Classifications of periodontal diseases and clinical forms
Plan :
Introduction
1. Reminders on periodontal health
2. Periodontal diseases
3. Etiopathogenesis of periodontal disease
4. Interests of a classification
5. Classification systems
6. Classification criteria
6.1 Anatomopathological criteria
6.2 According to the mode of evolution
6.3 Topographic criteria
6.4 According to the Elementary Lesion
7. Classification of periodontal diseases
7.1 The 1989 classification of the American Academy of Periodontology (AAP)
7.1.1 Periodontitis
7.1.2 Gingivitis
8. Classification by GC Armitage (1999)
8.1 Gum diseases
8.1.1 Plaque-induced gingival diseases
8.1.2 Non-plaque induced gingival diseases
8.2 Periodontitis
8.3 Innate or acquired adverse periodontal conditions
9. New classification of periodontal and peri-implant diseases and conditions 2017
9.1 Key concepts and basic rules of the new classification of periodontitis:
9.2 Gingival health
9.3 Plaque-induced gingivitis
9.4 Non-plaque induced gingival diseases
9.5 Periodontitis
9.6 Peri-implant conditions
9.7 Classification of gingival recessions
Conclusion
Bibliography
Introduction: Periodontal diseases are recognized as being inflammatory and of bacterial origin. As such, many complex phenomena will come into play in their natural history and pathogenesis.
The classification aims to consider all of these mechanisms and to weight them according to recent scientific and epidemiological data, in order to compare them with the patient’s own data and arrive at a periodontal diagnosis. From this diagnosis, put in relation to the occlusal and possibly preprosthetic data, a treatment plan and a prognosis adapted to the specificity of each patient will result.
1. Reminders on periodontal health :
The periodontium is considered healthy when:
. the gum has a pale pink, orange peel appearance, does not bleed when brushing, chewing, spontaneously or when probing.
. the depth of the gingivo-dental sulcus varies between 0.8 and 2 mm, the epithelial attachment being at the level of the enamel-cement junction.
– on X-ray, the top of the bony crest is 2 mm below the enamel-cement junction.
2. Periodontal diseases : Classifications – Problem: Gingival diseases are inflammatory processes that only affect the superficial periodontium without reaching and/or destroying the deep periodontal structures (alveolar bone, desmodontium, cementum). Periodontitis is an irreversible destruction of the deep tissue periodontal components, i.e., the epithelial-connective tissue attachment, the desmodontium, the alveolar bone and the cementum.
Due to the difficulty in grouping all forms of periodontal diseases, no classification of periodontal diseases has been definitive. The classification according to clinical criteria has been the most frequently used. But in the last ten years, knowledge of periodontal diseases has been developed, in order to try to keep pace with the progress of science, etiology and pathogenesis; bacteriological or biological criteria could also be used.
3. Etiopathogenesis of periodontal disease : Periodontal disease is a multifactorial disease, some of whose factors are directly involved in triggering the disease, while other factors aggravate and amplify and/or maintain the progression of the different phases of periodontal disease.
Among these factors, we find the direct local etiological factors or initial irritation factor represented by the bacterial biofilm; the indirect local factors or functional factors. The general etiological factors or systemic factors. Constitutional etiology (age; heredity, sex, race).
Biofilm bacteria attack the periodontium directly through enzymes,
indirectly through the action of toxins and antigens that stimulate immune cells, which trigger the secretion of antibodies. However, the host response is variable. Immunological phenomena play an important role in this pathogenesis; thus the presence of general factors modifies this response by reducing natural defenses, limiting the repair capacity and causing an abnormal response.
Periodontal pocket / Clinical attachment loss:
It is the pathological increase in the depth of the sulcus which results either from the apical migration of the epithelial attachment, or from the increase in the volume of the gingiva, or both.
The clinical attachment level: represents the distance separating the enamel-cement junction from the bottom of the pocket, the difference between the two measurements being the gingival recession (it is therefore the addition of the probing depth and the recession height, which is the main marker of periodontitis)
4. Interests of a classification: Classifying an attack: allows to make a correct diagnosis, carry out targeted treatment, carry out the differential diagnosis. It is essential to carry out epidemiological or clinical studies by making the results comparable with each other.
5. Classification systems : Specific features defining different periodontitis-related phenotypes have formed the basis of classification systems since periodontal diseases were first described in the literature. Inevitably, these systems have continually evolved.
Over the last 50 years, early epidemiological findings have established that the severity of periodontitis in the population is associated with age and oral hygiene (Scherp 1964). An overview of the most recent periodontitis classification systems, prior to the introduction of the current system, indicates that these systems have largely attempted to separate patients with levels of periodontal tissue destruction commensurate with their age and level of local etiology from more severe but less widespread manifestations.
6. Classification criteria : To classify periodontal diseases, many authors use classification criteria, namely:
6.1 Anatomopathological criteria: Three pathological processes are distinguished
. Inflammatory lesions (gingivitis/periodontitis)
. Degenerative lesions: This is a regressive process with partial or total degradation of certain elements of the periodontium. There are tissue changes: the cells are transformed into an inert substance and lose all functional activity.
. Benign/malignant tumor lesions: This is an excessive proliferation of qualitatively normal anatomical elements.
6.2 According to the mode of evolution:
. Acute form: painful lesion, sudden onset, short duration.
Chronic form: Slow onset, no pain, quiet progression
. Subacute form: consists of a warming of the chronic form, but less severe than the acute mode.
. Recurrent form: The lesion reappears after poor treatment; or successfully treated, but which, due to lack of supportive care, triggers a new process of destruction.
. Refractory mode: the lesion does not respond to treatment.
6.3 Topographic criteria:
. Location: Gingivitis: papillary, marginal or diffuse.
Periodontitis: superficial, deep or terminal.
. Extent: localized (less than 30% of sites) or generalized ( more than 30% of sites are affected)
6.4 According to the Elementary Lesion: The primary elementary lesion corresponds to the initial lesion process. The secondary elementary lesion represents an evolutionary stage of a primary lesion.
Classifications of periodontal diseases and clinical forms
. Primary lesions:
. Erythema: it is due to the permanent dilation of the capillaries, the gum presents an intense localized or generalized red coloration characterized by its disappearance on finger pressure (positive cup sign) and reappearance as soon as the pressure stops. -The macule: it is a flat lesion characterized by a circumscribed alteration of the color. Example: petechiae¸ ecchymosis…
. Papule: superficial, circumscribed lesion, solid and does not contain fluid.
. The plaque: it is like the papule¸ which is a superficial elevation but exceeds 0.5 mm.
. The nodule: more raised than the papule or plaque, forms deeper
. The vesicle: epidermal elevation, generally round, containing a clear serous or hemorrhagic liquid, its dimensions vary from those of a pinpoint to those of a large pea 0.5mm. The vesicles are fragile, transient. Their etiology is essentially viral. Example: Herpes, shingles, eczema.
. The bubble: it is an epidermal elevation with damage to the basal, of variable size (more than 5mm, the bubble is only a large vesicle. It contains a serous or hemorrhagic fluid.
. Pustule: circumscribed elevations of the skin, 1 to 5 mm in diameter, containing a purulent exudate from the outset and surrounded by an inflammatory halo. Pustules are often of infectious origin; they should not be confused with secondarily infected vesicles.
. Secondary lesions: Follow primary lesions
. Erosion: loss of substance limited to the epithelium. Erosion is painful and heals without scarring.
. The crack: it is the linear loss of the integrity of the epithelium.
. Ulceration: this is a deep loss of substance with destruction of the gingival epithelium and the upper part of the underlying connective tissue.
. Necrosis: this is the tissue death of a portion of the gum caused by the presence of fusospirillary bacterial germs.
Gangrene: the mortification reaches the deep periodontal tissues, eschars form which can leave considerable loss of substances and major scars.
. Tumor: Pathological growth due to cellular proliferation. The tumor can be benign or malignant.
7. Classification of periodontal diseases:
7.1 The 1989 classification of the American Academy of Periodontology (AAP) distinguishes several forms of periodontal disease based on the age of onset, the speed of progression and any associated general problems: we distinguish:
7.1.1 Periodontitis:
. Adult periodontitis: this is by far the most common. It affects people generally over 35 years old. It has the particularity of being directly related to various deposits (plaque, tartar). Tissue destruction extends over years or decades. There is no immune dysfunction and no genetic involvement.
. Early-onset periodontitis: differentiated according to the location or generalization of the lesions. Most often they are characterized by a small amount of dental plaque and tartar compared to the extent of bone lysis. This can be prepubertal, juvenile or rapidly progressive periodontitis.
. Prepubertal periodontitis affects very young subjects with deciduous or mixed dentition. Its progression is rapid, associated with alveolysis affecting both deciduous and permanent teeth. It should be noted that these conditions are very rare and most often associated with a systemic disorder, and that they can be considered as the oral expression of a systemic syndrome.
. Juvenile periodontitis: affects adolescents and very young adults (up to 25 years old). It is described in two forms: localized or generalized. Localized juvenile periodontitis affects the incisors and the first permanent molars.
. Generalized juvenile periodontitis affects slightly older patients, in late adolescence or young adults. In addition, lesions are found on other teeth (canines, premolars, second molars).
. Rapidly progressive periodontitis: affects young people, between 20 and 35 years of age. The lesions are generalized, affecting the majority of teeth, without any particular distinction or specific location. Some patients may have a history of juvenile periodontitis. The majority of patients have functional defects in neutrophils or monocytes.
.Periodontitis associated with systemic diseases
.Ulceronecrotic periodontitis
. Refractory periodontitis that does not respond to conventional periodontal therapy
7.1.2 Gingivitis:
. Inflammatory gingivitis of bacterial origin: the initiating factor of this gingivitis is the accumulation of dental plaque on the teeth. One or more of the following clinical signs may be observed: change in color (red), contour, and texture. There is the presence of edema, bleeding (induced or spontaneous), the consistency is soft, and radiologically, there is no bone loss.
. Gingivitis and hormonal changes
. Gingivitis and drug interactions
. Gingivitis and dermatological diseases
. Gingivitis and systemic diseases
. Specific infections
. Ulcerative-necrotic gingivitis.
Classifications of periodontal diseases and clinical forms
8. GC Armitage classification (1999) : A new classification of periodontal diseases was proposed in 1999 (Armitage). The result of a global consensus conference, it is intended to be a more clinical and more exhaustive synthesis than before of the evolution of knowledge over the last ten years. It also marks a concern for simplification in the face of a previous classification system considered too narrow and too rigid.
The criteria selected:
This new classification:
. No longer takes into account the patient’s age.
Early-onset forms are called aggressive periodontitis .
. According to the 1999 classification, the term “chronic periodontitis” replaces “adult periodontitis”. Indeed, this clinical form of periodontitis does not only affect adults; it can also be observed in children at an early stage.
. Refractory periodontitis disappears as an entity
. It specifies the class of “gingival diseases” (induced and not induced by bacterial plaque
. It develops and better identifies the characteristics of periodontitis associated with systemic diseases.
. It includes the term “necrotic periodontal diseases”
. Periodontal abscess appears in the classification
. Endoperiodontal lesions are also part of the classification.
Some conditions are classified as “innate or acquired adverse conditions” in which mucogingival defects are taken into account .
The table below represents the current classification of periodontal diseases.
8.1 Gingival diseases:
8.1.1 Plaque-induced gingival diseases
. Gingivitis associated with plaque only
. without local factors
. with local factors (tooth shapes, overflowing fillings, dental fracture)
. Gingival disease associated with systemic factors
. associated with endocrine changes:
. puberty gingivitis
. gingivitis associated with menstrual cycles
. gingivitis during pregnancy, pyogenic granuloma
. gingivitis and diabetes mellitus
. Gum diseases associated with blood clotting disorder: leukemia, other disorders
. Gum diseases modified by drug treatments: anti-epileptic medications; oral contraceptives.
. Gum diseases modified by malnutrition: vitamin deficiency (vitamin C); other deficiency
8.1.2 Non-plaque induced gingival diseases:
Specific bacterial origin: Neisseria gonorrhea, Treponema, Streptococcus
Viral origin: Herpetic gingivostomatitis, Herpes, Shingles, other
Fungal origin: Candidiasis, Linear gingival erythema, other
Genetic origin: gingival fibroma
Systemic origin:
. Mucocutaneous disorders: lichen planus, pemphigus, erythema multiforme, lupus erythematosus
. Allergic reaction: filling material (mercury, nickel, acrylic) Material to toothpaste, mouthwash, food
. Traumatic injury: chemical contact, injury, burn
. Reaction to foreign bodies
. Other origins: autoimmune reactions
8.2 Periodontitis:
Chronic periodontitis: can be localized or generalized.
. Periodontitis, manifestations of systemic diseases:
. Periodontitis associated with hematological disorders: neutropenia, leukemia, infection
to HIV
. Periodontitis associated with genetic disorders:
. familial neutropenia
. Down syndrome
. Papillon-Lefèvre syndrome
. Chediak-Higashi syndrome
. Agranulocytosis
. Cohen syndrome
. Ehlers-Danlos syndrome
. hypophosphatasia
. leukocyte adhesion deficiency syndrome
. histiocytosis x
. Periodontitis of undetermined origin
. Ulcerative-necrotic periodontal diseases : ulcerative-necrotic gingivitis, ulcerative-necrotic periodontitis.
. Periodontal abscess: gingival abscess, periodontal abscess, pericoronary abscess.
. Periodontitis associated with endodontic pathology: combined endo-periodontal lesions
8.3 Innate or acquired unfavorable periodontal conditions: anatomical factors favoring plaque retention. The morphology of the teeth or their positions, their overlapping can create unfavorable periodontal conditions. Insufficient or absent keratinized adherent gingiva can contribute to the development of periodontal disease.
An inadequate mucogingival complex, abnormal insertion of frenulums which can be the cause of attachment losses associated with recessions.
Occlusal trauma (primary or secondary) also constitutes an unfavorable condition for maintaining periodontal health.
9. New classification of periodontal and peri-implant diseases and conditions 2017:
In order to update the classification system, and taking into account the rapid scientific progress of the last 20 years, a joint workshop was organized by the American Academy of Periodontology and the European Federation of Periodontology in Chicago, USA in 2017. The result of this historic workshop is a revised disease classification that guides comprehensive treatment planning and allows for a personalized approach to patient care.
This classification indicates the severity and extent of the disease, takes into account the expression of the disease and the general health of the patient.
9.1 Key concepts and basic rules of the new classification of periodontitis: The new classification system of periodontitis is fundamentally different from the 1999 system because, with the exception of specific forms (necrotizing periodontal diseases and periodontitis as a manifestation of systemic disease), periodontitis is recognized as a single nosological entity that is further classified using a two-vector system (stage and grade).
The stage reflects the severity of the disease (expressed by loss of attachment and bone loss), but also the factors of tooth loss occurring following periodontitis.
Furthermore, this reflects the anticipated complexity of treatment required to eradicate/reduce the current level of microbial challenge and inflammation, and to restore the patient’s masticatory function.
The grade describes other biological dimensions of the disease, including the observed or inferred rate of progression, the risk of further deterioration due to environmental exposures (such as smoking) and comorbidities (such as diabetes), and the risk that the disease or its treatment may harm the overall health of the individual patient.
Major changes:
Gingivitis
. Definition of periodontal health status
. Possible periodontal health on reduced periodontium (notion of “treated periodontitis”)
Periodontitis
. A single diagnosis of periodontitis
. Dual characterization of periodontitis: 4-level “stage” and 3-level “grade”
.Classification of endo-periodontal lesions
. Classification of abscesses
Systemic associations
. Major effect on the development of periodontitis: certain rare diseases
. Variable effect on the development of periodontitis: frequent diseases (e.g. diabetes) and those affecting the periodontium independently of the presence of biofilm (e.g. cancers)
. Diabetes and tobacco use should be considered as descriptors
Gum recession
. Classification of gingival recessions
. The term “biological space” replaced by “supra-crestal attachment”
The different chapters of the classification:
Periodontal health and gum disease:
Three possible states:
. Gum health
. Plaque-induced gingivitis
. Non-plaque induced gum disease
9.2 Gingival health: Clinical diagnosis. Gingival health without periodontitis
. Gingival health in an intact periodontium: characterized by absence of bleeding on probing, absence of erythema, edema, loss of attachment and bone loss. Physiological bone levels range from 1 to 3 mm apical to the enamel-cementum junction.
. Gingival health on a reduced periodontium: concerns patients with gingival recessions or having undergone coronal elongation for example, is characterized by the absence of gingival bleeding on probing, absence of erythema, edema. Presence of a clinical attachment and reduced bone levels.
Gingival health with treated periodontitis : On reduced periodontium:
. Gingival health in a reduced periodontium after successful treatment of periodontitis: characterized by the absence of bleeding on probing, erythema, edema and the presence of reduced clinical attachment and bone levels.
For intact periodontium and reduced and stable periodontium, gingival health is defined as ≤10% bleeding sites with probing depths ≤3mm.
For intact and reduced periodontium, gingivitis is defined as ≥10% bleeding sites with probing depths ≤3mm. (Fig1)
Classifications of periodontal diseases and clinical forms
Loss of attachment Pocket depth Bleeding on probing Radiographic alveolysis | Without Periodontitis | With Treated Periodontitis | ||||
Intact periodontium Reduced periodontium * | Reduced periodontium | |||||
| HealthNo ≤ 3mm < 10% No | GingivitisNo ≤ 3mm ≥10% No | HealthYes ≤ 3mm < 10% Possible | GingivitisYes ≤ 3mm ≥10% Possible | HealthYes ≤ 4mm < 10% Yes | GingivitisYes ≤ 3mm ≥10% Yes | |
(Fig1). Gingival health and gingivitis. Clinical diagnosis
* Patients with gingival recessions or having undergone crown elongation for example
9.3 Plaque-induced gingivitis:
. Associated with biofilm only
. Modified by systemic or local factors:
. Systemic factors (modifying factors)
(Smoking, Hyperglycemia, Nutrition, Pharmacological agents (prescribed, non-prescribed and recreational), Sex steroids, Puberty, Menstruation, Pregnancy, Oral contraceptives, Hematologic disorders).
. Local risk factors (predisposing factors): Plaque retention factors (such as overcontours), Dry mouth
. Medicated gingival growth
9.4 Non-plaque induced gingival diseases
. Genetic Disorders / Developmental Disorders: Hereditary Gingival Fibromatosis
. Specific infections
. Bacterial origin: Neisseria gonorrhoeae, Treponema pallidum, Mycobacterium tuberculosis, Streptococcal gingivitis
. Viral origin : Coxsackie virus (foot-and-mouth disease), Herpes virus type I&II (primary or recurrent), Varicella-zoster virus (chickenpox and shingles – trigeminal nerve), Molluscum contagiosum, Papillomavirus (squamous cell papilloma; condylomata acuminata; common wart; focal epithelial hyperplasia)
. Fungal origin: Candidiasis, Other mycoses (histoplasmosis; aspergillosis)
. Inflammation and Immunity:
. Hypersensitivity, Plasma cell gingivitis, Erythema multiforme
. Autoimmune diseases of the skin & mucous membranes:
– Pemphigus vulgaris
– Pemphigoid
– Lichen plan
– Lupus erythematosus: Disseminated or Discoid
. Granulomatous inflammatory lesions (orofacial granulomatosis): Crohn’s disease, Sarcoidosis
. Reaction processes
. Epulides: Fibrous epulis, Calcified fibroblastic granuloma, Vascular epulis (pyogenic granuloma), Peripheral giant cell granuloma
. Neoplastic tumors:
.Pre-neoplastic tumors: Leukoplakia, Erythroplakia
. Malignant tumors: Squamous cell carcinoma, Leukemic infiltration, Lymphoma, Hodgkin’s, non-Hodgkin’s.
. Endocrine, nutritional & metabolic diseases: Vitamin deficiency, Vitamin C deficiency (scurvy)
. Traumatic injuries:
. Physical/mechanical: Frictional keratosis, Mechanical gingival ulceration, Self-inflicted injury (self-mutilation), Chemical (toxic) burn.
. Thermal aggression: Burning of the gums
. Gingival pigmentation: Melanoplasia, Tobacco melanosis, Drug pigmentation (anti-malarial, minocycline, Amalgam tattoo).
9.5 Periodontitis: Three possible diagnoses:
. Periodontitis
. Necrotic periodontal diseases
. Periodontitis clinical manifestation of other diseases
Other classifications:
. Endo-periodontal lesions
. Periodontal abscesses
Periodontitis is defined by 3 components:
- identification of the patient as a case of periodontitis
- Identification of the specific type of periodontitis,
- Description of clinical signs and other elements that may affect treatment
Stages and grades:
. The stage characterizes the severity and complexity of treatment. Severity is based on the assessment of attachment loss, bone destruction, and periodontal history of tooth loss.
Complexity concerns the presence and evolution of pocket depths, furcation lesions or infra-bony defects, dental mobility, secondary occlusal trauma, loss of occlusal alignment. (Fig2)
. The grade gives additional information on: (Fig3)
. biological aspects,
. past and future progress,
. the prognosis of treatment
. the risk that the disease or its treatment will affect the patient’s health
Additional descriptors: (1) distribution : molars, PM and/or incisors;
(2) extent : localized < 30% of sites, generalized ≥ 30% of sites
Stage 1 | Stage 2 | Stage 3 | Stage 4 | |||
Severity | Loss of interdental attachment * | 1 to 2 mm | 3 to 4 mm | ≥ 5 mm | ≥ 5 mm | |
Radiographic alveolysis | Coronary third < 15% | Coronary third 15 to 33% | ≥ 50% | ≥ 50% | ||
| Missing teeth due to periodontal reasons | 0 | 0 | ≤4 | ≥5 | ||
| Pocket depth | ≤4 mm | ≤5 mm | ≥6 mm | ≥6 mm | ||
| Radiographic alveolysis | HorizontalEssentially | HorizontalEssentially | Vertical ≥3 mm | Vertical ≥3 mm | ||
| Complexity | Inter-radicular lesions | No or class I | No or class I | Class II or III | Class II or III | |
| Crestal defect | No or light | No or light | Moderate | Severe | ||
| Rehabilitation NeedComplex ** | No | No | No | Yes | ||
(Fig2). Periodontitis. Severity/Complexity
* At the most affected site.
** due to masticatory dysfunction, secondary occlusal trauma (mobility ≥ 2), occlusal collapse, less than 20 residual teeth (10 antagonist pairs), etc.
Progress rate | Grade A Slow | Grade C Moderate | Grade D Fast | |
Criteria | Loss of attachment or alveolysisRadiographically over the last 5 years | No | <2 mm | ≥2 mm |
| Alveolysis percentage/age ratio | <0.25 | 0.25 to 1 | >1 | |
| Ratio of plaque quantity to periodontal destruction | Important/low | Normal | Low/high | |
Modifying factors | Daily cigarette consumption | No | <10 | ≥10 |
Diabetes | No | YesHbA1c <7.0% | YesHbA1c ≥7.0% |
(Fig3). Periodontitis. Progression rate
9.6 Peri-implant conditions are included in the classification and are stratified into peri-implant health, peri-implant mucositis, peri-implantitis and peri-implant soft and hard tissue deficiencies
9.7 Classification of gingival recessions: A classification of mucogingival recessions by Cairo et al. has been adopted and is based on the assessment of the level of the marginal gingiva in relation to the interdental tissues adjacent to the recession defects .
Type 1 (RT1): no interproximal attachment loss. JAC not clinically detectable (neither mesial nor distal to the tooth)
Type2(RT2): interproximal attachment loss * ≤ vestibular attachment loss **
Type3(RT3): interproximal attachment loss * > vestibular attachment loss **
* measured interproximal from the JAC to the bottom of the sulcus or pocket
** measured vestibularly from the JAC to the bottom of the sulcus or pocket
Conclusion: Our knowledge of periodontal diseases is set to evolve constantly. Research into the involvement of certain genes in periodontal disease must continue in order to hope for direct benefits for diagnosis (genetic tests evaluating the biological processes that lead to the destruction of periodontal tissues), for therapy (better knowledge of the genetic risk allowing a better understanding of the patient’s response), and for prognosis (targeting the subject who will develop a disease or the one who sees an existing disease progress).
. Bibliography:
1. Duyninh.T; Jame.O; Bousque.P; Gibert.P; Orti.V: classification of periodontal diseases; Medical-surgical Encyclopedia 23-441-A-10 (2004)
2. Mattout.P; Mattout.C: periodontal and implant therapies. Quintessence International. 2003
3. Struillou.X/ classification of periodontal diseases. Journal of periodontology and oral implantology. Vol21-no 04- 31/10 2002
4. Tenenbaum.H. Classification of periodontal diseases: periodontology: from diagnosis to practice; Bercy.Tenenbaum. De Boeck University. 1996
5. Lindhe.J. Clinical Periodontology and Implant Dentistry; Seventh Edition. 2022.
6. Newman.MG; Newman and Carranza’s Essentials of Clinical Periodontology. 2020
Classifications of periodontal diseases and clinical forms
Wisdom teeth can cause infections if not removed.
Dental crowns restore the function and appearance of damaged teeth.
Swollen gums are often a sign of periodontal disease.
Orthodontic treatments can be performed at any age.
Composite fillings are discreet and durable.
Composite fillings are discreet and durable.
Interdental brushes effectively clean tight spaces.
Visiting the dentist every six months prevents dental problems.