6. Lesions of the oral mucosa (Péter Novák MD)
6.15. Periodontal diseases (Péter Vályi DMD - László Párkányi DMD)DMD)
6.15.6. Non-bacterial lesions of the periodontal tissues and peri-implant lesions (Vályi P.)lesions (Vályi P.)
PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS Aetiology
Since periodontal tissues are connected to the pulpal tissues through the apical foramen, a pulpal disease can influence the periodontium and vice versa: periodontal diseases can affect the health of the pulp. Endo-periodontal lesions can develop in different ways. Lateral root canals, which can be found in the apical and middle third of the root, are on average 4-250 micrometres in diameter. Most of the time they have capillaries inside them. Through these, periodontal vessels can carry nutrients into the pulp chamber. Pulpal and periodontal processes can communicate through these connections. The other form of connection is the dentine tubules. Excessive root planing is not proven to cause pulp necrosis, but it is a possibility. Iatrogenic harm is much more common: when a false way is created during root canal treatment, it enables irrigating solutions to pass through to the periodontal space, thus creating an infection. Root fracture can be another cause of problems. Root perforation can also occur as a result of internal resorption. Trauma can disrupt the neurovascular connection of the pulp chamber, which can also lead to endo-periodontal lesions, sometimes even without infection.
Inflammation of the vital pulp does not result in periodontal lesions. Most bacteria causing pulpal infections are also periodontal pathogenic bacteria, although the bacterial composition of the necrotic pulp is much less complex than that of periodontal pockets. Necrotic pulp is a good substrate for these Gram negative bacteria.
From the pulp chamber there are two ways for the infection to proceed to the periodontal space: the apical foramen and the lateral root canals. In most cases, it is diagnosed as periapical periodontitis and damages the periodontal tissues around the apex. Infections exiting lateral root canals lead to lateral periodontitis. Infections exiting at the furcation level imitate the clinical picture of true furcation lesions.
There are three ways in which the infection can proceed: through the periodontal space and bone, under the periosteum reaching the marginal periodontium and passing through both the bone and the periosteum (and mucosa) into the vestibule through a fistula.
The degree of damage depends on the amount of bacteria, their virulence factor and host defense system.
Inflammation can go two ways, depending on host defense reactions. Acute periapical inflammation (purulent,
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serous) will develop, if host defense is insufficient. If the immune system functions properly, granulation tissue containing inflammatory cells can embed the inflammation, which can be present asymptomatically for years. If the inflamed area is surrounded by a fibrocellular connective tissue cover, bacteria from the pulp chamber rarely get to the surrounding tissues.
When acute inflammation is present, the excessive amount of inflammatory products spreads fast. When reaching the periodontal pocket, it is hard to differentiate from a periodontal abscess.
For differential diagnosis patient records, evaluation of clinical symptoms (location of swelling, configuration of pocket, direction of percussion tenderness, nature of pain, vitality test, degree of tooth destruction) and radiological examination can be of help. Previous chapters discussed the difference between a periodontal and a pulpal abscess. The morphology of the pocket can be helpful when probing: an apically narrowing pocket indicates a periodontal lesion, while an apically widening pocket is a sign of pulpal disease.
Continuous resorptive and rebuilding processes of the bone are separated from the dental hard tissues by periodontal ligaments and cementoblasts. If this barrier is injured and the root cementum gets in direct contact with the active bone cells, a resorptive process begins on the root. It only shows clinical signs when it is accompanied by an infectious or inflammatory process. Minimal surface resorption is present in case of occlusial trauma or smaller injuries on the cementum, caused by orthodontic treatment. The damage caused by osteoclasts in these cases is quickly repaired by cementoblasts. Replacement resorption can take place when periodontal ligaments get injured following tooth trauma or if autografts (containing vital bone cells) are used to fill periodontal pockets. This resorption ends with large resorption lacunas, which cannot be repaired by cementoblasts, therefore, osteoblasts gradually replace the defect by creating bone. This is most commonly recognised on radiographs without any clinical signs.
External inflammatory resorption is caused by granulation tissue developing around the root. This can happen after major trauma, accompanied by pulpal infection and necrosis. This scenario is associated with continuous irritation caused by the infection, as well as replacement resorption. The same process takes place after periodontal therapy, when treated root surfaces are populated by epithelial cells instead of fibroblasts.
Classification of endo-periodontal lesions
Several classifications are present, but the most recognised one is the Guldener and Langeland classification:
1. primary endodontal lesionThe necrotised pulp is causing the periapical or lateral periodontal lesion. The inflammatory products can deflect into the gingival sulcus and to the vestibule through a fistula.
2. primary periodontal lesionPeriodontal inflammation and consequent attachment loss can lead to the opening of accessory root canals. Pulp can get infected through these canals.
3. combined endo-periodontal lesion Pulp necrosis and periodontal lesion caused by persisting severe periodontitis develop at the same time.
DEVELOPMENTAL AND ACQUIRED PERIODONTAL DEFECTS AND CONDITIONS
Periodontal conditions or mucogingival deformities which influence the development and progression of periodontal inflammatory diseases, but can also occur independently of dento-gingival plaque.
Localised periodontal conditions, modified by tooth- related predisposing factors Anatomical factors of the tooth
Changes in the shape of the tooth can modify interdental spaces and shapes of the papillae or lead to their absence. Interdental spaces might be too narrow (crowded teeth) or too wide (pronounced curvature of clinical crowns). These deformations can be the result of rare anatomical structures, fissures engaging the root or enamel pearls.
Effects of restorations
Incorrect marginal closures of crowns, fillings, micro-mechanical retentive structures can irritate the gums.
Besides facilitating plaque accumulation, their direct traumatising effect can harm the periodontal tissues.
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Lack of keratinised gingiva
Periodontal health can be maintained in the lack of keratinised gingiva with good oral hygiene. However, lack of keratinised gingiva may inhibit appropriate oral hygiene, which can lead to inflammation. When performing restorations with crowns, a minimum of 3 mm keratinised gingiva is necessary to preserve periodontal health, especially in thin biotype.
Shallow vestibule
Shallow vestibule may prevent proper oral hygiene Pronounced frenule
Pronounced frenule can prohibit proper oral hygiene. Highly attached frenule can damage the marginal gingiva.
Gingival overgrowth, pseudo-pocket, irregular gingival contour
These conditions make appropriate individual oral hygiene impossible. They support plaque-induced inflammatory diseases and their progression.
Gummy smile
Gummy smile is mostly an aesthetic concern, but gums can be mechanically irritated as a result of mouth breathing.
Gingival overgrowth, pigment disorders
These disorders were mentioned in detail at the beginning of this chapter.
Mucogingival deformities on the edentulous ridge
The edentulous ridge suffers constant involution following teeth loss. If the tooth was affected by periodontal disease, cyst, surgical trauma or developmental disorder, its loss leads to various tissue deficiencies.
The ridge may lose volume horizontally as well as vertically. Seibert, Allen and Wang classified defects into
• Horizontal (H, Class I, Type A),
• Vertical (V, Class II, Type B) and
• Combined (C, Class III, Type C) defects.
Studer determined the severity of the horizontal defect relative to the dentate arch, and that of the vertical defect based on the papilla height of the adjacent tooth: 0-3 mm: moderate, 3-6 mm: advanced, 6 mm severe bone resorption.
According to the studies of Seibert and Allen, defects are combined in more than half of the cases, horizontal only in one-third of the cases, and isolated vertical defects are extremely rare . In less than 1 of 10 there is no deficiency at all.
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Correction of the edentulous ridge is inevitable for both fixed partial dentures and implant restorations.
However, not only tissue deficiency, but also shallow vestibule, gingival overgrowth, pronounced, highly attached frenules can cause problems associated with the edentulous ridge.
Occlusal trauma
All adaptive and pathological changes in the periodontium caused by overload of the masticatory function are called occlusal trauma. Unfavourable forces can appear after the adjustment of occlusion, early tooth contact and parafunction. Early contact can be the result of tooth loss, periodontitis, changes in dentition (elongation, tooth malposition or mobility) or poorly designed restorations. In case of primary occlusal trauma, the tooth is periodontally healthy, but is subject to increased loading forces. In secondary occlusal trauma, the force might even be normal, but affected teeth are periodontally compromised.
Occlusal trauma can lead to qualitative and quantitative changes in periodontal tissues, which can regenerate in part or completely if the damaging forces no longer exist. As a result of the pathological process, the periodontal space gets wider, the alveolar bone starts to resorb, vascular changes take place in the ligaments, degenerative changes in the cementum and the amount of collagen decreases in the alveolar bone. The pathological mobility of tooth can be divided into two stages: progressive (increasing) and stabilised (persistent).
Clinical signs of occlusal trauma: high tooth mobility, increasing tooth mobility, tooth wearing, facets on teeth, tooth migration, tooth tilting, failure of restoration, pain. The radiographic image shows extended periodontal space, which is „U‖; „V‖; or sandglass shaped. Cementiculi can develop within the periodontal space and hypercementosis can occur on the apical portion of the root.
Two types of forces can reach the tooth. One way, or orthodontic type forces are present if resorptive and rebuilding processes induced by orthodontic movement are not evenly distributed, because of over forcing.
Jiggling type forces create resorptive forces on both sides of the tooth. Widening of the periodontal space and bone destruction (together with increased mobility) will go on until adaptive measures compensate for high forces.
Occlusal trauma is not responsible for periodontal inflammatory diseases by itself, but forces exceeding adaptive capacity of the periodontium may trigger inflammatory processes. Several human studies proved that occlusal trauma contributes to the severity of plaque induced inflammation, and it even influences the success of the therapy in a negative way.
LESIONS OF PERI-IMPLANT TISSUES
Implant failures can be classified as early and late. Early failures develop around the implants before osseointegration. Late failures can affect implants in function. Implant loss can be due to overloading (improper size, surface characteristics, bone quality) or infection.
Alberktsson and Izidor applied the following definitions on implants, based on definitions related to natural dentition:
Peri-implant mucositis: reversible soft tissue lesion around implants
Peri-implantitis: inflammation affecting osseointegrated implants in function, resulting in supporting bone loss Incidence
The longest study on periimplantitis was conducted by Roos and Jansaker (implants placed 9-14 years ago).
They found that 16% of study subjects and 6.6% of implants were affected. According to Zitzmann and Berglundhs, who refined the criteria, over 56% of patients and 28% of implants revealed a lesion.
Periimplantitis had a 2-10% prevalence in a 5-year period. Peri-implant mucositis was present in more than two-thirds of the patients with implants in function for 9-14 years.
Risk factors
Based on available data, peri-implant and periodontal infections have a lot of risk factors in common. Peri-implant diseases are much more likely to occur in patients with a history of periodontitis, smoking, inadequate
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oral hygiene or local disturbing factors present. Further risk factors are diabetes mellitus and genetic factors (IL-1 gene polymorphism). Overloading does not cause bone resorption by itself but facilitates inflammation.
Characteristics of the lesion
Plaque induced changes in the peri-implant mucosa are similar to gingival inflammation in the first three weeks.
Following this, fibroblasts appear in a much higher number in the inflamed gingiva than in the mucosa. Apical and horizontal spread of the lesion is much wider, reparation is much less pronounced. Inflammatory cells are widespread in the mucosa, inflammation is much less contained. (bordered)
A large portion of the soft tissues gets infiltrated. A large number of inflammatory cells (macrophage, plasma cell, lymphocyte) appear in the histological specimens. The biofilm is not separated from the connective tissue by an epithelial barrier. A large number of PMN cells are present in the lesion, even further away from the implant surface, perivascularly. Elastaze-activity and lactoferrin-concentration is higher in the sulcus in periimplantitis compared to the healthy mucosa.
The composition of the biofilm is similar in periodontal and peri-implant lesions.
Symptoms:
Bone resorption on the radiographic image. Inflammatory signs (swelling, reddish peri-implant mucosa, bleeding on probing, suppuration) are noticeable in peri-implant soft tissues. Stability of the implant is maintained for a long time.
Peri-implantitis
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Radiological signs of peri-implantitis
6.16. Periodontitis and systemic diseases. Focal infection (Péter Vályi DMD - László Párkányi DMD)
It has been suspected since the time of Hippocrates that oral diseases can have an effect on systemic diseases.
From the late 19th century till the beginning of the 20th century, „oral sepsis‖ and „focal infection‖ were well known terms, but pointless and brutal tooth extractions did not fulfil expectations: systemic conditions did not improve in most patients after the treatment. As a result of modern diagnostic procedures and broader immunological knowledge, in the late 20th century studies confirmed that oral infections can cause damage to distant organs and can influence the development of systemic diseases.
DENTAL FOCUS OF INFECTION
Focal infection is a chronic, isolated, symptomless inflammation, from which bacteria or their toxins and antigens spread to distant organs, where they provoke inflammatory and immune reactions, causing secondary diseases. Focal infections can be categorised based on their relation to the oral cavity (open, closed) or by aetiology (periodontal, endodontic). There are major differences between periodontal and endodontic infections in duration, possibility of spreading (bacteraemia–involved surface area) and incidence (bacteraemia can develop from periodontal pockets during daily oral hygiene or even chewing), as well as in number and types of bacteria. Some bacteria spread directly to specific organs (e.g.: T. forsythensys and P. gingivalis prefer the endothelium); this is called tropism. There are also differences in the frequency of clinical symptoms. The spread of bacterial products can be direct or indirect. Classification of focal infections, ways of spreading and target organs are listed in the table below:
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Classification of dental foci, ways of spreading and target organs
The damaging effect of focal infections is also due to the special anatomical conditions: bacteria can get from the oral cavity directly to the heart through veins, and form there directly into the systemic circulation without passing through the liver, which plays a major role in immune responses. Adhesion to Kupffer cells (fixed macrophages) in the liver causes increased adhesion of granulocytes and release of chemotactic substances, cytokines, which activate further components of the immune system. Passing by this mechanism, pathogens can easily get to targeted organs. In the targeted organs they need to attach and reproduce. Previous chapters mentioned the virulence factors of bacteria which can dodge immune responses and secure their survival in targeted tissues.
Focal dental infections trigger destructive procedures not only by the spread of bacteria themselves (metastatic infection) but also by releasing toxins (metastatic damage)). In this case, these toxins can be isolated, and linked to specific bacteria, and their antigens provoke immune response and inflammation in the target organs (metastatic infection). Antigens of these toxins act as super-antigens (toxic shock syndrome), furthermore they can lead to autoimmune diseases by cross-reactions, stimulating the production of autoantibodies.
SECONDARY DISEASES IN TARGET ORGANS
Quite rarely, severe infections can spread from the head and neck region directly between cervical muscles, mediastinum, cranium (cerebral abscess) and sometimes to masticatory muscles. Infection in the sinuses and deeper facial tissues is much more common.
From digestive system diseases, Helicobacter pylori can persist in periodontal pockets maintaining underlying diseases, e.g. duodenal abscess. Periodonto-pathogenic bacteria may be the aetiological factor of autoimmune inflammatory intestinal diseases (P. gingivalis).
Long-term artificial respiration or aspiration among frail elderly patients can lead to respiratory infections, caused by oral pathogens. Relationship between pneumonia, lung abscess, COPD and periodontitis is confirmed by epidemiological studies.
Inflammations originating from the head and neck region can lead to autoimmune diseases of the kidneys through antigen-triggered immune complexes in the target organ. Possible relationship between dental infections and liver abscesses have also been mentioned in some studies.
Ophthalmological (uveitis, endophthalmitis) and dermatological (erythema nodosum, pustulosus palmo-plantaris) diseases have also been linked to dental infections as aetiological factors, with some supporting
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evidence. Joint diseases have also been related to dental infections, but evidence is lacking to prove this hypothesis. Relationship with cardiovascular, genital diseases and diabetes mellitus will be detailed in Chapter 5.13.