Bilateral cervical lymph nodes are visible, and these two major causes are actually the cause

Acute suppurative lymphadenitis and chronic lymphadenitis are important causes of bilateral cervical lymph nodes. The common pathogens of acute suppurative lymphadenitis are Staphylococcus aureus and hemolytic Streptococcus; chronic lymphadenitis can be a consequence of acute lymphadenitis, or it can be a reaction to the stimulation of low-toxic infection of the face and neck and the body's strong resistance.

1. Acute suppurative lymphadenitis: The common pathogens of acute suppurative lymphadenitis are Staphylococcus aureus and hemolytic Streptococcus. The source of infection can be any purulent inflammation of the mouth, face, scalp and neck, such as odontogenic infection (apical periodontitis, periodontitis, pericoronitis and gingivitis, etc.), perimaxillary space infection, jaw inflammation, oral mucosal infection and ulcers, tonsillitis, pharyngitis, furunculosis of the facial skin and scalp, etc. The infection can also come from injuries to the oral and maxillofacial area. Among them, those secondary to odontogenic infection and oral infection are the most common. Especially for infants and children, whose overall resistance is low and whose lymph node barrier defense structure is imperfect, upper respiratory tract infection and tonsillitis can easily cause this lymphadenitis.

The pathological changes of acute suppurative lymphadenitis (including catarrhal inflammation) are degeneration and exudation. In the early stage, the lymph nodes are congested, the sinus cavities are dilated, the reticuloendothelial cells are shedding, and there is infiltration of neutrophils and monocytes in the lymph sinuses of the marginal sinuses and paracortical areas of the lymph nodes. After these cells engulf bacteria, they denature and collapse, forming cell fragments and denatured substances. At the same time, the lymphatic sinuses are enlarged and may have varying degrees of sinus cell hyperplasia, and there is also immunoblastic hyperplasia in the deep cortical area. As these cells increase in number, the meshwork between the cells decreases, and the sinuses and cords become less recognizable. In the late stage, there is cell necrosis, lymph nodes are destroyed and necrosis occurs. After a large amount of necrosis is formed, it becomes an abscess, which can break through the capsule to form lymphadenitis or glandular cellulitis. Of course, there are cases where acute inflammation turns into chronic lymphadenitis due to timely medication or enhanced immune function of the body.

2. Chronic lymphadenitis: Chronic lymphadenitis can be a consequence of acute lymphadenitis, or it can be a reaction to the stimulation of low-toxic infection of the face and neck and the body's strong resistance.

In addition to degeneration and exudative changes, chronic lymphadenitis often presents as a variety of reactive hyperplasia with extremely complex morphology. Especially at this time, the clinical inflammatory symptoms are not obvious, so differential diagnosis is also difficult. Its pathological morphology of reactive hyperplasia can be roughly divided into five types: ① necrotic fragment type; ② diffuse hyperplasia type; ③ follicular hyperplasia type; ④ vascular hyperplasia type; ⑤ fibrous nodular type. In general, the early stage of lymphadenitis is mainly characterized by exudation and necrosis, the middle stage is mainly characterized by reactive hyperplasia of lymphoid tissue, and the late stage is mainly characterized by vascular hyperplasia and fibrosis. Relatively speaking, the proliferative changes in the middle stage are easily confused with malignant lymphoma or metastatic carcinoma; some atypical changes also need to be differentiated from a variety of other lymph node lesions.