containing ointment, metronidazol gel (e. g., Elyzol, p. 292). The patient may be instructed to rinse at home with mild hydrogen perborate solution.
Subsequent appointments: Motivation, repeated oral hygiene instruction, plaque and calculus removal.
Recall: Short-interval (information! plaque control).
Prognosis: With treatment and patient compliance, good.
Ulcerative periodontitis always develops—often very rapidly—from a preexisting ulcerative gingivitis. Probing depths may be shallow because the destruction of tissue occurs simultaneously with the attachment loss. While the clinical signs associated with NUG can be eliminated by proper treatment, ulcerative periodontitis (NUP) always leads to irreversible damage (attachment loss, bone loss). Acute and subacute phases occur cyclically. Acute phases are always accompanied by pain, in contrast to simple gingivitis. Ulcerative periodontitis is seldom generalized.
Therapy: Similar to the case with ulcerative gingivitis, in the acute phase of NUP careful and complete plaque and calculus removal should be performed. This mechanical therapy can be supported by topical medicaments. After the pain subsides, systematic instrumentation (debridement) follows. In advanced cases, minor surgical procedures may be necessary after all acute symptoms subside: In mild cases, gingivoplasty; in advanced cases, contouring flap surgery. A strict recall program is absolutely necessary, because NUP has a tendency toward recurrence.
A 26-year-old male (see also Fig. 172) who was systemically healthy, presented complaining of severe pain and “inflamed gingiva.” A similar inflammation had occurred one year previously, but it resolved after the use of mouthwashes, without treatment by a dentist. The patient smoked ca. 40 cigarettes per day.
|API: 80%||PBI: 3.2|
|PD: 3–5 mm||TM: 0–1|
|Second acute phase (one year later)|
Diagnosis: Generalized, acute ulcerative gingivoperiodontitis.
Therapy: In acute stages, careful supragingival cleaning, chlorhexidine rinses; “slow release” medicaments (e. g., metronidazol: Elyzol gel) may be used if pockets are present. After the acute symptoms subside, systematic supra- and subgingival plaque and calculus removal. Surgical intervention (gingivoplasty) was indicated in this case, but was not performed.
Recall: Not desired by the patient.
Prognosis: Questionable; patient non-compliance.
Types I A 2 a
Changes in the body’s hormonal balance generally do not cause gingival inflammation, but can increase the severity of an already existing plaque-induced gingivitis. In addition to insulin deficiency (Diabetes mellitus; pp. 132, 215), it is primarily the female sex hormones that often are associated with the progression of plaque-elicited gingivitis:
• Puberty gingivitis
• Pregnancy gingivitis
• Gingivitis from the “Pill” (rare)
• Gingivitis menstrualis and intermenstrualis
• Gingivitis climacterica
Epidemiologic studies have demonstrated that gingival inflammation during puberty is somewhat more pronounced when compared to the years preceding and following puberty (Curilovi ć et al. 1997, Koivuniemi et al. 1980, Stamm 1986). If oral hygiene is poor and/or if the adolescent is a mouth breather, a typical gingival hyperplasia may ensue, especially in the maxillary anterior area (Figs. 178 and 179). Therapy: Oral hygiene instruction, plaque and calculus removal; gingivoplasty if the hyperplasia is severe. Mouth breathing may require consultation with an appropriate medical specialist (ENT).
This condition is not observed in every pregnant woman. Even if oral hygiene is good, however, the gingivae will exhibit an elevated tendency to bleed (Silness & Löe 1964). Therapy: Oral hygiene; recall every one to two months until breast-feeding is discontinued.
Gingival reaction to oral contraceptives is rare today (Pankhurst et al. 1981). Symptoms: Slight bleeding, rarely erythema or swelling.
Therapy: Oral hygiene.
This gingival condition is exceedingly rare. Desquamation of gingival epithelium occurs during the twenty-eight day menstrual cycle, similar to vaginal epithelium. In exceptional cases, the desquamation can be so pronounced that a diagnosis of “discreet” gingivitis may be made, even less frequently gingivitis menstrualis or intermenstrualis (Mühle-mann 1952).
Therapy: Good oral hygiene to prevent secondary plaque-associated gingivitis.
This alteration of the mucosa is also rare. The pathologic alterations are observed less on the marginal gingiva than on the attached gingiva and oral mucosa, which may appear dry and smooth, with salmon-pink spots. Stippling disappears and keratinization is lost. Patients complain of xerostomia and a burning sensation.
Therapy: Careful oral hygiene (pain!), and topical vitamin A-containing ointments and dentifrices. In severe cases, the gynecologist may elect to intervene by means of systemic estrogen supplements.
The following pages depict puberty gingivitis and pregnancy gingivitis.
This 24-year-old woman was eight months pregnant. She presented complaining that she “bites the swollen gums” on the left side of her mouth (gravid epulis). A severe, generalized gingivitis was also in evidence.
|API: 70%||PD: 7 mm in the region of teeth 34 and 35, otherwise up to 4 mm (pseudopockets)|
|PBI: 3.2||TM: 0–1|
Diagnosis: Severe generalized pregnancy gingivitis with a large pyogenic granuloma (epulis) near teeth 34–35.
Therapy: During the pregnancy, repeated oral hygiene instruction, motivation, plaque and calculus removal; gingivoplasty (electrosurgery, laser) around teeth 34 and 35. After breast-feeding is terminated, re-evaluation and further treatment planning.
Recall: Frequency depends on patient compliance.
Prognosis: With treatment, good.
Some systemic medications, in combination with microbial plaque, can elicit gingival overgrowth. This adverse effect is best known for phenytoin (diphenylhydantoin, p. 121), which has been used for decades in the treatment of most types of seizure disorders.
Phenytoin is also often prescribed following skull trauma and neurosurgical procedures, so that relatively many persons (up to 1 % of the population?) take the drug at some time during life.
It is also well known that phenytoin can cause teratogenic damage, and therefore must never be taken during pregnancy. In the case depicted here, neither the patient nor her treating physician were aware of this potential side effect. The 22-year-old epileptic had taken phenytoin for many years, including during the first seven months of her pregnancy. She developed prominent gingival overgrowth, which was particularly pronounced in the maxillary right quadrant. Probing depths up to 7 mm (pseudopockets) were associated with copious hemorrhage (BOP). Fortunately, the child was born with no birth defects.
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).
|• 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
• Clinical and radiographic symptoms
• Clinical cases depicting the various 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. 519–522). 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.
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.
(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.
(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.
|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|
(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.
(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.
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 atta–chment 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.
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).
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).
|A||Narrow: horizontal resorption|
|B||Average: horizontal resorption, incipient vertical resorption|
|C||Wide: vertical resorption, bony pocket|
The infrabony pocket (infra-alveolar vertical bone loss) may exhibit various forms in relation to the affected teeth (Goldman & Cohen1980, 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.
|A||Three-wall bony defect|
|B||Two-wall bony defect|
|C||One-wall bony defect|
|D||Combined bony defect, crater-like resorption (“cup”)|
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.
Periodontal bone loss around multirooted teeth presents a special problem when bi- or trifurcations are involved. Partially or completely open furcations tend to accumulate plaque (Schroeder & Scherle 1987). Exacerbations, abscesses, progressive loss of attachment and rapid deepening of periodontal pockets occur frequently, especially with through-and-through furcation involvement. In addition, open furcations are particularly susceptible to the development of dental caries.
Modified from Hamp et al. (1975), three classes of horizontally measured furcation invasion are acknowledged:
|Class F1:||The furcation can be probed in the horizontal direction up to 3 mm.|
|Class F2:||The furcation can be probed to a depth of more than 3 mm, but is not through-and-through.|
|Class F3:||The furcation is through-and-through and can be probed completely.|
|A||F0:||Pocket on the mesial root, but without furcation involvement.|
|B||F1:||Furcation can be probed 3 mm horizontally.|
|C||F2:||Furcation can be probed deeper than 3 mm.|
|D||F3:||Through-and-through furcation involvement.|
This classification of bifurcation involvement in the mandible is also applicable to the maxilla, where trifurcation involvement is virtually impossible to diagnosis on the radiograph. In the case of maxillary trifurcations, it is imperative to differentiate between which roots the invasion exists and the extent of the horizontal bone loss. For a complete diagnosis, probing most be performed not only from the buccal, but also from distopalatal and mesiopalatal aspects.
> 7 mm
Therapy: Class F1 and F2 furcation involvement may be successfully treated by root planing alone or by flap procedures (conventional and regenerative). Class F3 furcations are usually treated by means of hemisection or by amputation of one root (p. 381).
The primary symptoms of periodontitis are attachment loss and pocket formation. Pocket epithelium exhibits the following features (modified from Müller-Glauser & Schroeder 1982):
• irregular boundary with the subjacent connective tissue, exhibiting rete pegs; toward the periodontal pocket, epithelium is often very thin and partially ulcerated
• in the apicalmost region, the pocket epithelium becomes a very narrow and short junctional epithelium
• transmigration of PMNs through the pocket epithelium
• defective basal lamina complex on the connective tissue aspect.
Within the subepithelial connective tissue, collagen is lost and numerous inflammatory cells invade. In acute stages, pus formation and microabscesses occur. Bone is resorbed, and deeper osseous marrow is transformed into fibrous connective tissue.
These obligate primary symptoms of periodontitis must be present simultaneously for a diagnosis of “periodontitis” (= inflammation-induced attachment loss); they can occur in different forms and in measurable degrees of severity.
The additional symptoms, listed below, are not obligate in every case of periodontitis, but they may modify or complicate the disease picture:
• Gingival shrinkage
• Gingival swelling
• Pocket activity: bleeding, exudate, pus
• Pocket abscess, furcation abscess
• Tooth migration, tipping, extrusion
• Tooth mobility
• Tooth loss
During the course of periodontitis, especially the slowly progressive, chronic type in adults, gingival shrinkage may occur with time. Gingival shrinkage can also occur after spontaneous transition of an acute exacerbation into a chronic, quiescent stage, or following comprehensive periodontal therapy or after draining of abscesses. Whatever the cause, shrinkage leads to exposure of root surfaces.
This type of shrinkage must not be confused with true gingival recession, which can occur in the absence of clinical inflammation. True recession occurs without the formation of periodontal pockets and is most often observed on the facial aspect of roots. On the other hand, gingival shrinkage due to periodontitis may also be quite pronounced in the papillary regions.
If, as a result of shrinkage, the gingival margin is located apical to the cementoenamel junction, clinical probing of any pockets will underestimate the actual loss of attachment. True attachment loss must be measured from the cement-oenamel junction to the base of the pocket.
Enlargement of the gingiva is a symptom of gingivitis that may remain if progression to periodontitis occurs.
If the gingivae are edematous or hyperplastically enlarged beyond the cementoenamel junction, pocket depth (probing depth) may be overestimated, while true attachment loss may be underestimated (Fig. 212).
The activity of a pocket and the frequency of active episodes are of more importance than absolute pocket depth in mm, especially in regard to treatment planning and prognosis. Bleeding on probing, presence of exudate, and suppuration after application of finger pressure are all signs that an active phase of periodontitis is in progress (Davenport et al. 1982). Such signs are often observed in the aggressive forms of periodontitis, but may also be seen in older patients with chronic periodontitis and reduced host immune response.
Pocket and Furcation Abscess
An additional symptom of active periodontitis is the pocket or furcation abscess. This develops during an acute exacerbation if necrotic tissue cannot be either resorbed or expelled (for example, due to closure of the coronal gingiva above deep pockets, furcations and retentive areas). An abscess (macronecrosis) may also be the consequence of injury, for example biting upon hard, sharp foodstuffs, improper oral hygiene efforts (e. g., a broken toothpick), or iatrogenic trauma. In rare instances a periodontal abscess can develop into a submucosal abscess (Parulis).
An abscess is one of the few manifestations of periodontitis that may elicit pain. If an abscess is expansive, extending to the apical region, the tooth may become sensitive to percussion. A painful abscess must be drained on an emergency basis, either by way of the pocket orifice itself or via incision through the lateral wall. An abscess may release spontaneously through a fistulous tract or via the gingival margin.
A fistula may be the result of spontaneous opening of an abscess if the gingival margin is sealed. If the underlying cause (active pocket) is not eliminated, the fistula may persist for an extended period of time without any pain. The orifice of the fistula is not always located directly above the acute process; this can lead to improper diagnosis of the location of an abscess (probe the fistulous tract with a blunt probe!).
In advanced periodontitis, additional clinical symptoms include shrinkage (gingival recession) or swelling of the gingiva; tooth migration and tipping of individual teeth or groups of teeth can occur. The result of such tooth movements is the creation of diastemata, which can present an esthetic problem. There are many factors that could be responsible for tooth migration and it is not possible in every case to determine the specific cause. It is nevertheless clear that compromised tooth-supporting apparatus is a prerequisite for tooth migration, tipping etc. Numerous other factors may also play a role: missing antagonists, functional occlusal disturbances, oral parafunctions (lip biting, cheek biting, tongue thrust etc.).
A tooth exhibiting a deep pocket on one side and intact periodontal fiber structure on the other side may migrate not so much as a result of pressure exerted by granulation tissue in the pocket, as by forces deriving from the still intact collagenous supracrestal fiber bundles in the healthy tissues. The fact that migrated teeth usually exhibit their unilateral pocket on the side opposite the direction of wandering would appear to support this hypothesis.
The figures below present typical clinical measurements (probing depth, recession of the marginal gingiva, clinical attachment loss) (see also p. 171).
Clinical Attachment Loss
Pocket activity and tooth mobility are symptoms of severe, advanced periodontitis. Elevated tooth mobility must, however, be interpreted carefully because it can be influenced by numerous factors.
Even in a healthy periodontium, the teeth exhibit physiologic differences in mobility depending on number of roots, root morphology and root length (p. 174).
Even in a healthy periodontium, occlusal trauma can lead to an increase in tooth mobility (p. 461). In cases of periodontitis, it is the quantitative loss of bone that is the primary determinant of tooth mobility, but superimposed occlusal trauma can increase tooth mobility still further. In such cases, one may observe a continuously increasing (progressive) tooth mobility, which is very unfavorable in terms of single tooth prognosis.
The final “symptom” of periodontitis, the one which ultimately stops the disease process, is tooth loss. It seldom occurs spontaneously because extremely mobile teeth that are no longer functional are usually extracted prior to spontaneous exfoliation.
This 51-year-old male had received restorative dental care at irregular intervals. The dentist had never performed any periodontal diagnostic procedures, nor any therapy. The patient himself complained of occasional gingival bleeding and calculus that bothered him. He was unaware of any periodontal disease and felt that he was completely functional in mastication.
Findings: See charting and radiographic survey (p. 109).
Diagnosis: Slowly progressing, mild to moderate chronic periodontitis (Type II).
Therapy: Motivation, oral hygiene instruction and follow-up initial therapy. Closed scaling and root planing. After reevaluation, modified Widman procedure at several sites. No systemic therapy. Possible bridgework in mandibular posterior segments.
Recall: Every 4–6 months.
Prognosis: Even if the patient’s compliance is only average, the prognosis is good. In cases such as this, the dentist or periodontist is always “very successful.”
|API||93%. Oral hygiene is poor. Almost all of the interdental spaces harbor plaque.|
|PBI||2.9. The index is very high. All papillae bled during performance of the PBI.|
For decades, this 61-year-old male patient had “scrubbed” his maxillary anterior teeth using a horizontal motion. He had never received oral hygiene instructions, and virtually all of other areas of his dentition were completely neglected. Restorations were inadequate.
Findings: See chart and radiographic survey (p. 111).
Diagnosis: Moderate to severe generalized chronic periodontitis (Type II B). The pronounced gingival shrinkage in the maxillary anterior sextant should not be confused with classical gingival recession!
• Immediate: Extraction of teeth 18, 17, 28 and 46 and the root of 41. The crown will be used as a temporary pontic by attaching it to the adjacent teeth (acid etch).
• Definitive treatment: Motivation, modification of oral hygiene, extraction of 26 and 31. Initial periodontal therapy (definitive debridement) and possible subsequent surgical procedures and a cast framework partial denture.
Recall: Every 4–6 months.
Prognosis: For the teeth to be maintained and treated periodontally, the prognosis is good.
|PI||69%. With the exception of the maxillary anterior and some facial surfaces in the mandibular anterior regions, plaque was present on almost all tooth surfaces.|
|BOP||75% of the pockets examined bled after gentle probing.|
This 31-year-old female immigrated to Switzerland from Ethiopia ten years previously. She complained of loose teeth and the formation of a diastema between her maxillary central incisors. Hemorrhage occurred during tooth brushing. She had never undergone any periodontal treatment.
Diagnosis: Aggressive, moderate periodontitis; an ethnic component must be considered.
Therapy: Motivation, oral hygiene instruction and follow-up initial therapy. Systemic administration of metronidazol and amoxicillin (van Winkelhoff et al. 1989). After reevaluation, flap surgery in quadrants 1, 2 and 4 (excluding the maxillary anterior). Extraction of teeth 18 and 28.
Supportive Therapy: Recall at 3-month intervals.
Prognosis: With good patient compliance, the prognosis is good.
|API||64%. Interdental hygiene is inadequate; smooth surfaces are relatively clean.|
|PBI||Bleeding was more or less pronounced from all inter-dental papillae. The papilla bleeding index is very high at 2.3.|
This 32-year-old female was referred by her general dentist because of multiple periodontal abscesses. She complained for years about ever-recurring pain and “pus discharge” from her gingiva.
Diagnosis: Aggressive, moderate, localized profound and acute periodontitis (active stage).
Therapy: Incision of the abscess; motivation, oral hygiene instructions and check-up, immediate extraction of teeth 25, 37, 32, 31, 41 and 42. Temporary replacement for mandibular anterior teeth. Supra- and subgingival scaling. Systemic antibiotic supportive therapy (metronidazol), and topical application of metronidazol (p. 289) at recall appointments. At Phase 1 evaluation, decision concerning additional procedures, depending upon patient compliance (radical, maintenance or regenerative/GTR).
Supportive Therapy: Initially, very short-interval recall.
Prognosis: With the exception of teeth 15, 24 and 37, and with good patient compliance, the prognosis is average.
This 15-year-old female was referred from her private dentist because of “suddenly occurring” periodontal defects on all first permanent molars.
Bitewing radiographs had been taken periodically to check for dental caries, and gingival findings were noted. Thus, the localized osseous defects were not “serendipitous findings.”
Findings: See charting and radiographs (p. 117).
Diagnosis: Incipient LJP (Type III A). Typical involvement of first molars, with as yet no pocket formation around incisors.
Therapy: Improvement of interdental hygiene, especially in the molar areas. After initial therapy, modified Widman surgery with intensive root planing (direct vision!) on all involved molars.
Microbiologic DNA test (e. g., PadoTest): Aa present, pocket type 4 (p. 185).
Systemic medicinal support with tetracycline (p. 289). Possible filling of osseous defects.
Recall: Repeated professional plaque control during the wound healing phase; subsequent 6-month recall.
|API||64%. Only ten of the 28 interdental spaces examined were free of plaque (-), despite the fact that the dentition appeared relatively clean (Fig. 239).|
|PBI||2.9; number of bleeding sites, 80! Upon cursory inspection, the gingiva appeared to be inflammation-free. Only after recording the PBI was the massive gingivitis identified.|
This 2½-year-old boy was referred from his private dentist. The medical history, gathered from his parents (Japanese mother, Swiss father) revealed that the mandibular deciduous incisors and the maxillary right deciduous incisor had “fallen out” in the previous few months. The left deciduous incisor and also the lateral incisor and canines in the maxilla were highly mobile, but their roots exhibited no resorption. This case is difficult to classify in the absence of an identification of possible hematologic defects. Even though most of the teeth are affected, the relatively mild gingival inflammation and the absence of gingival hyperplasia speak against the generalized form of PP (Type IV B). Laboratory studies should be performed to rule out hypophosphatasia.
Findings: See charting and radiographs.
Diagnosis: Localized, pre-pubertal periodontitis (PP, Type IV B).
Therapy: Palliative or extraction (Page et al. 1983b). Intensive periodontal preventive maintenance upon eruption of the permanent teeth.
Prognosis: Poor for the deciduous dentition, questionable for permanent teeth.
As they traverse their clinical course, plaque-induced inflammatory gingival and periodontal diseases may be enhanced or co-initiated by hormonal disturbances and the side effects of systemic medications. Additional oral pathologic alterations accompanying systemic diseases are frequently observed on the gingiva and in the periodontium. In this milieu, clinical differentiation between gingivitis and periodontitis on the one hand and diseases of the oral mucosa on the other may become blurred.
It is impossible in this Color Atlas of Periodontology to depict and describe each and every oral pathologic alteration that also manifests on the gingiva or in the periodontium. A comprehensive treatment of all such oral lesions can be found in the Color Atlas of Oral Pathology (Reichart & Philipsen 1999).
In the pages that follow, several of the relatively frequently occurring diseases or alterations will be described:
Primarily Gingival Alterations
• Hormonal complications (p. 91)
• Hyperplasia caused by medicaments
• Gingival overgrowth, tumors
• Autoimmune diseases, desquamati/>