Myeloma is multiple myeloma, or plasma cell sarcoma. The disease was first described by Rustizky in 1873 and named Multiple Myeloma (MM), which is a tumor of the hematopoietic system and is a malignant tumor caused by abnormal hyperplasia of plasma cells. The abnormal plasma cells, i.e. myeloma cells, infiltrate the bone marrow and soft tissues and produce M-globulin, causing bone destruction, anemia, renal impairment and abnormal immune function. In recent years, the incidence of multiple myeloma has been on the rise. The incidence rate is 2 to 3/100,000, and the age of onset is mostly in middle and old age, mostly between 50 and 60 years old, and less frequently below 40 years old. However, multiple myeloma with oral and maxillofacial swelling as the first symptom is often misdiagnosed and mistreated, especially when it is manifested by mandibular swelling, which is usually difficult to distinguish from jaw tumor, and blind surgery may cause unnecessary harm to patients [1, 2, 3]. In this paper, we analyze the clinical manifestations, biological behavior and pathological manifestations, and propose the principles of diagnosis and treatment, taking into account the literature.
I. Case presentation
The patient was a 68-year-old male who was admitted to the hospital on 2004-4-7 with the primary cause of a painless swelling in the right mandible for 2 months. On February 5, 2004, the patient unconsciously discovered a swelling in the right mandible, the size of an apricot kernel, and in mid-January, the affected tooth was extracted due to toothache, but there was no significant discomfort. He came to our hospital on March 22, 2004 for further treatment and was admitted as “mandibular swelling”. Since the onset of the disease, he had good mental, dietary and sleep status, and normal bowel movements. Past history: suffered from tuberculosis in 1970, fell in 1996 and caused left rib fracture, and fell in 2003 and caused right femoral stem fracture, which was treated with surgery and blood transfusion in Baoding Hospital in Hebei. Personal history: Grew up in Hebei, no history of exposure to epidemic water, radioactive substances, or chemical poisons. He has a healthy wife, one son and four daughters, all of whom are in good health. Family history: Both parents are deceased. He denied any family history of similar diseases or hereditary diseases. Admission examination: general condition was good, and no abnormalities were found in the heart, lungs and abdomen. Specialized examination: left-right asymmetry of the maxillofacial area, the right mandibular area was obviously bulging, with a palpable swelling of about 6.0×5.0×3.0 cm in size, normal skin color on the surface, low skin temperature, clear boundaries on palpation, inactive, hard, no pressure pain, no ping-pong-like sensation, locally soft, cystic feeling, only the left mandibular lateral incisor remained in the upper and lower dentition, and the remaining teeth were missing for denture repair. The right lower lip was numb, cheek puffing was normal, the right corner of the mouth was not strong enough when smiling, and no enlarged lymph nodes were palpated in the submaxilla and neck bilaterally. The whole-mouth surface tomography showed that the right mandibular body part showed a large area of bone density reduction with neat edges of bone density reduction and buccal bone defects in the mandibular body part. PET (positron emission tomography) showed a right mandibular mass with multiple abnormal hypermetabolic foci in bone and soft tissue, consistent with a malignant lesion. The abnormal hypermetabolic foci in the lower right side of the bladder, and prostate-related examination was recommended. The right mandibular tumor was considered to be metastatic cancer. The possibility of metastatic cancer had been informed to the patient’s family, and the patient’s family strongly requested surgery with the main purpose of clarifying the pathology.
After adequate preoperative preparation, an enlarged resection of the right mandibular mass was performed under general anesthesia on 2004-4-13, with a submaxillary incision approach. Intraoperative freezing was consistent with plasmacytoma, and no tumor was seen at the cut edge. Postoperative symptomatic treatment. Postoperative pathological return: plasmacytoma of the right mandible, size 7.5×3.5×1.3 cm, considered as multiple plasma cell myeloma in combination with clinical considerations, no tumor tissue was seen in the lymph nodes. Immunohistochemical staining: tumor cells showed LCA (+), Kappa (-), Lambda (+), Vimentia (+), Actia (-), HMB (-), CK (-). The patient was discharged from the hospital on 2004-4-22 and transferred to the hematology department for further treatment and regular review.
II. Diagnosis and treatment thought process
(A) Etiology
The etiology of this disease is unknown and may be related to the following factors.
1. clinically some chronic infections and inflammatory conditions, such as chronic osteomyelitis, chronic hepatitis, pyelonephritis, tuberculosis, etc. can be accompanied by malignant proliferation of plasma cells. This may be the result of long-term chronic stimulation of the reticuloendothelial system by antigens, and also raises the possibility that any chronic stimulation of the reticuloendothelial system leading to the development of myeloma may be caused.
2. Based on experimental observations in animals, it has been found that the disease may be directly caused by viral infection, and long-term viral infection may manifest as proliferation of the reticuloendothelial system.
3. Since the incidence of multiple myeloma is higher in workers engaged in radiation than in the general population, ionizing radiation is considered to be one of the causes of the disease. Studies on survivors of the atomic bombings in Japan from 1950 to 1976 showed that the incidence of the disease was 4.7 times higher than normal after receiving 100 cGy of air.
4. Multiple myeloma is associated with certain genetic factors. Chromosomal abnormalities are 0 in occult multiple myeloma; 18% in newly diagnosed active type; 63% in progressive type; and the most common chromosomal abnormality is [t(11;14) q13;q32)].
Different hypotheses exist about the origin of multiple myeloma, among which the more recognized is the tumor precursor cell theory. It is believed that TdT-, CALLA+ pre-B cells in the bone marrow are stimulated by some antigen, proliferate, become malignant, and differentiate directly into CALLA+ preplasma cells without passing through the sIg+ B cell stage in the middle, from which clonal expansion occurs and differentiate into malignant plasma cells, forming myeloma. In addition CALLA+ cells can enter the peripheral blood and cause dissemination of myeloma to form multiple lesions. Normally differentiated pre-B cells in the peripheral blood are stimulated by antigen during their transformation into resting B cells, which become malignant and return to the bone marrow to be inoculated with tumor precursor cells, resulting in multiple myeloma.
In this case, after repeated and detailed medical history, the patient did not have a history of long-term exposure to radiation, pesticides and other irritants, and had been growing in rural areas without the possibility of physical or chemical stimulation such as radiation. However, the patient had a history of two fractures and suffered from tuberculosis for a long time, whether it stimulates the growth of tumor and whether it has any induction and promotion effect is yet to be studied.
(B) Cytology of multiple myeloma
1. Cytokinetics of myeloma cells
In the early stage of multiple myeloma, i.e. preclinical stage, the cell proliferation time is less than 72h, and it takes about 1~2 years before the clinical manifestation of myeloma gradually appears. And when its clinical manifestation is obvious, the proliferation time of tumor cells is gradually prolonged, which is about 4~6 months. When the tumor proliferates to a certain volume, the number of myeloma cells can remain on the horizontal line for several months or even years. Multiple myeloma cells are terminal cells, which need to be supplemented by the proliferation and differentiation of malignant B cells with clonal expansion and differentiation ability that are in the earlier differentiation period. This period is called the cell stabilization phase. Studies have shown that if myeloma cells are killed during the stable phase, the proliferative phase also increases. Therefore, it is necessary to use cell cycle specific drugs along with cell cycle non-specific drugs during the treatment process to achieve better results.
2. The rate of monoclonal immunoglobulin synthesis in myeloma cells.
Myeloma cells have the ability to synthesize huge immunoglobulin (M protein), and the M protein produced in 2-4 hours is equivalent to the total amount of immunoglobulin contained in the cells. Studies have projected that each myeloma cell contains about 5 to 10 million molecules of M protein, and each myeloma cell synthesizes 2.5 to 38 Pg of M protein per day.
3. Total number of myeloma cells in the patient’s body
The total number of myeloma cells in the body is directly proportional to the clinical severity (e.g. the degree of osteolytic lesions). When there are multiple osteolytic lesions, the number of tumor cells in the body has exceeded 2×1012. If the total number of tumor cells is about 5%-7% of body weight, it can be fatal.
(C) Cellular immunological changes of multiple myeloma
1. Alteration of T cell subsets
The absolute number of T3+, T4+, and T8+ cells is decreased in stage I, II, and III, while the absolute number of T8+ cells is increased in stage I, normal in stage II and III, and the percentage is increased in all stages. The increase in T8+ cells is thought to be an early compensatory effect of the tumor clone proliferation.
Alterations in T cell function
Perri et al. concluded that Th cell function is normal in patients with multiple myeloma, while Ts mimetic B cell activity is higher than normal, and B cells in patients with multiple myeloma are more sensitive to Ts cell activity in multiple myeloma. Due to the defective T cell function, the synthesis and secretion of normal polyclonal immunoglobulins in the organism are reduced, and there is an abnormal increase of immunoreactive M proteins in the body. In addition, the phagocytic and chemotactic functions of granulocytes in patients are significantly lower, antibody-dependent cytotoxicity is reduced, and NK cell activity is decreased, resulting in increased susceptibility of the organism to pathogenic micro-organisms.
3. Alteration of cytokine activity
Abnormal peripheral blood cytokine production in patients with multiple myeloma The cytokines associated with the development of multiple myeloma are IL-1, IL-2, IL-4, IL-5, IL-6, etc. Studies have shown that a decrease in IL-4 (BSF-1) – B-cell stimulating factor-1 – leads to a decrease in peripheral blood B cells, resulting in inhibition of normal immunoglobulin synthesis. Myeloma cells secrete IL-6 (BSF-2), which in turn has a BSF-2 receptor on its surface that promotes tumor proliferation through its own positive feedback effects. a study by Cimino et al. found that IL-1 and SLR-2R in the serum of patients did not differ from normal controls. Studies on the changes of IL-2 levels are inconclusive.
4. Changes in B lymphocytes
Tienhaara et al. showed that the total number of peripheral blood B lymphocytes and the absolute number and percentage of CD20+ cells corresponding to age were significantly reduced in the control group of patients with multiple myeloma. Therefore, the immune function corresponding to B lymphocytes is also low or defective.
(iv) Clinical manifestations [4, 5, 6, 7, 8]
Multiple myeloma has a slow onset, and patients may have an asymptomatic period of several months to more than 10 years. During this period, there may be increased sedimentation, M globulin or proteinuria of unknown origin, which is called “preclinical”.
The clinical manifestations of multiple myeloma are complex and varied. According to the clinical analysis of 2547 cases in China, the main symptoms are bone pain, anemia, fever, infection, bleeding, renal insufficiency, arthralgia, gastrointestinal symptoms, neurological symptoms, skeletal deformation and pathological fracture. The clinical manifestations are mainly due to the infiltration of malignant proliferating plasma cells, skeletal and extramedullary tissues and the increase of M globulin.
1. Infiltrative clinical manifestations
(1) Bone pain: Myeloma cells proliferate relatively indefinitely in the bone marrow cavity, invade the bone and periosteum, and cause bone pain. Bone pain is often the early and main symptom, among which lumbosacral pain is the most common, followed by chest pain, limb and other parts of pain. Early pain is mild and can be wandering or intermittent, and thus easily mistaken for rheumatic pain. In the later stages, pain is more intense, aggravated by activity and weight bearing, and relieved by rest and treatment. Bone pain is often an early and important clue for diagnosis.
(2) Bone deformation and pathological fracture
Myeloma cells infiltrate and destroy the cortical blood supply, causing diffuse osteoporosis limited bone destruction and can form local masses, which are often multiple. The occurrence of cotton ball-like nodules at the junction of the thorax, ribs and clavicle has diagnostic significance for the disease. Bone destruction can easily cause pathological fractures, and often multiple fractures exist simultaneously.
(3) Damage to hematopoietic organs
Since the tumor foci are mainly in the red bone marrow, anemia is common and may be the first symptom. Anemia is mostly moderate and severe in later stages; thrombocytopenia is common and may be accompanied by bleeding symptoms.
(4) Extramedullary infiltration The spleen, liver, lymph nodes and kidneys are the most common organs and tissues invaded. The chance of solitary soft tissue myeloma in respiratory tract and oral cavity is more than other sites.
(5) Neurological lesions
They may appear first or later. The most common is paraplegia caused by compression of the spinal cord in the thoracic and lumbar spine. Pathological fractures are also another important cause of bone marrow compression, and in most cases, corresponding burning nerve root pain can occur prior to paraplegia. Cranial tumors can cause direct compression causing corresponding clinical symptoms. Peripheral neuropathy is dominated by progressive, symmetric sensory-motor deficits in the distal extremities.
2. Clinical manifestations caused by large amount of M protein and its polypeptide chain
(1) Renal function impairment
About half of the patients with multiple myeloma have renal function impairment. M protein and its polypeptide chains can cause renal tubular degeneration, dilation and occlusion, leading to destruction of renal units and renal failure. Renal failure can be chronic or acute, and is the second leading cause of death after infection in this disease.
(2) Susceptibility to infection
The massive production of M protein, reduced formation of normal immunoglobulins and increased metabolism of r-globulin catabolism are the main reasons for susceptibility to infection. Patients with this disease are susceptible to infection, 15 times higher than normal. Gram-negative bacillary infections have predominated in recent years; viral (e.g., herpes nodosum) infections have also increased, and infection is often the main cause of death in this disease.
(3) Hyperviscosity syndrome
Increased blood viscosity in patients with multiple myeloma is associated with a large increase in M protein in the serum and changes in the viscosity of the protein itself. The increased blood viscosity affects blood circulation and intracapillary perfusion, causing stasis and ischemic and hypoxic changes in tissues and organs. Among them, the brain, eye, kidney and extremities are the most obvious.
(4) Hemorrhagic dumping of blood
Common for this disease, the causes vary. Decreased platelet production, platelet dysfunction due to M protein, and direct mimicry of factor VIII activity by M protein are all causes of hemorrhage.
3. Other
(1) Associated with other tumors
Autopsy shows that about 19% of patients with this disease may have other tumors in combination, and the incidence of non-lymphoreticular system tumors increases significantly, especially breast cancer, brain cancer, and biliary tract tumors. Combinations of Hodgkin’s disease, lymphosarcoma, reticulocytic sarcoma, myelofibrosis, Kaposi’s sarcoma, etc. have also been reported.
(2) Close relationship with lymphocytic and autoimmune diseases
Golderberg et al. reported that their incidence of rheumatoid arthritis was much higher than the incidence in the general population. Concomitant dermatomyositis and other diseases have also been reported.
(E) Laboratory tests
1. Peripheral blood picture
Anemia is generally moderate. The anemia is of the normocytic normal pigment type. The size of red blood cells varies, and a small number of young granular and juvenile red blood cells can be seen in the blood. In the late stage, there is often a decrease in whole blood cells due to bone marrow infiltration and suppression by chemotherapeutic drugs. The erythrocyte sedimentation rate is significantly increased due to a significant increase in plasma globulin.
2. Bone marrow examination
Bone marrow aspiration biopsy has specific diagnostic significance for this disease. The lesion site shows that the bone marrow nucleated cells are mostly proliferating actively or significantly active. When the plasma cells are above 10% with abnormal morphology, the possibility of this disease should be considered. Myeloma cells vary in size and morphology, and the nuclear chromatin is loose and detailed, and the perinuclear lightly stained ring is mostly absent. The cytoplasm is basophilic, dark blue and opaque foamy, and some cells have Russell vesicles in the cytoplasm. Some tumor cells have Russell vesicles in the cytoplasm, and some are filled with large, pale blue vacuoles and have a three-dimensional appearance, called grape cells. A few binucleated, trinucleated and multinucleated tumor cells are also seen. According to the 6th European Hematology Conference in 1957, myeloma cells are classified into 4 grades: Grade I: mature (small) plasma cell type. Grade II: Juvenile plasma cell type. Grade III: protoplasmic cell type. Grade IV: reticulocytic type. If the disease is suspected but the puncture is negative, it should be noted that: (1) the bone marrow tissue is viscous and interspersed with areas of extreme proliferation of tumor cells and poor hematopoietic cells, and it is not easy to obtain bone marrow tissue if the puncture site happens to be in a poorly proliferated area. In the early stage of the disease, the bone marrow lesions are focal and nodular in distribution, so it is advisable to do multi-site and regular punctures. Since the sternum is easily involved, sternal puncture should be an important diagnostic step if necessary. It can be combined with X-ray puncture at the lesion site to achieve a high positive rate.
3. Abnormal globulin
(1) This week (coagulation) protein
In 50~80% of myeloma patients, urine is positive for Benzylparaben. In the early stage of the disease, Benzedrine often appears intermittently, but it appears frequently in the late stage. Therefore, even if Benzedrine is negative, the disease cannot be ruled out, and the urine should be checked repeatedly and regularly. In addition, this week’s protein is not unique to this disease, other diseases such as metastatic carcinoma of the bone, multiple sarcomas, fibrocystic tumors and many other diseases can also show positive reactions.
(2) Hyperglobulinemia and M protein appearance
In about 95% of patients, serum globulins are increased and the ratio of albumin is inverted. An abnormal electrophoretic pattern, M globulin, can be seen in acetate membrane electrophoresis, which is mainly a densely stained and dense band of single-peaked raised immunoglobulins, with a few double peaks. Applying immunoelectrophoresis, according to the different components of M protein, it can be divided into: ①IgG type accounting for 50%-60%. ②IgA type accounts for 20%-25%. (③) Coagulation lysin or light chain type accounted for 20%. ④IgD type accounts for 1.5%, often accompanied by into the light chain. ⑤IgE type and IgM type, accounting for only 0.5% and 0.1%,. (6) “Non-secretory” myeloma, in which M protein cannot be isolated from the serum, accounts for about 1%.
4. Others
Due to extensive bone destruction, a large amount of calcium enters the blood circulation, resulting in hypercalcemic blood; in patients with advanced stage and renal insufficiency, blood phosphorus may be significantly increased. Serum alkaline phosphatase is mostly normal or mildly elevated, which is different from bone metastasis cancer. Serum urea nitrogen and creatinine are increased.
(F) X-ray examination [2, 3]
1. There is often no positive change in skeletal X-ray examination in the early stage of the disease. According to the study of tumor cell dynamics, only when the unit tumor cells proliferate to a certain number can the foci of destruction visible on X-ray appear. Magnification photography is helpful for early detection.
2. Extensive osteoporotic changes
The tumor is characterized by extensive bone density loss, thinning of bone trabeculae, thinning of bone cortex, chestnut-shaped bone destruction, uneven cortex, and intermittent discontinuity. The site of osteoporosis is prone to pathological fractures, especially in the ribs and spine.
3. Multiple Bone Destruction
If the tumor grows rapidly, it often shows osteolytic destruction with soft tissue masses and blurred margins; if it grows slowly, it shows swelling changes with clear margins. Bone destruction can be manifested in several ways.
(1) Penetrating: When tumor cells proliferate in multiple confined nodes to form spherical nodes, they appear as multiple round translucent areas without sclerotic margins or periosteal changes, and the edges of the lesions are sharp. It is most common in the skull.
(2) Honeycomb pattern: It is a number of cystic bone rupture ring areas of similar size, overlapping close to each other.
(iii) Rat bite: a dentate area of destruction with blurred margins, fused into a large area of destruction.
(iv) Soap bubble shape: capsular bone defects of varying sizes, separated by curved thin walls.
⑤ Eggshell shape: seen at the end of long bones, it is a thin layer of bone cortex remaining after severe bone destruction.
4. Sclerotic bone changes: Rarely seen, and the sites and modes of sclerotic bone changes are also diverse.
(VII) Other auxiliary examinations
In recent years, it has been found that CT scan for multiple myeloma has the following advantages: (1) All X-ray findings can be confirmed. (2) The larger extent of the lesion, especially the extent of extramedullary infiltrative lesions, can be better determined. (3) The detection of multiple myeloma lesions that are negative on X-ray, especially in the early stages of the lesion.
Since the skeletal invasion in patients with multiple myeloma is mainly osteolytic. Measurement methods of increased bone formation such as alkaline phosphatase and radionuclide scan are not helpful.
Clinical staging and staging.
1. General staging There are five types: isolated, multiple, diffuse, extramedullary, and leukemic, and each type can be interconverted.
2. Immunoglobulin typing: IgG, IgA, IgG, IgD, light chain, EgE, non-chemotropic, etc.
3. Special types are named as smoldering myeloma, isolated myeloma, myeloma with more than two M proteins, and hemimolecular IgA multiple myeloma, etc.
4. Staging According to Duriie staging criteria as follows.
Stage I: The following conditions must be met: hemoglobin > 100g/l (10g/dl) normal blood calcium, normal bone X-ray or isolated osteolytic lesion, M globulin IgG 1-2×1012 units/m2.
Stage II: between stages I and III.
(H) Diagnosis and differential diagnosis
The diagnosis of a typical case of multiple myeloma is not difficult. It is mainly based on the finding of abnormal plasma cell infiltration by bone marrow aspiration biopsy, destructive bone changes by X-ray, and the presence of M protein or/and light chains in urine by serum electrophoresis. The diagnosis should be accompanied by a good differential diagnosis.
1. Bone marrow aspiration biopsy reveals a large number of myeloma cells
This is the main diagnostic basis. However, plasmacytosis can also be seen in rheumatoid arthritis, metastasis of intra-myeloid tumors, chronic inflammation and many other diseases, but in the above diseases, plasma cells usually do not exceed 10% and there is no morphological abnormality.
2. Bone destructive changes This should be differentiated from tumor bone metastasis, senile osteoporosis, hyperparathyroidism, etc.
3. Hyperglobulinemia
Mainly M protein and/or proteinuria (this week’s protein can be detected in urine), but M protein and this week’s protein can also be seen in other diseases such as metastatic cancer, macroglobulinemia, multiple sarcomas, etc.
(ix) Treatment
There is no cure for this disease, but systemic chemotherapy and supportive therapy have made significant progress in the reduction of myeloma cells, improvement of clinical symptoms and signs, and recovery of health status.
Chemotherapy is the most effective chemotherapeutic agent for cell cycle non-specific drugs. Phenylalanine nitrogen mustard and cyclophosphamide are the first choice. In the past, MDC (multidrug combination chemotherapy) was the mainstay, and the MP regimen (marfalan + prednisone) is now recommended as the standard regimen of choice for induction of remission in multiple myeloma. the VAD regimen is also considered to be an induction regimen with fewer drugs, high efficacy, and rapid efficacy.
2. Supportive therapy
For patients with concomitant symptoms, symptomatic or emergency treatment of red blood cell transfusion and injection of androgens to promote normal hematopoiesis to correct anemia. For hypercalcemia, apply high-dose prednisone or/and add calcitonin, etc. Treatment of hyperuricemia with oral allopurinol. Those with increased blood viscosity use penicillamine or consider plasma separation to control infection and improve renal function. For spinal cord compression, apply high-dose hormones, local radiotherapy or emergency laminectomy and decompression. For bone pain, apply analgesic drugs and radiotherapy. For those with pathological fracture, treat according to general fracture treatment principles. Internal fixation can be done. If the lesions of the extremities involve soft tissues, palliative amputation can be considered.
3. Radiotherapy The disease is sensitive to radiotherapy. In case of local bone pain or pathological fracture, local irradiation can reduce the symptoms, but it will not help much in the course of the disease.
4. Other
In addition to the traditional treatment methods, people began to explore new ways to treat this disease, such as alpha-interferon treatment of this disease, in vitro studies have confirmed that the combination of alpha-interferon and mafenamic acid has a synergistic effect, and with prednisone full use has a strengthening effect. Other scholars began to study bone marrow transplantation (BMT) for this disease, homozygous homogeneous BMT has good efficacy, but cannot avoid late relapse, how to solve this problem still needs further exploration.
III. Review
MM lesions invade red bone marrow sites throughout the body, and this feature is similar to bone metastases, and MM clinical and X-ray manifestations are complex and difficult to diagnose. When a patient undergoes X-ray examination because of local symptoms and bone destruction is found, first of all, it must be differentiated from local masses, and MM with a mandibular mass as the first symptom needs to be differentiated from a local mass in the mandible. In this case, the patient was first seen in the local hospital, so as a surgeon, we must always have a warning line to catch the distinctive traces of the disease, and we must not “see the forest for the trees”. The diagnosis of “mandibular tumor” and the treatment plan of “partial mandibular osteotomy and mandibular reconstruction with free iliac bone graft” proved to be a common problem of many surgeons, that is, they overly believe that “surgery is the only effective way to solve the problem”. “, focusing only on the local and not the whole body. The patient was referred to our hospital because he thought the surgery was relatively large. Then, after detailed history taking and clinical examination we gradually found out that the disease is different from ordinary primary mandibular swelling. Firstly, the swelling could be basically identified as malignant tumor for several reasons: from the imaging point of view, the swelling showed osteolytic changes, and there were symptoms of nerve damage, and the patient showed symptoms such as lower lip numbness and lower lip muscle weakness, while from the medical history and general condition, the change of osteomyelitis could be excluded. Secondly, the patient had a swelling as the first symptom, and the mandibular bulge appeared first, followed by numbness of the lower lip, which was significantly different from the pathogenesis of central carcinoma of the mandible. From the imaging point of view, the growth of the swelling did not take the inferior alveolar nerve canal and the bone marrow cavity as the long axis for growth, but was an osteolytic change starting from the destruction of the lower edge of the mandible, and did not show periosteal reaction and osteogenic changes. Finally, the age of the patient did not suggest the possibility of osteosarcoma. So at this point, we gradually put our eyes on the whole body, tending to the diagnostic consideration of the mandible as a metastatic lesion with the primary foci in other parts of the body. With the consent of the patient’s family, PET showed: right mandibular mass with multiple abnormal hypermetabolic foci in bone and soft tissue, consistent with the manifestation of a malignant lesion. The abnormal hypermetabolic foci in the lower right side of the bladder and prostate-related examination were recommended. The right mandibular tumor was considered to be metastatic cancer. The patient’s family has been informed of the possibility of metastatic cancer, and the patient’s family strongly requested to do the surgery as soon as possible with the main purpose of clarifying the pathology. In this case, excision of the local mass was performed and no repair was performed.