Periodontal diseases (parodontopathies) include an array of conditions ranging from simple to complicated ones, from repairable to irreparable ones. Their diagnostics and therapy is a domain of specialists - periodontists - however, it would be a professional neglect if a doctor of general medicine would have lacked a basic knowledge from the field that is so important for preservation of teeth and thus health of his/her future patient.
The periodontium are tissues surrounding a tooth. These are the following:
1. The gum (gingiva) which may be:
a) free - forms a kind of rim around a tooth neck. Between the rim and the tooth surface there is a sulcus that may be up to 1 mm in depth.
b) attached - divided from a free gingiva by the paramarginal groove that marks the sulcus’ depth from the outside
c) interdental papilla filling the interdental space.
2. Periodontal membrane that lines the periodontal slit.
3. The tooth root surface cement.
4. Compacts of a tooth socket.
A tooth is set in an alveolus in such a way that it may move slightly upon a mastication load. This movement distributes a chewing pressure evenly on the whole bone socket and prevents a momentary localized overloading. The periodontal membrane that fills the space between an alveolus and a tooth root, provides for this function. The main structures of this membrane are bundles of collagenous fibrils arranged into several groups of ligaments. Some fasten a tooth to its socket, others fix a gum to the bone base. Another groups of ligaments project along a tooth to the socket’s edge at the interdental space, connect adjacent teeth and their net forms ligamentum circulare at the alveolus edge, that closes a periodontal slit. Ligaments in an alveolar slit lead from lamina dura of an alveolus to the cement of a root’s surface. They are S-shaped at rest and straighten, stretch and distribute a tooth load by pulling on the whole socket’s walls not until a stress is applied. Two areas are important for good health of the periodontium: attached gingiva and its width, and the place where an epithelium attaches to a tooth neck at the bottom of a sulcus - the attachment.
3.1 Factors Causing Parodontopathies
Factors that cause parodontopathies to occur are both internal and external with mutually overlapping effects.
1. Internal causes:
Age - changes of the periodontium may occur already in childhood and the time factor just enable the disease to evolve.
Heredity - concerns anatomic anomalies only (upper or lower frenulum, shallow vestibule).
Toxic substances - damages by hydantoinates and salts of heavy metals.
Infection - exacerbations and multiple abscesses arise during infectious diseases after stopping a treatment with antibiotics.
Race - does not play a role, differences are caused only by exogenous factors at different races.
Gender - men have higher incidence of parodontopathies. Worse dental hygiene plays certain role at men as well.
Vitamins - vitamin deficiency does not exist in our country, so there are no reasons for a vitamin therapy.
Endogenous factors - high levels of estrogen cause growth of bacteroides melaninogenes in a plaque. Incidence of parodontopathies is significantly higher at liver cirrhosis, chronic alcoholism, juvenile diabetes and Down’s syndrome.
2. External causes.
Orthodontic anomalies worsen hygienic conditions of the oral cavity.
Traumatic occlusion worsens an existing damage of the periodontium, although it does not cause a disease by itself.
Anatomical deviations of mucous membranes - lip frenula that have a high attachment and pull the marginal gingiva, makes it to become anemic and chronically irritated. Shallow vestibule causes chronic irritation by an analogous mechanism.
Wrong stomatologic work - overhanging fillings, non-fitting crowns, crowns in supra-occlusion or infra-occlusion, braces of dentures etc.
Tartar - both supra- and sub-gingival that acts as a plaque carrier and is basically a mineralized plaque by itself.
Soft dental coating - the plaque - is the most significant factor of a parodontopathy origin. It is an acquired item and it plays a key role in the occurrence of dental caries. It covers surfaces of teeth and dentures and may be removed by mechanical means only. The plaque undergoes certain maturation during which its microbial flora changes (it is developed in 14 days). At the deepest layers, filamentous bacteria form a palisade layer, the middle part is made of a mesh of the same microorganisms, filled with other microbes. There is materia alba on the surface, a structureless thin layer, removable by a spray. Microbial composition of the plaque varies, although it seems that the higher the number of gram-negative rods, the more invasive the plaque is. New data are being generated on the plaque’s influence on the periodontium and course of immunological reactions inside periodontal tissues. It seems that the plaque produces many antigenic substances that induce B and T lymphocytes sensitization and their increased counts in a gingiva. An immunological reaction in the periodontium neutralizes the plaque antigens. On the other hand, during binding of the complement, the tissue necrosis and lymphokines release take place causing an inflammation.
3.2 Classification of Parodontopathies According to the Czech Nomenclature
Diagnosis X-ray changes
a) G. acuta acute inflammation 0
b) G. chronica chronic inflammation 0
II. Periodontitis gum inflammation, bone resorption
marginalis true gingival pockets,
prevailing exudative part
III. Parodontosis slight or no inflammation, bone resorption
part, true gingival pockets
IV. Periodontium atrophy atrophy of periodontal bone atrophy
tissues, without gingival
I. Gingivitis (gum inflammation)
During an acute gingivitis, an erythema, catarrhal, sero-hemorrhagic, purulent, vesiculous, pseudo-membranous or ulcerous inflammation occurs. At chronic gingivitis, catarrhal, hyperplastic, atrophic or ulcerous inflammation occurs.
I. a) Gingivitis acuta
1. Gingivitis acuta simplex
Etiology - frequently occurs together with respiratory tract diseases, influenza or an infectious exanthema.
Pathologic anatomy - hyperemia, erythema.
Clinical picture - without great difficulties, slight itching may sometimes occur.
Therapy - treatment of the basic disease, improved oral hygiene.
2. Gingivitis acuta catarrhalis
Etiology - exogenous factors or whole-organism diseases.
Pathologic anatomy - a diffuse soaking of the gingival tissue by lymphocytes and polynuclear leukocytes infiltrate.
Clinical picture - both apposing and spontaneous pain. Bleeding caused by touching, or exudation sometimes appear; regional lymph nodes take part in the process.
Therapy - adjusted oral hygiene, removal of exogenous causes, mouth washing with disinfectant and astringent solutions. If not cured, this disease tends to become chronic.
3. Gingivitis acuta during gingivostomatitis herpetica
Etiology - Herpes hominis virus.
Pathologic anatomy - vesicular inflammation.
Clinical picture - mostly child’s disease (maximum incidence between 1 and 3 years of age), although it affects adults between 17 and 30 years as well. The disease has an influenza-like prodromal stage marked by headaches, pains of arms and legs, nausea, sore throat. These signs are followed by a fever, sometimes quite high; the disease is rarely afebrile. Herpetic blisters appear inside a mouth. These blisters are round or oval shaped, size ranging from 1 to 10 mm, often with broken tegmens, covered with a fibrin deposit. Blisters sometimes merge into one surface and typical efflorescences can be found on its edges only. An inflammatory rim forms around the lesions. It is preferentially located at the palate gingiva behind the upper incisor teeth and on the hard palate mucosa. It may also appear on the tongue, lips, gingiva or inside a pharynx. The disease is always accompanied by catarrhal gingivitis. A necrotic decomposition of papillae tips or inflammatory hyperplasia appear as well. The sub-mandibular lymph nodes often react, and a multiple, gray and wet fur covers the tongue. The disease is accompanied by dry mouth and mucous membranes (due to breathing by mouth).
Mucous lesions inside a mouth are very sensitive and children refuse solid food and even to swallow the saliva (virtual hypersalivation). This is probably the reason why this disease is sometimes misdiagnosed by pediatricians as the foot and mouth disease (stomatitis epizootica). This disease has a similar clinical course, although it is very rare at children and a direct contact with infected cattle has to be proven.
Therapy - mouth washes with disinfecting solutions or with a solution of “Framykoin”. Small children should have mouth washed with 1-2% solution of methylene blue or gentian violet. At complicated cases, antibiotics are administered to prevent secondary infection. Antipyretics and supportive therapy with vitamins B and C should be added in case of high fever. Currently, drugs that affect the capacity of viruses to grow and live - acyclovirs (Zovirax) and iododeoxyuridine (IDU). These drugs are administered both as a general treatment and locally. Patients’ diet should be bland and pulpy.
4. Gingivitis acuta ulcerosa
Etiology - fusiform bacteria, borrelias, anaerobic streptococci, vibrios; accompanied by severe failures of immune reactions.
Pathologic anatomy - ulcerous inflammation.
Clinical picture - the disease appears without prodromes, begins at perfectly healthy persons mostly at their second or third decennium. It is linked to presence of teeth. An organism - weakening disease may be present in an anamnesis. The disease frequently occurs in groups of young people (boarding houses, dormitories, military bases, at students during a pre-exam period etc.), and under situations with increased mental or physical stress. An acutely inflamed gingiva with ulceration at interdental papillae tips that has a destructive character, can be observed. Ulcers appear predominantly at places of increased local irritation, e.g. at wrong fillings, denture braces, cutting wisdom teeth, roots etc. After a careful removal of a necrotic tissue, a papilla appears to have its tip cut off. The disease acute phase may either take a course with high fever or it may be afebrile. If the disease is not diagnosed and cured on time, it enters a chronic stage that causes irreparable damage of the periodontium.
Therapy - mushy diet. Careful local washes with hydrogen peroxide, administration of vitamins B and C. Penicillin should be used in more serious forms of the disease. At acute phase, all stomatologic, especially stomato-surgical treatments are contraindicated.
Caveat! At every ulcerous gingivitis that after a timely and intense care does not show any recovery or has low inflammatory reaction, it is imperative to examine the blood count for possible white cells disorder. The differential diagnostics should take into account a possibility of infectious mononucleosis that is often accompanied by ulcerous gingivitis.
I. b) Gingivitis chronica
1. Gingivitis chronica catarrhalis
Etiology - mainly external factors.
Pathologic anatomy - hyperemia, slight edema of the gingiva, inflammatory infiltrate, granulous tissue.
Clinical picture - the disease begins as chronic and exacerbates acutely later. An inflammatory rims appear together with formation of a granulous tissue that is not painful spontaneously but is sensitive to pressure. An increased bleeding occurs.
Therapy - removal of irritation factors. Oral hygiene, massages, irrigation and mouth washes with astringent solutions.
2. Gingivitis chronica desquamativa
Etiology - unclear.
Pathologic anatomy - diffusive erythema and an epithelium peeling.
Clinical picture - the gingiva has a dotted or a “map-like” spotted appearance and bright red color. The epithelium smears under a slight pressure. Very high painfulness.
Therapy - a causal therapy does not exist. Corticoids and estrogens are sometimes used with success. Removal of factors causing a local irritation.
3. Gingivitis hyperplastica
a) Gingivitis hyperplastica pubertalis - iuvenilis
Etiology - unknown.
Clinical picture - frequently occurs at girls of pubertal age. Its appearance is favored by bad oral hygiene, orthodontic anomalies, or previous gingivitis. A small, not painful swelling of palatal papillae appears first, that becomes hypertrophied at later stages. After the end of puberty, this disease may either disappear or it is transformed into a chronic form at some subjects.
Therapy - is the same as in case of a chronic gingivitis. Sclerotization of interdental papillae by calcium is sometimes advisable. If a hyperplasia is so large that it causes obstruction during eating, it is possible to perform a gingivectomy.
b) Gingivitis hyperplastica gravidarum
Etiology - occurs at about 50% of pregnant women during the second or third month of pregnancy. After the end of lactation, the disease often disappears. Its appearance is supported by bad hygienic conditions or earlier gingivitis.
Clinical picture - various forms ranging from light hyperplasia of the pale gingiva to heavy edematous soaking and interdental papillae hyperplasia can be found. Papillae may even cover the teeth crowns, they loose its shape, the gums are livid, bleeding and contain granulous tissue. Hyperplasia may sometimes be restricted to a narrow section of dentition. This form is called a gestation tumor - epulis gravidarum.
Therapy - if hyperplasia obstructs during eating, a gingivectomy is indicated.
c) Gingivitis hyperplastica during the vitamin C deficiency
This disease, associated with malnutrition, occurs very rarely in this country. Its signs are hyperplasia and exulceration of gingiva with bleeding.
d) Gingivitis hyperplastica diphenylhydantoinica
Etiology - hyperplasia of the epithelium of a non-inflammatory origin, that is induced by a medication used by epileptics.
Clinical picture - the gingiva is smooth and pale, inflammatory changes may come at later stages. Young individuals are more prone to hyperplasia, this susceptibility decreases after 30 years of age. The disease occurs at 50% of epileptics, often preceded by a chronic gingivitis or bad oral hygiene.
Therapy - oral hygiene improvement, removal of irritating factors, dental massages. If a hyperplasia obstructs mastication (during frequent recurrences), gingivectomy is indicated. A neurologist has to be consulted for a possible change of a medication.
e) Gingivitis hyperplastica during leukemia
Etiology - occurs most often at acute forms of leukemia.
Pathologic anatomy - diffusive infiltration of connective tissues with white blood elements that are characteristic for a particular type of the disease.
Clinical picture - gingival hyperplasias appear at the oral side at first, more often at the frontal section. They are not painful, and inflammatory signs are missing. The surface of a gingiva may exulcerate and bleeding may occur. Gingival bleeding may take place even without the presence of ulcers. Other oral mucous membranes are notably pale.
Therapy - is completely in the hands of a hematologist. A dentist takes care of a patient’s oral hygiene and removal of local harmful effects.
Caveat! Any oral surgical interventions are contraindicated. Necessary extractions may be performed after consulting a hematologist only.
Periodontitis is always accompanied by the inflammatory part, the chronic gingivitis. Inflammation proceeds into depth to the alveolar tips. This process results in attachment damage, deepening of a periodontal pocket and impairment of periodontal ligaments. The periodontal slit gradually widens and the bone is being resorbed. Besides chronic gingivitis, true gingival pockets can be found. These pockets are shallow at the beginning, but they get deeper with time and teeth get loose. Loose teeth are noticed first by a dentist during an examination. A patient feels just paresthesias at this period (itching feelings, insecure feelings during occlusion), sometimes even foetor ex ore. Teeth moving or fanned spreading of teeth sometimes appears. In some cases, gaps between teeth occur as a result of teeth movement. In case of a deep periodontal pocket, a periodontal abscess may appear as a result of a purulent exacerbation. Periodontitis course may change and even take different courses at the upper and lower jaws.
Parodontosis is a chronic disease of the degenerative nature. It lacks an inflammatory process, which may sometimes occur at the terminal stage. This diseases is regarded as a form of periodontitis at individuals who have reduced immunity against microbes of the plaque. During clinical examination, we can find a pale gingiva with shallow pockets, loose teeth, especially at the molar area, that does not correspond to an X-ray finding. It affects mostly young individuals before age of 30, who practice a good oral hygiene. As the disease progresses, true pockets get deeper and an inflammation appears, so that the finding is the same as for periodontitis.
IV. Atrophy of periodontium.
Etiology of periodontal atrophy is not known, although the alveolar compact matter state plays an important role. Clinically, teeth necks get exposed, inflammatory changes are not present. Teeth remain firm, neither periodontal pockets, nor widened periodontal slits are present.
Therapy for periodontitis, parodontosis and periodontal atrophy is fulfilled according to a plan outlined at the beginning of the treatment. This plan proceeds from simple tasks to more complicated ones. At the first instance, all exogenous harmful effects are removed (plaque, tartar, teeth overload, orthodontic anomalies) including defective dental work. An inflammation should be eliminated by the local use of disinfecting and astringent solutions. Patient’s cooperation is essential at this stage, who can significantly influence results of the therapy by a regular care at home (massages, irrigation, oral hygiene). This conservative cure is followed by a surgical therapy that aims at elimination of pockets and their contents, removal of pathological tractions (high attachments of a frenum, transient folds and the shallow vestibule), ensuring sufficiently wide attached gingiva and restoring a physiological shape of gums and the bone base. If needed, therapy is supplemented with a prosthetic work that provides for functional completion of teeth and its splinting.