Secondary amyloidosis in chronic osteomyelitis
One of the main causes of secondary (systemic) amyloidosis is long-standing purulent inflammation. A typical example of such a condition is chronic hematogenous osteomyelitis, which develops as an outcome of the acute septic form of the disease.
The mechanism of complication development is closely associated with severe morphological changes in bone tissue:
- Focuses of suppuration (abscesses) are constantly present in the bone marrow.
- Zones of bone tissue necrosis form around the abscesses — sequestration occurs with the formation of bone cavities containing necrotic fragments (sequestra).
- Periosteal formation of new bone actively proceeds in adjacent areas, leading to its sharp thickening and pronounced deformation. The periosteum undergoes sclerosis.
- Fistulous tracts form, through which pus and small sequestra escape outward.
It is chronic intoxication and continuous tissue decay against the background of prolonged pus discharge from fistulas that trigger the pathogenetic mechanisms of secondary amyloidosis. Without timely and adequate surgical debridement of the purulent focus, the process progresses steadily.
Amyloidosis as an extraintestinal complication of dysentery
In addition to purulent-destructive processes in the bones, secondary amyloidosis can develop against the background of prolonged intestinal infections accompanied by deep ulcerative lesions of the mucous membranes. In particular, it has been described as one of the severe extraintestinal complications of dysentery.
During the healing stage of dysenteric ulcers (which begins even before clinical recovery), the following processes occur:
- Ulcerative defects of the intestinal wall are actively filled with granulation tissue.
- Granulations gradually mature with the formation of dense connective tissue.
- With extensive and deep lesions, coarse scars form, capable of causing cicatricial stenosis (narrowing of the intestinal lumen).
Along with local changes (such as perforations, bleeding, or toxic megacolon), systemic reactions develop. Extraintestinal complications of severe dysentery, in addition to infectious-toxic shock, liver abscesses, bronchopneumonia, and toxic arthritis, include systemic amyloidosis resulting from pronounced exhaustion (cachexia) and prolonged immune imbalance.
Stromal amyloidosis in oncomorphology
Amyloid deposits can be not only systemic, but also local in nature. In pathological anatomy of the skin, local amyloidosis is considered one of the microscopic criteria in the study of malignant epithelial neoplasms.
In particular, histological examination of basal cell carcinoma reveals specific changes in the interaction between the tumor parenchyma and its stroma. The weakening of the connection between these components is accompanied by:
- Deposition of amyloid deposits directly in the stroma, between growths of solid tumor cell complexes.
- Formation of mucinous cysts in the central zones of tumor complexes due to degenerative processes.
- Accumulation of melanophages in the stromal component and increased cell pigmentation during melanocyte proliferation.
Unlike other differentiation features (such as the formation of "horn pearls" and intercellular bridges characteristic of squamous cell carcinoma), the detection of amyloid in the stroma using standard hematoxylin and eosin staining serves as an important additional landmark for the morphologist.
Differential diagnosis of organ lesions
When studying pathological anatomy, it is important to differentiate amyloidosis from other severe dystrophic and necrotic processes in organs that occur during infections.
For example, in pronounced intoxication against the background of diphtheria, necrotic nephrosis develops in the kidneys rather than amyloidosis (which is sometimes mistakenly assumed by students). Diphtheria exotoxin causes direct cell damage, which is also accompanied by adrenal hemorrhages (acute insufficiency), severe paralysis due to nerve ganglion damage, and croup development when localized in the respiratory tract. Systemic amyloid deposition, however, requires a different pathogenetic background — chronic inflammation with prolonged antigenic stimulation.
To remember the main causes of secondary amyloidosis from the course, use the "Bones and Intestines" association: chronic Osteomyelitis (fistulas and sequestra) + severe Dysentery (non-healing ulcers).
Class and exam questions
How is amyloidosis detected in skin tumor tissue?
The presence of prolonged purulent inflammation, abscesses, and fistulas leads to continuous tissue decay and chronic intoxication, which triggers the production of abnormal proteins precipitating in tissues as amyloid.
How is amyloidosis detected in basal cell carcinoma tissue?
Amyloid deposits in the stroma between tumor complexes are visualized using conventional histological staining of specimens with hematoxylin and eosin.
Does renal amyloidosis develop in diphtheria?
No, in pronounced diphtheritic intoxication, necrotic nephrosis develops in the kidneys; amyloidosis is not typical for this acute infection.
What else to study on this topic
- Pathological anatomy of chronic hematogenous osteomyelitis
- Histological structure of basal cell and squamous cell carcinoma
- Ulcer healing stage and complications in dysentery
- Complications of diphtheria (nerve and muscle damage, necrotic nephrosis)
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