Periodontitis

PERIODENTITIS (periodontitis, paradentitis), inflammation of the periodontium (pericementum, root membrane). The tissues surrounding the tooth are anatomically and physiologically interconnected and form a single biological system; therefore, inflammatory processes arising in the periodontium are not localized only within it, but also occur in the adjacent tissues surrounding the tooth: in the nearby bone substance, the bone marrow of the alveolus, and involve the cementum of the tooth root, etc. Therefore, for the last 10 years, it has not been customary to consider the pathology of the periodontium independently, without connection to the processes occurring in the entire complex of tissues surrounding the tooth, which are currently called the paradentium (paradentium, paradontum). The paradentium tissue system includes the cementum, periodontium, alveolar process, external periosteum, and gingiva. Damage to one of these three tissues (periodontium, cementum, alveolar process) necessarily affects the other two. The outer surface of the alveolar process is covered by the gingiva, which is a continuation of the oral mucosa. Directly beneath the gingival mucosa lies the external periosteum of the jaw's alveolar process. The gingival mucosa is covered by stratified squamous epithelium, the surface edge of which is shed from time to time during chewing and other mechanical actions. The gingival mucosa lies above the upper edge of the jaw's alveolar process, covering the lower third of the tooth crown and forming so-called gingival papillae between the teeth. The epithelium covering the connective tissue base of the papilla bends toward the enamel-cementum surface of the tooth, thus creating a depression known as the gingival pocket. The epithelium of the gingival pocket fuses with the Nasmyth's membrane of the enamel, so that the bottom of the pocket lies above the enamel-cementum boundary of the tooth. Only in pathological cases does the epithelium vegetate deeper along the cementum, thus rupturing the bottom of the pocket. The physiological gingival pocket is very shallow; under the influence of mechanical or other irritation, when the epithelium loses its connection with the Nasmyth's membrane and gradually begins to penetrate deep into the forming crevice toward the root surface, we have a pathological gingival pocket. Previously, a (physiological) gingival pocket was understood as the slit-like space lying between the gingival papilla and the lower third of the tooth crown, and it was believed that the bottom of this pocket lay at the level of the enamel-cementum boundary. The error of this concept has now been proven. Beneath the gingival epithelium lies connective tissue consisting of collagen fibers with an admixture of elastic ones. In the area of the papilla up to the enamel-cementum boundary, this tissue does not have a regular direction, is loose, and differs from the underlying layer, called the "ligamentum circulare dentis" (circular ligament). This ligament lies between the enamel-cementum boundary of the tooth and the upper edge of the alveolar process. The connective tissue bundles that make up the circular ligament have specific directions. According to Witzel, they run in the following order: from the neck of the tooth, fibers run obliquely to the lingual and labial surfaces of the gingiva, ending in its connective tissue. The second group of fibers, the circular one, encircles the neck of the tooth, runs parallel to the upper edge of the alveolus, and is fixed to the soft tissues surrounding the tooth. The proximal surfaces of adjacent teeth are connected by means of fibers running in a horizontal, and at times in an oblique, direction. The fourth group of fibers runs from the neck of the tooth obliquely and ends in the external periosteum of the alveolus on the lingual and buccal surfaces. This entire system of fibers encircles the neck of the tooth, creates a tightly closing ring around it, which, along with the periodontium, plays the role of a supporting and fixing apparatus for the tooth. A continuation of this ring is the connective tissue of the periodontium, which fills the entire space between the surface of the tooth root and the inner wall of the alveolus. The thickness of the periodontium in the upper jaw (according to Weski) is 0.2–0.25 mm, and in the lower jaw 0.15–0.22 mm. The periodontium consists of dense connective tissue bundles having a more or less horizontal direction in the upper part, and an oblique one in the rest, with the upper part of the bundle line being at the alveolus and the lower part going toward the cementum, obliquely toward the apex. In the apical part, which is looser, the fibers take on a horizontal direction. The connective tissue bundles of the periodontium are intertwined with each other. Between them are areas of loose tissue surrounding the vascular and nerve bundles that nourish the periodontium. The connective tissue fibers of the tooth ligament (periodontium) end at one of their ends in the mass of the alveolus, forming so-called Sharpey's fibers, and at the other end transition into the cementum. Thus, this ligament, on one side adjacent to the inner surface of the alveolus, serves as its periosteum, and on the other side, transitioning into the cementum, is the periosteum of the cementum—the pericementum. In the first case, the cells running along the alveolus are carriers of osteoblasts, and in the second, of cementoblasts. Between the elements of the connective tissue of the periodontium, clusters of epithelial cells are found, epithelial rosettes, so-called "debris epitheliaux paradentaires Malassez" (epithelial paradental rests of the enamel organ). The circulatory system of the periodontium is extremely richly developed. Penetrating from the depth of the alveolar floor and from the alveolar processes of the bone together with the vessels nourishing the pulp and the tooth ligament, the blood vessels form an extremely rich, branched network permeating the entire tissue of the periodontium up to and including the papillae. The entire circulatory system of the periodontium, in the form of glomeruli, plexuses, etc., anastomoses with the nearest vessels of the bone, which ensures the proper inflow and outflow of blood. The lymphatic system is even more developed and is connected by anastomoses with the lymphatic vessels of the bone system. A healthy periodontium is a very strong, stable formation. It can withstand pressure during chewing of up to 100 kg. The alveolar process of the jaw is divided by means of bony septa into individual cells, each corresponding to the root of a tooth. The cell consists of bony plates, which on the labial and lingual surfaces merge with the compact mass of the jaw body. The interalveolar septa, pointed toward the tooth neck and widened at the base, consist of spongy bone substance, bounded on the sides by plates of compact bone mass. On the floor of the alveolus, there is an opening for the passage of the neurovascular bundle, and the interdental septa are perforated by small canals through which vessels and nerves penetrate into the periodontium tissue. The alveolus, corresponding to the shape and direction of the tooth, is immobile and resists the pressure and tension to which the tooth is subjected. The function of the apparatus supporting the tooth is mainly mechano-static. It is expressed in the counteraction to the pressure that the tooth experiences during chewing. The pressure exerted on the crown is distributed to the root, the soft tissues surrounding it, and the tooth alveolus. The apparatus in which the tooth is included does not represent a static system in which individual parts are immovably connected to each other. A certain mobility of the tooth is possible and exists. It is caused not by elastic tissue, which is not present in the tooth ligament, but by the special arrangement of collagen fibers in the periodontium. The latter, in a state of rest, are free, not stretched, and wavy. This circumstance, as well as the special structure of the vascular system of the paradental tissue, ensures a certain mobility of the tooth. The relative physiological mobility of the tooth is not the same in all periods of a person's life and apparently also fluctuates in different individuals. In a young organism, in which the growth of the jaws is not yet finished and where, consequently, the periodontium is thicker and looser, the mobility of the tooth is greater. In old age, the mobility of the tooth weakens due to the loss of elasticity of the fibers themselves. In addition to age-related factors, individual characteristics also have significance. The connective tissue of the periodontium does not have the same morphological structure in individuals of different constitutions. Even long before the modern doctrine of constitution, Baume, in his manual on dental diseases, stated that "in some individuals there exists a certain predisposition to inflammations of the root membrane." He refers to Mummery, who, on the basis of statistical data, proves that "some people suffer from inflammation of the periodontium more often than is encountered in others." "The character of the periosteum apparently exerts a significant influence; teeth weakly anchored in their alveoli, having consequently a thicker root membrane, are apparently more often subjected to periodontitis than teeth firmly fixed in the alveolus by a thin and tightly stretched periosteum; until now, little attention has been paid to these predisposing factors." As can be seen, Baume quite definitely attaches importance to the structure of the connective tissue of the periodontium in the development of pathological processes. A thick or thin periodontium, tightly stretched or loose, i.e., fibrous or loose, is evaluated by Baume as tissue that reacts differently to a pathogenic factor. In reality, upon careful histological study of the periodontium tissue, it is seen that its connective tissue presents various degrees of morphological variations.

There are periodontal tissues consisting of dense fibrous connective tissue poor in cells, and of delicate loose tissue. The periodontium, which performs the function of a ligament fixing and supporting the tooth in the alveolus, has a coarser structure in the lateral section than in the apical part. When studying pathological processes occurring in the periodontium, especially in its apical part, the morphological structure must be taken into account. Without considering this point, a whole series of phenomena will be incomprehensible. Inflammation of the paradentium—paradentitis (periodontitis)—is divided by localization into apical paradentitis (at the apex of the tooth root) and marginal. Etiological factors can be infection, trauma, and medications used in dental treatment. Most often, infectious apical paradentitis is encountered as a consequence of putrid decay of the tooth pulp. The gangrenous mass of the root canal content, in the presence of a wide apical foramen, has direct contact with the periapical tissue. In the absence of direct contact of the canal content with the periodontium, the food mass filling the pulp chamber of a tooth destroyed by caries pushes the root canal content beyond the apical foramen. The putrid mass of the root canal can also be pushed beyond the apical foramen during mechanical cleaning of the root canal with nerve extractors, Miller needles, and similar instruments. In a closed gangrenous tooth, putrid gases push bacteria beyond the apex with their pressure. Purulent, diffuse melting of the entire coronal and root pulp can also cause apical paradentitis. From the point of view of pathological anatomy, apical paradentitis is divided into exudative and proliferative. The first form is encountered most often in acute cases, the second in chronic ones. The causative agents of infectious apical paradentitis are most often streptococcus and staphylococcus; anaerobic infection is also possible. Specific causative agents—actinomycetes and the tuberculosis bacillus—are rarely encountered. Acute and chronic apical paradentitis of infectious origin are distinguished. Clinical picture: in the initial stage, in the first 12-24 hours, a previously insensitive tooth becomes very sensitive to percussion upon pressure or eating. Subsequently, pain from touching the tooth intensifies, chewing on this side becomes impossible, and a sensation arises that the tooth has seemingly lengthened. Simultaneously, continuous spontaneous pains appear, at first dull, then acute, pulsating, and agonizing. Intake of hot food or drink intensifies the pain; cold relieves it for a very short period of time. Due to the agonizing pains, sleep is lost. The submaxillary lymph nodes increase sharply in volume and become painful. After 1-2 days, swelling of the gingival mucosa of the corresponding tooth and sometimes of neighboring teeth appears, the transitional fold of the cheek smooths out, then the cheek swells, and collateral edema of the lower, and sometimes the upper eyelid (when the process occurs in the upper jaw) forms. The accumulated pus breaks through into the submucosa of the alveolar process, forming a gingival abscess on the labial or buccal, less often on the lingual surface and on the hard palate. Sometimes a fistula forms on the chin or cheek. The temperature rises to 37.2-37.8° and even to 39-39.5°. When the pus is emptied into the oral cavity or extraorally, all acute phenomena begin to subside: the temperature drops, pains become less, the swelling disappears completely, and the acute process transitions into a chronic one. The formed fistulas of the cheek, chin, and gum do not close completely until the offending tooth is extracted or subjected to apicoectomy. The process does not always proceed in the manner described above. Sometimes all phenomena take on a more violent character. Limited paradentitis becomes diffuse. Pain upon percussion is felt not in one, but in a group of teeth; the purulent infiltrate captures the territory of the mucosa of several teeth. The latter become mobile, strong swelling of the cheek appears, and its skin becomes dense and shiny. Subsequently, a sharp picture of perimaxillary phlegmon is obtained. If the process occurs in the lower jaw in the region of the 7th and 8th teeth, the masticatory muscles are involved, and trismus of the jaw occurs. The general condition is severe, the temperature is high, the pulse is rapid, and there are chills. In almost all such cases, leukocytosis is noted, which is rarely encountered in ordinary apical paradentitis; the number of band neutrophils increases, young forms appear, and sometimes the number of eosinophils decreases. The described picture corresponds no longer to apical paradentitis, but to acute osteomyelitis (for details, see Osteomyelitis). In the initial stage, it is difficult to differentiate acute apical paradentitis from incipient osteomyelitis, because the pathological-anatomical boundary of apical paradentitis and osteomyelitis is almost always blurred. Furthermore, every acute apical paradentitis, from the point of view of topography, is simultaneously to a certain extent a limited apical ostitis and apical osteomyelitis. Pathological-anatomical picture: sharp hyperemia of the periapical part of the periodontium in the initial stage (the first few hours) is accompanied by extravasates and serous infiltration of the tissue. With the appearance of abundant infiltration by polymorphonuclear leukocytes, purulent melting of the apical periodontal tissue begins. The adjacent bone trabeculae of the alveolar floor are resorbed, and the delicate tissue of the bone marrow becomes permeated with leukocytes and loses its structure. The pus breaks its way through the entire wall of the alveolus, accumulating under the periosteum, in the submucosa of the gum or hard palate. Thus, the periodontium, bone, bone marrow, external periosteum, and gingival mucosa are involved in the process. Sometimes the pus breaks its way not through the wall of the alveolus, but between the cementum and the periodontium or between the periodontium and the alveolus, rising (in the lower jaw) or descending (in the upper jaw) to the alveolar margin and destroying along the way the so-called circular ligament of the tooth. In such cases, the pus is emptied from the gingival pocket. Therapy. It is necessary to open the offending tooth and pass through the root canal to provide an exit for gases and pus. This measure often reduces pain. Gingival, palatal, and cheek abscesses must be opened. To reduce pain during infiltration of the surrounding tissues, various types of dry heat are prescribed—heating pads (water, electric) and light (Sollux, blue lamp, etc.). X-ray irradiation. Internally, painkillers (pyramidon 0.3 two to three times a day). Multi-rooted teeth are subject to extraction. Well-preserved central and lateral incisors, canines, and premolars (of the upper and lower jaw) can, after the disappearance of acute phenomena, be subjected to an apicoectomy operation and thus be saved. Chronic apical infectious periodontitis. The outcome of acute apical paradentitis can be complete cure upon apicoectomy or a transition to a chronic state. The exudative form, which prevails in acute inflammation, gradually transitions with the emptying or resorption of pus into a proliferative one, characterized by the formation of granulation tissue in the periapical region. Over time, the proliferated granulation tissue resorbs and destroys the bone substance of the alveolus and the body of the jaw (for details, see Granulomas, Granulomatosis—dental granuloma). More often, chronic apical paradentitis proceeds from the very beginning in the form of granulating periodontitis. Treated and untreated gangrenous teeth, as well as depulped teeth resulting from inflammation of the tooth pulp, have a chronically inflamed apical periodontium in the majority of cases. Clinical picture—subjective sensations are absent, gingival fistulas are often encountered, and X-ray examination reveals widening of the periodontal space or a sharply defined granuloma or cystogranuloma. Pathological-anatomical picture of chronic apical paradentitis. Instead of normal periodontium in the apical part, one finds proliferated granulation tissue, sometimes younger, sometimes more mature, rich in lymphoid cells, plasma cells, mast cells, macrophages, and eosinophils. The floor of the alveolus is ulcerated and lacunarly resorbed. In the apical part of the root, the cementum is eaten away and lacunarly eroded. The granulations are often surrounded by a fibrous connective tissue ring. Upon extraction of a tooth affected by such a process, a loose piece of flesh the size of a pinhead, a pea, or larger is found on the root apex. Therapy. Drug therapy, which has been used until recently, has not justified itself. All attempts to sterilize the canal with the help of various chemical and antiseptic substances have not been crowned with success. Often, the disinfection of the root canal achieved turned out to be temporary: the canal became infected again after a very short period—2-4 weeks. Therefore, for the time being, only the extraction of the corresponding tooth or resection of the root apex with removal of the granulating focus can be considered a radical method of therapy for chronic apical paradentitis.

Healing of chronic apical periodontitis can sometimes occur if natural obliteration of the root canal and its regio ramificationis takes place, and, accordingly, there is a complete cessation of infection access to the surrounding periapical tissue. According to the doctrine of oral sepsis (see Sepsis), teeth affected by chronic apical periodontitis, even those proceeding latently, represent a chronic infectious focus from which infection can penetrate via the bloodstream and lymph into other tissues and cause a whole range of chronioseptic and toxic diseases. Weber and Pesch examined 119 apical granulomas, and all proved to be infected. Feldman and Gutner examined 146 granulomas and granulating apical processes and established the following: 1) In every apical periodontitis at any stage of its development, there is the presence of pathogenic microflora; there are no so-called sterile apical processes. 2) A positive finding during bacteriological examination was obtained both in acutely developing apical periodontitis, during the exacerbation of a chronic process, or in a chronic, subjectively completely unnoticeable granulating apical focus. The cited circumstances, as well as the crisis of medicinal therapy for pulpless teeth that has emerged over the last decade, compel modern odontology to seek methods of radical therapy for chronic apical periodontitis. Acute and chronic hematogenous apical periodontitis arise as a result of the introduction of infection via the bloodstream and lymph into the apical periodontium. Clinical picture: In a completely intact tooth or group of teeth not affected by a carious process, all characteristic signs peculiar to apical periodontitis appear. X-ray reveals greater or lesser destruction of periapical tissues, a sharp decrease in the reaction to an induction current. Trepanation of the tooth is painless. The pulp is putridly decomposed, ichorous. Therapy: in cases of small destruction of periodontal tissue—apicoectomy; in more extensive cases, i.e., in the presence of a cyst—the corresponding operation. Acute and chronic marginal periodontitis arise as a result of trauma to the edge of the gum (with the addition of infection) by a sharp crown edge, a clasp, a prosthetic hook, heavy dental calculus deposits, overhanging fillings pressing on the gum, toothpicks, etc. Elimination of the etiological factor quickly leads to healing even in those cases where there is a small abscess at the edge of the gum. The abscess must be opened. Small growths in the gingival pocket can be mechanically removed. It is useful to cauterize once or twice with a weak solution of 5% chromic acid, resorcinol, etc. Traumatic apical and lateral periodontitis: A blow, a fall, or a bruise can cause a fracture of the tooth in the root part, as well as the loss of the entire tooth. Infection almost always joins periodontal trauma. Acute traumatic lateral and apical periodontitis can sometimes arise during canal preparation with a drill or bur when the lateral wall of the root or its apical part is perforated. Clinical picture: in case of a tooth fracture in the root part, the fragment is slightly mobile, the mucosa is sharply edematous and painful. Avulsion of the tooth from the bottom of the alveolus and instrumental damage to the periodontium give the picture of acute apical periodontitis. Pathoanatomical picture: when infection joins the trauma, this acute inflammation of the apical and lateral periodontitis has an exudative character, gradually passing into a proliferative form. Therapy: teeth avulsed from the bottom of the alveolus, as well as those fractured in the root part, must be reinforced with a splint and temporarily taken out of articulation, for which the bite should be raised. Rest often contributes to healing and recovery, especially if infection is absent or weak. Prognosis for lateral and apical periodontitis caused by instrumental perforation during the widening of the root canal of a devitalized tooth is poor. The acute process passes into chronic granulating periodontitis, and only in the absence or weakness of infection can one expect healing. Chronic traumatic apical periodontitis is the result of chronic, slowly acting trauma or the outcome of an acute process. Gradual overloading of one or a group of teeth by an excessively protruding antagonist, an incorrect prosthesis, or certain harmful occupational habits [e.g., in seamstresses (the habit of biting off thread with front teeth), in musicians playing wind instruments, etc.] leads to the crushing of the apical periodontium, to the rupture of the neurovascular bundle nourishing the tooth, and to the death of the pulp. Accidental trauma, often unnoticed by the patient, which caused the rupture of the neurovascular bundle with subsequent death of the tooth pulp, leads to chronic apical periodontitis. Clinic: chronic apical traumatic periodontitis proceeds unnoticed. The appearance of a fistula near intact teeth suggests the presence of inflammatory changes in the periapical region. An accidental X-ray examination or a change in the color of the tooth signals the presence of a process in the apical periodontium. Therapy: elimination of the cause, if it still exists, and the same treatment as for infectious apical periodontitis. Medicinal or chemical apical and marginal periodontitis: Medicinal periodontitis, both apical and marginal, are the result of the action of medicines and chemicals used in the therapy of complicated caries (pulpitis and gangrenous teeth). As Feldman's studies on dogs, cats, and other animals have shown, all medicinal substances used by conservative dentistry, both for temporary dressings intended to disinfect the root canal and when filling the root canal with pastes containing various medicinal mixtures, irritate, cauterize, and necrotize the periapical tissue to one degree or another. Inflammatory phenomena caused by medicinal substances are of varying intensity and depend, all other conditions being equal, on the structure of the root canal, the width of the apical foramen, the degree of branching of the regio ramificationis, the structure of the periodontium (density, fibrousness), the age of the patient, and the reactive capacity of the individual. Apical periodontitis arising as a result of treating a tooth with inflamed pulp is often not a consequence of the spread of pulp inflammation to the periapical tissue, but is caused mainly by the medicines used in the treatment and filling of the root canal. Arsenious acid (As₂O₃), used for devitalization of the tooth pulp, often causes periapical periodontitis, especially in childhood, as well as in adults when the paste remains in the tooth for more than one or two days. Apical periodontitis after the application of As₂O₃ occurs even when all existing rules for using arsenious paste are observed. This circumstance depends on the form of inflammation, the structure of the pulp, the topographo-anatomical features of the tooth, and the constitution of the patient. Some people are extremely sensitive to arsenic and sometimes, already a day after the application of arsenious paste, come with complaints of periodontitic pain. Clinical signs of apical arsenious periodontitis are almost the same as in infectious apical periodontitis, only more weakly expressed. Pain upon percussion, pressure, slight spontaneous pain. Rapid extirpation of the pulp reduces all painful phenomena. At times, slight pain upon percussion remains for 1–2–3 weeks. Arsenious apical periodontitis is caused by the penetration of arsenious acid through the apical foramen. Heinze managed to detect traces of As₂O₃ in the apical periodontium after only 24 hours. Feldman, in experiments on animals, saw lateral damage to the periodontium and the alveolar septum after a day, caused by the diffusion of arsenious acid through the dentinal tubules. The intensity of inflammatory changes in the periapical tissue varies within wide limits in different cases, manifesting as hyperemia and edema, focal or diffuse infiltration with lymphoid cells, formation of abscesses, resorption of cementum and dentin, the apical part of the root, and the bone tissue of the alveolar floor. Marginal arsenious periodontitis is caused exclusively by the accidental contact of arsenious acid with the gum papilla during application into the tooth cavity or by the sucking of this paste from the carious cavity of the tooth when the dressing applied to the tooth is not sufficiently hermetic. Arsenious paste, getting onto the papilla, spreads deep into the alveolus, damaging the periodontium and the alveolar bone tissue. The necrosis of the papilla that has begun may be limited only to the area of the gum adjacent to the cavity of the carious tooth, but necrosis of the alveolus and sequestration of the latter together with the tooth is also possible. The ulcerated surface of the papilla, covered with a grayish coating, is painful. The tooth subsequently becomes mobile and sensitive to palpation. To stop the process in case of spread necrosis of the alveolus, it is better to extract the tooth immediately. Using antidotum ars. in such cases is pointless.

Prophylactically, it is necessary to apply arsenious acid paste with maximum caution and observe a strict time limit of 24-48 hours. Similar to arsenious paste containing pure arsenious acid, a paste made from Scherbenko-Balt (Arsenicum metallicum), which is also used for pulp devitalization, acts on the apical and marginal periodontium. The Scherbenko-Balt paste, containing a smaller amount of arsenious acid, acts more weakly, more gently, and more slowly, but is also capable of causing a picture similar to the one described above. Medicamentous apical periodontitis is also caused by pastes used to fill the root canal. The latter contain various medicinal mixtures, which include phenol, chlorophenol-camphor, thymol, eugenol, clove oil, formalin, tricresol-formalin, and a number of others. All these antiseptic substances, as recent studies have shown, cause chronic apical periodontitis. The most destructive of the listed preparations for periapical tissue is formalin. In dogs, it causes sharp destructive phenomena not only of the apical periodontium but also of the lateral one (evidently caused by the diffusion of formalin through the dentinal tubules and cementum). Furthermore, formalin possesses the property, discovered by Feldman, of causing so-called periodontitis ossificans, i.e., simultaneously with the phenomena of inflammation, to lead to metaplasia an exudative process in the form of serous or fibrinous peritonitis, which eventually leads to adhesive periduodenitis. The clinical significance lies precisely in those adhesions with which all these processes end. The most frequent cause of the development of periduodenitis is gallbladder disease, specifically calculous cholecystitis (see Vol. VIII, art. 415, fig. 8). The reason for the development of adhesions in the area of the duodenum is often also diseases of the stomach, colitis of the flexura hepatica, and finally, diseases of the vermiform appendix in its abnormal position. Among other etiological factors, one should point to trauma, acute or chronic, in the area of the duodenum, and finally, trauma caused by surgical interventions in this area (especially the placement of tampons after operations on the biliary tract). Pathoanatomically, adhesive periduodenitis presents various pictures: in the mildest forms, narrow or more or less wide strands and connective tissue bridges are formed, extending from the anterior surface of the intestine to the lower surface of the liver or to the gallbladder. In the most severe forms, it is a matter of the formation of a thick layer of diffuse adhesions occupying the entire area between the liver, duodenum, stomach, transverse colon, and the anterior abdominal wall. Between these two extremes lies the whole variety of transitional stages. In the relatively rarely observed callous ulcers of the duodenum, the ulcer itself, together with the developed periduodenal deposits, can produce a large inflammatory tumor palpable through the abdominal walls. Adhesive periduodenitis rarely gives a clearly expressed clinical picture. In many cases, it does not manifest itself with any symptoms; in others, it is difficult to determine whether the symptoms depend on periduodenitis or the underlying disease or on the involvement of other neighboring organs in the process. As a consequence of periduodenitis, the following symptoms are noted: heaviness and pain in the epigastric region after eating; sometimes late pains (hunger pains); vomiting is usually absent; nevertheless, as a result of the pain and the fasting forced by it, patients lose weight and reach a state of severe exhaustion. In themselves, these symptoms are also characteristic of a duodenal ulcer, but a distinguishing feature is the absence of gastric and intestinal bleeding. A reference point for differential diagnosis can in certain cases be the radiographic picture: a clearly expressed fixed position of the pylorus to the right and upward and sometimes pocket-like protrusions of the walls of the duodenum. In those cases where periduodenitis is caused by cholecystitis, one can observe displacement and fixation of the pylorus, the bulb of the duodenum or its descending part in the area of the gallbladder, i.e., dextroposition of the pylorus; further, difficult unfolding of the duodenum, an elongated position of its upper knee, and a sharp angular bend in relation to the descending part of the intestine. The movement of contrast masses is slowed down despite increased peristalsis. On the basis of the cited symptoms, it is possible with some probability to exclude an ulcer, on the one hand, and gastric neurosis, on the other. In the course of chro- connective tissue fibers of the periodontium into osteoid and bone tissue, leading in places to the fusion of the alveolus with the roots of the tooth. Treatment of the root canal with strong antiseptic substances, such as hydrochloric and nitric acids, aqua regia, antiformin, etc., does not remain without influence on the periapical tissue. In general, it is necessary to say that all medications used both for the preservation of the root pulp and for the lifelong disinfection of the root canal not only do not achieve their goal but directly harm, irritate, cauterize, and cause inflammatory phenomena of varying intensity in the surrounding periapical tissue. The prophylaxis of apical periodontitis, insofar as they are the result of inflammation, death of the pulp, and subsequent medicinal treatment, comes down to the fight for a healthy pulp, for the treatment of uncomplicated caries, and for the sanitation of the oral cavity of the adult and child population. The fight against caries and the treatment of its initial stages predetermines the fight against apical periodontitis.