Marginal destruction of bone tissue. What is destruction (destruction) of bones? "Focus of destruction" in books

Date of: 04.03.2020

Bone destruction, in which bone beams are destroyed with their replacement by pathological tissue, always occurs in inflammatory and neoplastic processes. Focal destruction, depending on the etiology, has a peculiar display on the radiograph. The contours of the focus are usually unsharply outlined and vague.

Extensive bone destruction (destruction) of the vertebral bodies with the formation of large sequesters

Relatively large destructive foci with a diameter of more than 5-6 mm are easily detected by X-ray examination. The ability to recognize destructive foci depends not only on their size, but also on their location in the bone.

Foci located in the central sections of a normal bone mass may go unnoticed even with their relatively large sizes, while foci located in the cortical substance are relatively easy to detect. For successful recognition of destructive foci, especially in the early phases of development, a thorough methodical examination of the bone is necessary not only in two, but sometimes in additional special projections. A tomographic study is especially useful.

In the x-ray image, the destruction can be of varying degrees of focality, vastness, and can be located centrally (inside the bone) or superficially.

Huge cavities (caverns) in the femur and tibia with multiple tuberculous osteitis

Depending on the cause that caused it, destruction is called inflammatory, tumor, etc. However, destruction is a symptom, and in order to correctly identify it, you must first accurately establish the diagnosis. Therefore, it is unlikely that destruction should be etiologically characterized before establishing a diagnosis. You should simply describe its size, shape, contours, location, reaction of the surrounding bone.

Bone cavities, or cavities, are formed when total destruction all bone beams in the area of the destructive focus with the formation of more or less clearly defined walls. They may have different shape and sizes. Naturally, bone caverns are easier to detect on x-ray than small destructive foci, although here, too, the size of the cavities and the depth of their occurrence in the bone, as well as the thickness of the affected bone, are of great importance.

Destructive changes in bone tissue appear mainly 4-5 months after the onset of the disease. However, this is often the first objective sign of the disease. When a lesion appears in the bones, children become restless, but complaints of pain in the affected areas were noted only in children older than 1.5 years. Foci of destruction are determined first in the form of a dense swelling of the bone tissue with a gradual softening of it from the center to the periphery. For example, we give the following case history.

Lena S., born on March 8, 1959. A child from the 1st pregnancy. The parents are young. Pregnancy and childbirth proceeded normally. The girl was born with a weight of 3200 g. At birth, there were changes in the skin (the child was born "all in the husk", which quickly disappeared).

She was breastfed up to 1 year 1 month, complementary foods were introduced in a timely manner. She grew and developed correctly. At the age of 3 months, she suffered from purulent otitis media, which did not respond to antibacterial treatment. At the age of 1 year, for a month and a half, the child vomited for no apparent reason.

The present illness began acutely at the age of 1/2 in October 1960, with a rise in temperature to 39-39.7°C, pain in the ears, the appearance of a small papular rash on the chest and back, and lesions of the mucous membrane (stomatitis). The temperature was maintained for 10 days. Symptomatic treatment of skin phenomena and mucosal lesions, regarded as exudative diathesis and stomatitis, was carried out. Soon, purulent discharge from the ears appeared, there was a lesion of the skin of the scalp in the form of yellowish crusts against the background of hyperemia. Roseolous-papular lesions with yellowish crusts on the skin of the body spread to the abdomen, captured the external labia, the mucous membrane of the external genital organs. There were hyperemia and ulceration at the site of the lesion. Damage to the mucous membrane of the genital organs was accompanied by purulent discharge from the vagina and severe pain during urination. An ulcerative process with necrosis was also found on the gums. Destructive changes in the bones of the skull were detected 5 months after the acute onset of the disease. A blood test revealed a slight leukocytosis (up to 12,000 in 1 mm) and an accelerated ESR - up to 30 mm/h.

The diagnosis of Letterer-Zieve disease was made on the basis of characteristic skin changes, lesions of the mucous membranes, and the appearance of destructive changes in the bones of the skull. The appointment of periodic short-term courses of treatment with prednisolone for 3-5 days and 7-14 days gave a temporary improvement with a significant deterioration in the condition when it was canceled, and only long-term treatment with medium doses of prednisolone gave a positive result.

To illustrate the gradual development of the disease, we present the following observation.

Borya A., born December 29, 1959. Pregnancy 1st. Parents are young and healthy. During pregnancy, the mother noted constant pain in the lower abdomen. During childbirth, labor was stimulated.

The child screamed immediately. Birth weight 3900 g, height 53 cm. During the neonatal period, the umbilical wound festered for about 20 days. From 3 months he was supplemented with dry mixtures. Up to 6 months, the child grew and developed normally, did not get sick with anything. I got sick for the first time at the age of 6 months purulent otitis media who did not succumb antibiotic therapy. Anorexia appeared, he stopped gaining weight, but psychomotorly the boy developed correctly. During this period of time, the child was diagnosed with angina twice. At the age of 1 year, a rapidly increasing swelling behind the ear on the right appeared, which was regarded as a dermoid cyst. The tumor has been removed. Histological examination revealed a large number of reticular cells, eosinophils and single large cells with "foamy" protoplasm. Histological diagnosis: eosinophilic granuloma. IN postoperative period a fistula formed at the site of the scar, complicated by purulent lymphadenitis. At the age of 17 years, a second operation was performed - excision of the scar, followed by X-ray therapy in this area.

After 1.5 months, the disease worsened again. A pointed pink dry rash appeared on the skin in the area of the sternum and back. Behind the ear, at the site of the postoperative defect, a soft bulge 3X4 cm in size began to be palpated, a blurred exophthalmos was noted on the left. The shortening of the percussion sound in the interscapular region was determined. Wheezing was not heard, the liver protruded 4 cm below the costal arch, the spleen was palpated at its edge.

A blood test revealed normochromic anemia, ESR - 27 mm/h, blood cholesterol - 133 mg%. X-ray on the right parietal bone revealed 2 defects with uneven contours 3×3 and 1×1 cm in size. In the lungs, a significant uniform enhancement of the vascular and interstitial pattern was determined along with a large number of small foci.

The location of the rash and its nature, the presence of exophthalmos, bone defects, interstitial lung damage, enlarged liver and spleen, destructive changes in the flat bones of the skull, as well as histological examination data, indicate the presence of acute reticulo-histiocytosis (Letterer-Zieve disease). The child is dead. The diagnosis was confirmed by post-mortem examination.

Thus, in the initial period of Letterer-Zive disease, there are some characteristic clinical symptoms that come to light during a thorough questioning of the parents, in a detailed examination of the child.

Reticulo-histiocytosis is characterized by an undulating course of the disease with periods of relative well-being and deterioration. long time the process can be hidden, either not manifesting itself, or giving uncharacteristic disturbances in the general condition of the body.

Doctor of Medical Sciences, Associate Professor, Scientific Consultant of the Educational and Methodological Center "Exclusive Dent" (Kazan)

The assessment of the severity of inflammatory and destructive lesions of the bone tissue of the periapical region, the furcation zone and the interdental/interradicular septa is of key importance when planning the stages of diagnosis, treatment and rehabilitation of patients by dentists of any profile. This problem causes a lot of controversy when choosing orthopedic/orthodontic constructions, limiting the disruptive load, conservative/surgical management of patients burdened with endoperiodontal foci of infection (EPO).

Endoperiodontal focus of odontogenic infection is a combination of inflammatory and destructive processes in the apical periodontium and marginal periodontium. Given the aggressiveness of such foci of chronic infection, it is appropriate to mention the so-called endoperiodontal syndrome, in which there are systemic manifestations of microbial sensitization of the body: septic endocarditis, rheumatism, chronic pyelonephritis.

The issues of EPO etiopathogenesis have been discussed by domestic and foreign researchers for several decades, however, the issue of primary/secondary involvement in inflammatory process endodont/periodontal tissue remains unresolved.

To date, it has been postulated that the penetration of infectious agents - microbes and their toxins in the endodontic / periodontal system occurs by vascular system(by the vascular route) and through the main root canals, their branches, as well as through the dentinal tubules (by the tubular route).

Combined pulp and periodontal diseases are the cause of tooth loss in more than 50% of cases. Diagnosis is hampered by the fact that these diseases were previously studied as independent, and the similarity clinical symptoms often fell out of the field of view of specialists during differentiation, which is one of the factors of unsuccessful treatment of patients with this pathology.

The aim of this study was to develop an algorithm for assessing the severity of bone lesions in patients with endoperiodontal foci of infection.

We examined 98 patients with EPO (40 men and 58 women aged 22-72 years) who applied to the medical and surgical department of the Kazan dental clinic. medical university for the purpose of sanitation of the oral cavity and subsequent prosthetics. The full range of differential diagnostic measures included: analysis of anamnestic data, clinical examination of the patient, X-ray examination (targeted dental radiograph, orthopantomogram).

When collecting an anamnesis, we found out complaints associated with changes in the oral cavity (edema), the time of their occurrence, the dynamics of development, possible reasons and frequency of exacerbations.

When examining the oral cavity, attention was paid to the integrity/violation of the integrity of the periodontal attachment, the depth of the pocket, the nature of supra- and subgingival dental deposits, the presence/absence of granulations in the periodontal pocket and their nature (flaccid, cyanotic/juicy, prolapsing, bleeding), tooth mobility, the presence of fistulas (periapical or periodontal origin), the severity/smoothing of the phenomenon of stipling, the presence/absence of exudate (purulent, serous, hemorrhagic, or combinations thereof).

When analyzing the data of the X-ray method of research, the severity of the destructive process in the periodontium was assessed: with mild periodontitis, the initial degree of destruction of the bone tissue of the interdental septa was noted (significant fibrillation or disappearance of the endplates, the phenomena of intracortical, subcortical and trabecular osteoporosis, a decrease in the height of the interdental septa - less than 1/ 3 root lengths), moderate periodontitis is characterized by resorption of the bone tissue of the interdental septa from 1/3 to ½ of the root length, for severe periodontitis - bone resorption by more than 1/2 of the height of the interdental septa (until complete resorption of the alveolar septum).

When analyzing targeted dental radiographs, the degree of the destructive process in the periapical region was assessed: the size of the lesion (longitudinal and transverse), contours (clear/fuzzy), the tendency to merge periodontal and periapical foci of destruction.

In the course of our studies, we have identified the most common types of endoperiodontal lesions (illustrated by targeted dental images or fragments of orthopantomograms) (Fig. 1) .

A type of endoperiodontal focus, which is characterized by the expansion of the periodontal gap throughout, vertical destruction of the bone tissue of the alveoli. The cortical plate is partially preserved, with signs of subcortical osteoporosis; on the periphery of the focus there is a thinning of the trabeculae, an expansion of the intertrabecular spaces. The functional orientation of the trabeculae (vertical) is partially preserved. The height of the alveolar ridge is reduced.

As a rule, periodontal pockets are narrow and deep (up to 6-8 mm), filled with juicy (often prolapsing) granulations. Mobility of the 1st-2nd degree. Changing the axis of inclination of the tooth. We believe that a change in the direction of the disruptive load is essential in the formation of this type of destruction focus (Fig. 2) .

This type of endoperiodontal lesion is characterized by the presence of a focus of bone destruction in the periapical region with clear, even contours, round or oval. The integrity of the cortical plate is broken. Bone trabeculae along the periphery of the focus retain their functional orientation (horizontal), there are signs of a decrease in bone mineral density. Height alveolar process decreases due to resorption mixed type) trabecular bone of the alveoli.

Most common in multi-rooted teeth. Furcation bone defects (not associated with complications of endodontic intervention) are regarded as prognostically unfavorable factors. As a rule, changes in the position of the tooth in the dentition does not change. Periodontal pockets with a depth of not more than 5 mm, filled with flaccid cyanotic granulations. In 25% of cases, fistulas of periodontal and periapical origin are detected (differential diagnosis of the latter is difficult) (Fig. 3).

It is characterized by the presence of a focus of bone destruction with clear, even contours; often along the periphery of the focus, phenomena of increased bone mineral density are observed. The classic horizontal type of bone destruction forms "wide" periodontal pockets, the depth of which depends on the degree of bone loss. The pockets are often filled with flaccid granulations.

In later stages of the disease, the axis of inclination of the tooth may change and mobility may increase. An increase in the disruptive load can provoke an exacerbation of the disease. With the predominance of the extraosseous lever over the intraosseous one, the prognosis is unfavorable (Fig. 4).

This type of endoperiodontal focus is characterized by the presence of destructive bone changes with fuzzy uneven contours; on the periphery of the focus, pronounced phenomena of a decrease in bone mineral density are observed. Furcation defects often form with this combination.

In the later stages of the disease, the focus of bone tissue destruction in the septal area, spreading along the periodontal fissure, merges with the focus of destruction in the periapical region, resorption of the cement of the tooth root is possible, in more severe cases - of the dentin, which causes uneven contours of the tooth root. The axis of inclination of the tooth changes, it is possible to increase the mobility of the tooth even at early stages diseases. Periodontal pockets are deep, reaching the top of the tooth root, filled with abundant granulations. Increased disruptive load worsens the prognosis of the course of the disease.

The combination of chronic granulating periodontitis with a mixed type of destruction. It is characterized by the presence of a focus of bone destruction in the periapical region with fuzzy uneven contours; trabeculae along the periphery of the focus are thinned, their functional orientation is disturbed. The bone resorption of the alveolar crest is of a mixed type, however, in most of the observed cases, the vertical direction predominates. There is a tendency to merge periodontal and periapical foci. Possible resorption of the cement of the root of the tooth. Periodontal pockets are deep, often wide. The height of the alveolar process decreases, tooth mobility and a change in the axis of inclination occur in the early stages of the disease.

The combination of chronic granulating periodontitis with a horizontal type of bone destruction of the interdental/interradicular septa is characterized by the presence of a resorption focus in the periapical region with uneven fuzzy contours. On the periphery, the bone trabeculae are somewhat thinned, the functional orientation is not disturbed.

Root contours may be altered by hypercementosis (rare). Destruction of the alveolar ridge along the horizontal type, the periodontal gap is expanded throughout (the effect of functional overload). Periodontal pockets are wide; at later stages, fusion of periodontal and periapical lesions is possible. The height of the alveolar process decreases, a change in the position of the axis of the tooth and increased mobility are possible at advanced stages of the disease (Fig. 5).

Rice. 5a. Confluent focus of periodontal and periapical bone tissue destruction.

Rice. 5 B. Confluent focus of periodontal and periapical bone tissue destruction.

Rice. 5d. Confluent focus of periodontal and periapical bone tissue destruction.

The most severe and common variant of endoperiodontal lesions is a confluent focus of periodontal and periapical destruction. In most cases, it occurs under conditions of a long-acting increased disruptive load (a focus of traumatic occlusion). It is characterized by the presence of a significant focus of destruction, capturing the bone tissue of the periapical region and the bone tissue of the interdental septa; the latter are often completely resorbed. The unevenness of the contours of the root is due to the resorption of cement (dentin). Periodontal pockets are deep, reaching the apical part of the root, tooth mobility in all directions.

Thus, the marker radiological feature of the endoperiodontal focus of chronic infection is the focus of bone tissue destruction in the periradicular region of single-rooted and multi-rooted teeth in combination with the vertical type of destruction of the cancellous bone of the interradicular septa.

It is also possible to combine the destruction of bone tissue in the periradicular region of single-rooted and multi-rooted teeth with a horizontal type of destruction of the cancellous bone of the interradicular septa.

The merger of two foci of infection in the prognostic plan is extremely unfavorable and determines the indications for tooth extraction.

Literature

Balin V. N. Practical periodontology / V. N. Balin, A. K. Iordanashvili, A. M. Kovalevsky. - St. Petersburg: Peter Press, 1995. - 272 p.
Barer G. M. Therapeutic dentistry/ G. M. Barer: textbook at 3 hours - M .: Geotar-Media, 2008. - Part 2. - Periodontal disease. - 224 p.
Bezrukova I. V., Grudyanov A. I. Aggressive forms of periodontitis / I. V. Bezrukova, A. I. Grudyanov. Guide for doctors. - M.: MIA, 2002. - S. 126.
Briseno B. Periodontal-endodontic lesions / B. Briseno. Clinical dentistry. - 2001, No. 2. - S. 24-29.
Borovsky E. V. Therapeutic dentistry / E. V. Borovsky: a textbook for medical students. - M.: Medical Information Agency, 2007. - 840 p.
Herbert F. Wolf. Periodontology / F. Wolf Herbert, Edith M. Ratezhak, Klaus Ratezhak. Per with him. Ed. prof. G. M. Barera. - M.: Medpress-inform, 2008. - 548 p.
Diekov D. Regenerative treatment of periodontitis and endoperiodontal pathology using cupral and cupral depophoresis / D. Diekov. Maestro of dentistry. - 2004, No. 3. - S. 21-27.
James L. Gutman. Problem Solving in Endodontics: Prevention, Diagnosis and Treatment / L. Gutman James, S. Dumsha Tom, E. Lovdel Paul. Per. from English. - M.: Medpress-inform, 2008. - 592 p.
Cohen S. Endodontics. 8th edition, revised and enlarged / S. Cohen, R. Burns. Russian edition, ed. Doctor of Medical Sciences, Professor A. M. Solovieva. Publishing House STBOOK, 2007. - 1026 p.
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The process of destruction in the structure of bones, which gradually leads to its replacement with malignant tissue, granulations, pus - this is the destruction of the bone. A progressive pathological process is accompanied by a decrease in bone density and an increase in their fragility. Harmony in the development of bone tissue up to the age of twenty occurs normally, naturally. After this age limit, the formation of such tissues becomes slower, and the destructive process only intensifies.

Bones are a solid organ in our body, their functions are to provide musculoskeletal and protective functions. They are composed of hydroxyapatite, mineral substance, about 60-70% of bone weight and organic type I collagen about 30-40%.

When this composition changes, bone density decreases. This is one of the reasons why it is more difficult for older people to recover from any injuries than for a person at a young age. Small negative external factors can easily lead to injury, because weak bones are more susceptible to impact. A number of factors can speed up this process.

8 important reasons

The internal source of bone tissue destruction is osteoporosis. This disease has a systemic progressive character. Is it an exchange or clinical syndrome, which characterizes a decrease in density, an increase in fragility. The metabolism of this tissue decreases, it becomes less durable, and the level of fractures increases.

This disease was first found among the Indians of North America, around 2500-2000 BC. Also, the characteristic posture of this disease can be seen in the paintings of artists of Ancient China and Greece.

The degree of risk is determined, focusing on the objective data of the anamnesis and the results of examinations.

Osteoporosis leads to bone porosity. Several factors can also negatively affect this process. Bone destruction causes:

diseases caused by a disorder of one or more endocrine glands - endocrine, chronic diseases;
lack of nutrients, these are bone builders in our body - magnesium, potassium, vitamin D, the main cause of deficiency is an unbalanced diet;
the last independent menstruation, that is, the period of menopause;
lack of weight indicator;
Availability bad habits, aggravating their progressiveness;
heredity, threatens people who have blood relatives under the age of fifty who have been diagnosed with this disease;
past injuries that are aggravated by fractures;
professional athletes are also at risk, a large part of physical activity is the cause of this disease;

Important! Osteoporosis in running forms treated harder. More attention needs to be paid to prevention.

This will reduce the risk of disability, can save from lethal outcome. The risk lies in the absence of clear symptoms, pain, severe discomfort, or trouble in sensations. Most often, they are in no hurry to go for help, due to the "lack of pronounced symptoms." And with a fracture, respectively, contacting a specialist, unpleasant news is found.

Destruction of the bones of the skull

The most common defeat. After a long period of time, some bone foci are replaced by completely different ones. X-ray examination will help to identify a bone defect.

Foci of destruction can be ten centimeters in size and larger in diameter. In such cases, people feel a severe headache, earache. Pain sensations are predominantly observed at night in people with affected tubular bones.

Children show great passivity during this period. It manifests itself in a reduction in mobility, refusals to lift any object with your hands, or to walk corny.

The shape of the foci is oblong, elongated along the length of the bone. Complication in the area of the spine, the person stops moving.

Frontal bone destruction

The airspace inside her due to inflammatory disease performed pathologically by the content element. The filling is serous or purulent, edematous mucosa, or cyst. It is also possible to disturb the harmonious state of the walls due to fractures, tumor damage. Particularly doubtful cases require the use of iodolipol and mayodil introduced into the axillary part.

Destruction of the jaw bone

Reappears its action due to the germination of tumors. They develop from epithelial tissue into the oral mucosa. Up to ten percent is sarcoma, a larger percentage is cancer. Adenocarcinoma mammary, thyroid, prostate glands- one of the causes of metastases.

Important! It is X-ray intervention that will help to see isolated defects and various kinds of lesions.

Destruction of the femur

Consequence of violations of blood flow and necrotic elements. This disease is aggravated by the influence of increased alcohol consumption, the use of a cordiosteroid, joint injuries, and pancreatitis. The possibility of early diagnosis is possible with the use of tomography.

Destruction of the temporal bone

Diagnosed best with computed tomography and magnetic resonance imaging. Such methods are the most informative, they are accessible to most people and this allows you to limit the amount of the search.

In the pyramidal part of such a bone, tumors are often found: neuritis, fibroma, glomus, osteoma. The ear areas are most often affected.

Metastatic lesions are possible with cancerous tumor mammary glands, lungs, kidneys.

Important! Radiographically, it is possible to anticipate the manifestation of a tumor in this area, with an appropriate size. It is necessary to know the features of the structure of the bone, the basics of anatomy for the timely detection of the first signs of a different nature and approaches to their elimination.

Destruction of the humerus

It is a serious disease that acts from the bone element with the appearance of dead areas. Then it changes to adipose tissue. This disease is called ischemic necrosis. At the heart of the pathology is a change in the normal state of the blood supply to the bones. As a result, this tissue is deprived of 100% nutrition - it slowly dies off.

The worst thing is that this disease leads to irreversibility in the state of the bones. The minimum percentage of restoration of the structural part of the bones.

Important! Passage by the patient of all stages of the pathology occurs within a few months to 1-1.5 years. If destruction humerus has begun its action - it is no longer possible to stop this process. The patient goes through all the stages, as a result of which, most likely, leads to a wheelchair.

D destruction of the pelvic bones

Accompanied by long-term asymptomatic treatment. Most often, this is the wing of the ilium next to the sacrum - iliac joint. The first sign is a change in bones, swelling. Children and teenagers are most susceptible to this disease. The pain threshold is moderate, the sensation has a aching character. From a pathological point of view - the absence of fractures. It can only be treated surgically - bone resection. Large sizes form a defect and are shown by autoplastic and alloplastic substitutions.

Prevention measures

Because of special method diagnosis, greater accuracy in detecting changes in density is possible.

There is an ultrasound technique called densitometry. Thanks to this technique, even the smallest reduction in density can be determined. Other hardware interventions in the early stages are ineffective. For comparison: the X-ray machine will show the result at an indicator of twenty-five to thirty percent.

Experts discuss some of the signs that indicate the course of this disease: a decrease in growth of more than ten millimeters, the vertebral part is bent, the lower back and chest part hurts, especially when actively engaged in physical activity, you get tired quickly, working capacity is minimal.

Mobile life is the best preventive measure for development this disease. This:

balanced nutrition: the correct ratio of proteins, fats, carbohydrates, a large amount of fresh vegetables and fruits;
walking in fresh air;
morning exercises, physical training, not for wear;
minimizing harmful habits in the form of cigars, alcoholic beverages and the use of coffee drinks;
relaxing and invigorating massages.

Note! Before choosing exercises, approach consciously, it will not be superfluous to consult doctors or a fitness instructor. Within a few months of combining balanced nutrition plus moderate physical activity– the inert mass increases by several percent.

Medical therapy

Similar preventive measures therapeutic treatments. The difference lies in the greater direction of action. The disease itself is characterized by duration and complexity.

Note! A person should consume daily fish fat, eggshell powder, it is easier to digest.

Bone destruction treatment is helped by drug therapy. You are provided with a wide range of medicines. The specialist prescribes treatment on an individual basis.

Self-treatment is useless, the disease leads to a deterioration in the quality of living.

To minimize the occurrence of the disease, it is better to use preventive measures.

The contours of the focus are usually unsharply outlined and vague.

Extensive bone destruction (destruction) of the vertebral bodies with the formation of large sequesters

In the x-ray image, the destruction can be of varying degrees of focality, vastness, and can be located centrally (inside the bone) or superficially.

Huge cavities (caverns) in the femur and tibia with multiple tuberculous osteitis

Bone cavities, or caverns, are formed with the complete destruction of all bone beams in the area of the destructive focus with the formation of more or less clearly defined walls. They can have different shapes and sizes. Naturally, bone caverns are easier to detect on x-ray than small destructive foci, although here, too, the size of the cavities and the depth of their occurrence in the bone, as well as the thickness of the affected bone, are of great importance.

Types of bone tissue destruction

Fermin A. Carranza, Paulo M. Camargo, and Henry H. Takei

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Although periodontitis is infectious lesion gum tissue, the changes that occur in the bone are critical because bone destruction leads to tooth loss.

The height and density of the alveolar bone is maintained by a balance between local and systemic processes, between the processes of bone formation and resorption. When resorption occurs faster than new bone formation, both bone height and density decrease.

The bone level is a consequence of pathological processes, while changes in the soft tissues of the pocket wall reflect the current inflammatory state. Therefore, the level of bone loss does not necessarily correlate with the depth of periodontal pockets, the severity of pocket ulceration, and the presence or absence of pus.

Bone destruction caused by prolonged inflammation of the gum tissue

The most common cause of bone loss in periodontal disease is the spread of inflammation from the marginal gingiva to the supporting tissues of the periodontium. Bone inflammation and subsequent bone loss marks the transition from gingivitis to periodontitis.

Periodontitis is always preceded by gingivitis, but gingivitis does not always lead to periodontitis. In some cases, gingivitis never turns into periodontitis, and in other cases, after a short course, gingivitis quickly turns into periodontitis. The factors that are responsible for the involvement of supporting structures in the inflammatory process (that is, the transition of gingivitis to periodontitis) are currently not fully understood.

The transition from gingivitis to periodontitis is due to a change in the composition of the bacterial plaque. In the later stages of the disease, the number of spirochetes and flagellar microorganisms increases, and the number of cocci and rods decreases. As the severity of the lesion increases, the cellular composition of the infiltrated connective tissue also changes. At stage I of gingivitis, fibroblasts and lymphocytes predominate; as the disease progresses, the number of plasma cells and blast cells. Seymour et al. have described a stage of "repressed" gingivitis in which T-lymphocytes predominate; if B-lymphocytes become the dominant cell type, then the process begins to progress.

Heijl et al. were able to convert chronic gingivitis to progressive periodontitis in experimental animals by placing a silk ligature in the gingival sulcus and tying it around the neck of the tooth. This caused ulceration of the furrow epithelium, a change cellular composition inflammatory infiltrate from predominantly plasma cells to predominantly polymorphonuclear leukocytes, as well as osteoclastic resorption of the alveolar ridge. Recurrence of episodes of acute trauma over time can lead to progressive bone loss in marginal periodontitis.

The spread of inflammation to the supporting structures of the tooth depends on the pathogenicity of plaque and the resistance of the host organism. Resistance includes immunological activity and other tissue mechanisms such as degree of gingival fibrosis, width of attached gingiva, reactive fibrogenesis and osteogenesis that occur at the periphery of the inflammatory lesion.

Inflammation of the gum tissues spreads along the bundles of collagen fibers, follows the course of the blood vessels, and then into the alveolar bone through adjacent tissues around it (Fig. 14.1).

Figure 14-1 A, Area of inflammation extending from the gingiva to the subosseous level. B, Spread of inflammation along blood vessels and between collagen bundles.

Although the inflammatory infiltrate is concentrated in the marginal periodontium, the reaction is much more diffuse, often reaching the bone, and causing a response before ridge resorption or loss of attachment occurs. In the region of the maxillary molars, inflammation can invade the maxillary sinus, leading to thickening of the sinus mucosa.

Interproximal inflammation spreads to the adjacent connective tissue around the blood vessels, through the fibers, and then into the bony blood channels that penetrate the center of the alveolar ridge (Fig. 14-2),

Figure 14-2. Inflammation extending from the pocket area (above) between collagen fibers that have been partially destroyed.

on the side of the ridge (fig.)

Figure 14-3 A, Spread of inflammation to the center of the interdental septum. Inflammation penetrates through the transseptal fibers and enters the bone tissue of the center of the septum around the blood vessel. B, The cortical layer at the top of part of the septum has been destroyed, inflammation invading the space of the bone marrow.

or at an angle from the partition. In addition, inflammation can enter the bone through more than one channel. Less often, inflammation spreads from the gum directly to the periodontal ligament, and from there to the interdental septum (Fig. 14-4).

Figure 14-4 Inflammatory pathways from gingival tissues to supporting periodontal tissues in periodontitis. A, Interproximal, gingiva to bone (1), bone to periodontal ligament (2), and gingiva to periodontal ligament (3). B, Vestibular and lingual, from the gingiva along the external periosteum (1), from the periosteum to the bone (2), and from the gingiva to the periodontal ligament (3).

From the vestibular and lingual side, inflammation of the gum tissue spreads along the outer periosteal surface of the bone (see Fig. 14-4) and penetrates into the medullary spaces through the vascular channels in the outer cortical plate.

As it spreads from gingiva to bone, gingival and transseptal fibers break down into disorganized granular fragments, interspersed inflammatory cells, and edema. However, there is permanent recovery transseptal fibers along the entire crest of the interdental septum along the root as bone destruction progresses (Fig. 14-5).

Figure 14-5. Reorganization of transseptal fibers. Mesiodistal section through the interdental septum shows inflammation of the gum tissue and loss of bone tissue. Newly formed transseptal fibers protrude over the edge of the bone and are partially involved in the inflammatory process.

As a result, transseptal fibers are present even in cases of extreme bone loss.

Dense transseptal fibers form a hard covering of the bone and can be seen during periodontal flap surgery after removal of superficial granulation tissue.

After inflammation from the gum tissue reaches the bone (Fig. 14-6)

Figure 14-6. Due to the spread of inflammation reached the surface of the alveolar crest of the bone.

and bone marrow space, the bone marrow is replaced by leukocyte liquid exudate, new blood vessels and proliferating fibroblasts (Fig. 14-7).

Figure 14-7 Interdental septum, human autopsy specimen. An extensive inflammatory infiltrate penetrates the bone marrow from both the mesial and distal sections. The bone marrow was replaced by inflammatory cells and fibrous marrow.

The number of multinuclear osteoclasts and mononuclear phagocytes increases, and Howship gaps appear on the surface of the bone (Fig. 14-8).

Figure 14-8. Osteoclasts and Howship's lacunae during resorption of the crestal bone.

In the marrow spaces, resorption occurs from within, causing thinning of the surrounding bony trabeculae and enlargement of the marrow space, followed by bone destruction and reduction in bone height. As a rule, the adipose tissue of the bone marrow is partially or completely replaced by fibrous tissue in the resorption zone.

Bone destruction in periodontal disease is not a process of bone necrosis. There is cell activity along viable bone. If periodontal disease causes tissue necrosis and purulent process, it occurs in the soft tissue walls of the periodontal pocket rather than along the zone of underlying bone resorption.

The amount of inflammatory infiltrate correlates with the degree of bone loss, but not with the number of osteoclasts. However, the distance from the apical border of the inflammatory infiltrate to the alveolar ridge of the bone correlates both with the number of osteoclasts on the alveolar ridge and with total osteoclasts. Similar results were obtained in experimental periodontitis in animals.

Radius of action

Garant and Cho suggested that local bone resorption factors must be present in the vicinity of the bone surface in order to exert their effect. Page and Schroeder, based on Waerhaug's measurements on human autopsy specimens, concluded that the range of activity in which a bacterial plaque can cause bone loss is about 1.5-2.5 mm. Beyond 2.5 mm there is no effect; interproximal angular defects may only appear in spaces greater than 2.5 mm wide, as narrower spaces are completely destroyed. Tal confirmed this fact with measurements in humans.

Large defects well beyond 2.5 mm from the tooth surface (as in aggressive types of periodontitis) may be caused by the presence of bacteria in the tissues.

The rate of bone loss

In the study of the condition of the periodontium of tea plantation workers in Sri Lanka, who did not have oral hygiene and did not have access to dental care, Löe et al. found that the rate of bone loss averaged about 0.2 mm per year for the vestibular surface and about 0.3 mm per year for the proximal surfaces if periodontitis was not treated. However, the rate of bone loss can vary depending on the type of disease. Löe et al. defined the following three subgroups of patients with periodontal disease, based on interproximal attachment loss* and tooth loss:

Approximately 8% of people have rapidly progressive periodontitis, characterized by an annual attachment loss of 0.1 to 1.0 mm.
Approximately 81% of people have moderately progressive periodontitis with an annual attachment loss of 0.05 to 0.5 mm.
. The remaining 11% of people have minimal or no progressive disease (0.05-0.09 mm annually).

* Attachment loss can be equated with bone loss, although attachment loss occurs approximately 6-8 months earlier than bone loss.

periods of destruction

Periodontal destruction occurs episodically, with periods of remission and periods of destruction that result in loss of collagen and alveolar bone and deepening of the periodontal pocket.

Periods of destructive activity are associated with subgingival ulceration and an acute inflammatory reaction leading to rapid loss of alveolar bone. It has been suggested that this is due to the conversion of a T-lymphocyte-dominated lesion to a B-lymphocyte- and plasma cell-dominated lesion. Microbiologically, the number of non-attached, mobile, gram-negative microorganisms in the periodontal pocket increases. While periods of remission coincide with an increase in dense, loose, immobile, Gram-positive flora with a tendency to mineralization.

It has also been suggested that the onset of periods of destruction coincides with tissue invasion by one or more bacterial species, and then local defense mechanisms are activated.

Mechanisms of bone tissue destruction

Factors involved in bone destruction in periodontal disease are bacterial and host-mediated. Bacterial plaque products induce the differentiation of bone progenitor cells into osteoclasts and stimulate the release of mediators that have a similar effect. Plaque products and inflammatory mediators can also act directly on osteoblasts or their progenitors, inhibiting their action and decreasing their numbers.

In addition, in rapidly progressive diseases such as aggressive periodontitis, bacterial microcolonies or isolated bacterial cells which implies a direct effect.

Several host factors released by inflammatory cells are able to induce bone resorption in vitro and play a role in the development of periodontitis. These include prostaglandins and their precursors, interleukin-1α (IL-1α), IL-β, and tumor necrosis factor alpha-α (TNF-α).

When administered intradermally, prostaglandin E 2 (PGE 2) induces vascular changes observed in inflammation. When injected through the bone surface, PGE 2 induces bone resorption in the absence of inflammatory cells and few multinucleated osteoclasts. In addition, non-steroidal anti-inflammatory drugs (NSAIDs) such as flurbiprofen and ibuprofen inhibit PGE 2 production, slowing the bone loss that occurs in periodontitis in humans and Beagle dogs. This effect occurs when the gums become inflamed and ends 6 months after stopping the drug.

Bone formation in periodontal disease

Sites of bone formation are found immediately adjacent to areas of active bone resorption and along trabecular surfaces to strengthen the remaining bone tissue (supporting bone formation). This osteogenic response is clearly seen in experimentally generated bone loss in animals. In humans, this is less obvious, but has been confirmed by histometric and histological studies.

Autopsy specimens in the absence of treatment showed that there are areas in which bone resorption has ceased and new bone has formed on the previously eroded (corroded) surface of the bone. This confirms the intermittent nature of bone resorption in periodontal disease and is consistent with the various rates of progression observed clinically in untreated periodontitis.

Periods of remission and exacerbation (or inactivity and activity) seem to coincide with remission or exacerbation of gingival inflammation, manifested in changes in the degree of bleeding, the amount of exudate and the composition of the bacterial plaque.

Bone formation in response to inflammation, even in active periodontitis, has an impact on treatment outcome. The main goal of the treatment of periodontitis is to eliminate inflammation in order to stop the stimulation of bone resorption and the predominance of constructive processes.

Bone destruction caused by occlusal trauma

Another cause of bone destruction in periodontal disease is occlusal trauma, which can occur in the absence or presence of inflammation.

In the absence of inflammation, changes caused by occlusal trauma range from increased compression and stretching of the periodontal ligament and increased destruction of the alveolar bone to necrosis of the periodontal ligament, bone, and resorption of bone and dental structures. These changes are reversible if the traumatic forces are eliminated. However, persistent occlusal trauma leads to funnel-shaped expansion of the ridge portion of the periodontal ligament with resorption of the adjacent bone. These changes, resulting in an angular ridge, are an adaptation of the periodontal tissues to "absorb" increased occlusal forces, but the altered bone shape weakens the support of the teeth and causes them to move.

Combined with inflammation, occlusal trauma exacerbates inflammation-induced bone destruction and results in bone reshaping.

Bone destruction caused by systemic diseases

Physiological balance is regulated by local and systemic factors. If the general trend is towards bone resorption, there may be an increase in bone mass caused by local inflammatory processes.

This systemic influence on the alveolar bone response, as stated by Glickman in the early 1950s, occurs in all cases of periodontal disease. In addition to the virulence of the bacterial plaque, the severity of periodontal disease is influenced by the nature of the systemic component rather than its presence or absence. This concept of the role of systemic defense mechanisms was confirmed by studies of human immunodeficiency in destructive types of periodontitis.

In recent years, a possible relationship between periodontal tissue loss and osteoporosis has been identified. Osteoporosis is a physiological condition in postmenopausal women resulting in loss of bone mineral composition and structural changes bones. Periodontitis and osteoporosis have a number of risk factors (for example, age, smoking, diseases or medications that slow down regeneration). Some studies have indicated the relationship between skeletal density and oral bone density, as well as between ridge height and residual ridge resorption, as well as the relationship between osteopenia and periodontitis, tooth mobility and tooth loss.

Periodontal bone loss can also occur in generalized diseases (eg, hyperparathyroidism, leukemia, or histiocytosis X) through mechanisms that may not be characteristic of periodontitis.

Factors determining bone morphology in periodontal diseases

Normal alveolar bone variability

The morphological features of normal alveolar bone show significant variability that affects the bone contours caused by periodontitis. Next anatomical features significantly affect the structure of bone destruction in periodontal diseases:

Thickness, width and angle of interdental septa
The thickness of the vestibular and lingual alveolar plate
Presence of defects
Teeth alignment
Root and canal anatomy
The position of the root in the alveolar process
Proximity to another tooth surface

For example, angular bone defects cannot form in thin vestibular or lingual alveolar plates, which have little or no cancellous bone between the outer and inner layers of the cortical plate. In such cases, the entire crest is destroyed and the height of the bone is reduced (see Figure 14-9).

Figure 14-9 can be found on the companion website www.expertconsult.com

Exostoses

Exostoses are outgrowths of bone different size and forms. Palatal exostoses (torus) are found in 40% of people. They may occur as small nodules, large nodules, sharp ridges, spike-like protrusions, or any combination of these (Figures 14-10).

FigA, Vestibular exostosis of the upper second premolar and molars. B, palatal exostosis of the first and second molars. Note also the circular defect of the second molar (left).

Cases have been described where exostoses formed after the placement of free gingival grafts.

Occlusal trauma

Occlusal trauma may be a factor in determining the size and shape of bone deformities. There may be thickening of the cervical margin of the alveolar bone or changes in bone morphology (eg, angular defects, hardening bone) that are later superimposed by inflammatory changes.

Formation of strengthening bone tissue

Bone formation is necessary to strengthen bone trabeculae weakened by resorption. If this process occurs in the thickness of the jaw, then it is called central bone strengthening. If it occurs on the outer surface of the jaw, it is called peripheral bone strengthening. This can cause a change in the contour of the bone, which leads to the formation of bone craters and angular defects (Fig. 14-11).

Figure 14-11. protrusion of vestibular bone tissue. Peripheral bone strengthening along the outer surface of the vestibular cortical plate and ridge. Note bone deformity caused by hardening of the bones and protrusion of the mucosa.

The influence of food

Interdental bone defects often occur where proximal contact is missing or malformed. Pressure and irritation of the food bolus contributes to a change in the bone structure. In some cases, lack of proximal contact can lead to tooth displacement due to extensive bone destruction prior to food exposure. In these patients, food exposure is more of a complicating factor.

Aggressive periodontitis

A vertical or angular pattern of alveolar bone destruction can be found around the first molars in aggressive periodontitis. The cause of localized bone destruction in this type of periodontal disease is unknown.

Bone destruction in periodontal disease

Periodontitis, in addition to reducing the height of the alveolar process, changes the morphological features of the bone. For effective diagnostics and treatment, it is important to understand the nature and pathogenesis of these changes.

Horizontal bone loss

Horizontal bone loss is the most common form in periodontal disease. The bone decreases in height, but the edge of the bone remains approximately perpendicular to the surface of the tooth. The interdental septa, vestibular and lingual cortical plates are affected, but not necessarily to the same extent around the same tooth (Fig. 14-12, A).

FigA, Horizontal bone loss. Note the reduction in height of the marginal bone, the exposure of the cancellous bone reaching the furcation of the second molar. B, vertical (angular) bone loss on the distal root of the first molar.

Bone deformities (bone defects)

Various types of bone deformities can occur in periodontal disease. They are more common in adults, but also occur in the milk bite. Their presence can be detected by x-ray, but careful probing and surgical exposure of these areas is required to determine their exact shape and size.

Vertical or angular defects

Vertical or angular (angular) defects form in an inclined plane, leaving a depression in the bone near the root. The base of the defect is located more apically relative to the surrounding bone (Fig. B, and 14-14).

Fig B, vertical (angular) bone loss on the distal root of the first molar.

Figure 14-13. Angular (vertical) defects of various depths.

Figure 14-14. Angular defect on the mesial surface of the first molar. Note the involvement of furcation.

In most cases, angular defects are accompanied by intraosseous periodontal pockets. On the other hand, with an intraosseous pocket, there is always an angular defect lying at the base.

Angular defects were classified by Goldman and Cohen based on the number of bony walls. Angular defects can have one, two or three walls (Fig. 18).

Figure 14-15. One-, two- and three-wall vertical defects on the right lateral incisor. A, three bony walls: distal (1), lingual (2), and vestibular (3). B, defect with two walls: distal (1) and lingual (2). C, single wall defect: distal wall only (1).

Figure 14-16. Mid-level horizontal section of mandibular molars showing a double-walled bone defect distal to the second molar.

Figure 14-17. Single-wall vertical defect on the mesial surface of the lower first molar.

Figure 14-18. Circular vertical defect of the upper premolar.

The number of walls in the apical part of the defect is often greater than in its occlusal part, in which case the term combined bone defect is used (Figure 14-19).

Figure 14-19. Combined type of bone defect. Since the facial wall is ½ the height of the distal (1) and lingual (2) walls, this is a bone defect with three walls in its apical part and two walls in its occlusal part.

Vertical defects in the interdental spaces are usually visible on x-ray, although if a thick cortical plate is present, it may interfere with visualization. Angular defects may also appear on the vestibular, lingual, or palatal surfaces, but these defects are not visible on x-ray. Surgical exposure is the only reliable way to determine the presence and configuration of vertical bone defects.

Vertical defects increase with age. Approximately 60% of individuals with interdental angular defects have only one defect. According to reports, vertical defects detected radiographically most often appear on the distal and mesial surfaces. However, three-wall defects are more common on the mesial surfaces of maxillary and mandibular molars.

Bone craters

The bone crater is a cavity on the crest of the alveolar bone, limited by the vestibular and lingual wall (Fig. 14-20).

Figure 14-20. Schematic representation of the bone crater in the vestibulo-lingual section between the two lower molars. Left, normal bone outline. Right, bone crater.

Craters have been found to account for approximately one-third (35.2%) of all defects and about two-thirds (62%) of mandibular defects, and are also twice as common in the posterior than the anterior.

In 85% of cases, the height of the vestibular and lingual ridges of the crater is the same, and in the remaining 15% one of the ridges (vestibular or lingual) rises above the other.

The following reasons for the high incidence of interdental craters have been proposed:

Plaque accumulates in the interdental area, which is difficult to clean.
The normal flat or even slightly concave shape of the vestibular interdental septum in lower molars may contribute to crater formation.
The vascular structure of the gingival tissues and the center of the ridge provides a pathway for inflammation.

Bulbous bone contour

The "bulbous" bone contour represents bony extensions formed by exostoses (see Fig. 14-10), adaptation to stress, or by strengthening the bone. It is more common in the upper jaw than in the lower.

Structure change

The change in structure results from the loss of interdental bone, including the vestibular and lingual cortical plates, without concomitant loss of radicular bone, thereby altering the normal architecture of the bone (Figures 14-21).

Figure 14-21. Change in structure. The flap is raised, the uneven edge of the bone is visible.

Such defects are more common in the upper jaw.

Bone ledge

A ledge is a plateau-like edge of bone formed by resorption of thickened bone plates (Fig. 14-22).

Figure 14-22. Bone ledge formed by interproximal resorption.

Exist different kinds loss of bone tissue in periodontitis, in the same patient, bone loss can be different in different areas. Vertical bone loss is treatable through reconstructive periodontal surgery using a variety of osteoconductive materials, bioactive molecules and membranes. Often when extensive defects more than one material may be required to obtain good results. With horizontal loss of bone tissue and the presence of bone craters, restoration by conservative methods is usually not carried out; with these lesions, flap surgery combined with bone surgery is required.

Bone loss in the furcation area is more difficult to recover than loss in the interproximal area. With progressive damage III degree, the prognosis may be so unfavorable that removal is required as soon as possible, followed by implantation, in order to preserve the maximum amount of bone tissue.

Furcation involvement

The term furcation involvement means the involvement of bifurcation and trifurcation of multi-rooted teeth in the inflammatory process. However, the number of molars affected by furcation is unclear. While some reports report that the mandibular first molars are most commonly affected and maxillary premolars are the least affected, other studies suggest that the maxillary molars are more commonly affected. With age, the number of affected furcations increases.

The exposed furcation may be clinically visible or it may be covered by the wall of the pocket. The degree of involvement is determined by examination with a blunt probe, as well as the simultaneous introduction of warm air to facilitate visualization (Fig. 14-23).

Figure 14-23. A, Molar with clinically inflamed gingiva. However, there is a deep distal pocket.

Figure 14-23. B, Raised flap showing extensive bone loss and furcation involvement (Courtesy of Dr. Terry Fiori, Palo Alto, CA).

Furcation involvement is classified as class I, II, III, and IV, depending on the amount of tissue involved. Class I - initial loss of bone, class II - partial loss of bone tissue (dead end), class III - complete loss of bone tissue with a through defect of furcation. Class IV is similar to Class III, but with gingival recession exposing the furcation.

The type of destruction with involvement of the furcation varies in different occasions depending on the degree of involvement. Bone loss around each individual root may be horizontal or angular, often forming a crater in the interradicular region (Figures 14-25).

Figure 14-25. Radiograph (B) of varying degrees of bone loss on the skull. Involvement of the furcations of the first and second molar. Deep angular bone loss at the distal root of the first molar. Interradicular and interdental craters at the second molar and between the second and third molars, respectively.

To determine the presence of destruction, horizontal and vertical probing should be carried out around each root and in the crater area to establish the depth.

Furcation involvement is a stage of progressive periodontitis and has the same etiology. The difficulty, and sometimes the impossibility of controlling the plaque, determines the presence of extensive lesions in the furcation area.

The role of occlusal trauma in the formation of furcation lesions is controversial. Some assign a key role to trauma, believing that the furcation area is most sensitive to damage from excessive occlusal forces. Others deny the initiating effect of trauma and believe that the inflammation and swelling caused by plaque in the area of the furcation pushes the tooth out of the socket a little, which then leads to trauma and sensitivity.

Another important factor is the presence of enamel protrusions at the furcation, which occurs in about 13% of multi-rooted teeth, and the proximity of the furcation to the CEJ, which occurs in 75% of furcation involvement.

The presence of additional channels in the furcation area can cause inflammation to move from the pulp to the furcation area. This possibility should not be ruled out, especially when the mesial and distal bone maintain normal height. Accessory canals connecting the floor of the pulp chamber with the area of furcation were found in 36% of maxillary first molars, 12% of maxillary second molars, 32% of mandibular first molars, and 24% of mandibular second molars.

The diagnosis of furcation involvement is based on clinical signs and careful probing with a specially designed probe. X-ray examination useful, but the defect may not be visible with indirect projection of the image and due to radiographic obscuration due to neighboring structures.

Microscopically, furcation involvement has no unique pathological features. This is simply a stage of root canal expansion due to the periodontal pocket. In the early stages, there is an expansion of the periodontal space with cellular and exudative inflammatory exudation, followed by epithelial proliferation into the area of furcation from the adjacent periodontal pocket. The spread of inflammation to the bone leads to resorption and a decrease in bone height. Destructive processes can lead to horizontal tissue loss or angular defects associated with intraosseous pockets (Fig. 14-24).

Figure 14-24. Different degrees of furcation involvement in a human autopsy specimen. Furcation involvement was found in all three molars, with severe involvement of the second molar and an extremely severe involvement of the first molar, exposing almost the entire mesial root.

Plaque, tartar and bacterial debris accumulate on the exposed furcation.