Mucoid Swelling: The Reversible Phase
This is the initial and fully reversible stage of connective tissue disorganization. It is based on the accumulation of hydrophilic substances (primarily hyaluronic acid) and plasma proteins, especially globulins.
The reaction cascade is triggered by microcirculatory damage. Due to the resulting tissue hypoxia, the enzyme hyaluronidase is activated, leading to the weakening of chemical bonds between glycosaminoglycans (GAGs) and proteins. Simultaneously, fibroblasts begin to actively synthesize new GAGs.
Histological Picture:
- The ground substance swells, pushing stromal cells apart.
- Collagen fibers undergo fiber separation and swelling, but retain their bundle structure.
- Macroscopically, organs are unchanged at this stage.
Key diagnostic sign — metachromatic reaction. When stained with cationic dyes (e.g., toluidine blue), free acidic GAGs shift the medium pH, causing the tissue to acquire a lilac or purple color instead of blue.
Historical note: The term "mucoid swelling" was introduced by A.I. Strukov. Foreign pathologists rarely use this term, preferring "chromotropic edema" or similar concepts.
Fibrinoid Swelling: The Point of No Return
If the pathogenic factor continues to act, the process transitions into a profound and irreversible stage. Total degradation of collagen, fibronectin, and depolymerization of GAGs occur. Vascular permeability increases sharply.
In the lesion focus, fibrinoid is formed — a complex mass consisting of decaying fiber proteins, nucleoproteins from destroyed cells, and plasma proteins. Fibrin is an obligatory component.
Microscopic Changes:
- Collagen fibers merge into homogeneous masses.
- The tissue becomes sharply eosinophilic (plasma proteins block GAG residues, shifting the pH to the alkaline side).
- Metachromasia is completely absent because glycosaminoglycans are destroyed.
- The PAS reaction is sharply positive due to an abundance of glycoproteins.
The process is often accompanied by a cellular reaction (macrophages, plasma cells) and can be systemic (in rheumatic diseases) or local (spasm and damage to arterioles in hypertension).
Hyalinosis of Vessels and Tissues
Hyalinosis is the finale of profound destructive processes. It is always preceded by plasmorrhagia, fibrinoid swelling, inflammation, or necrosis.
Tissue becomes irreversibly dense, vessel walls thicken and become homogeneous, and their lumens narrow. This inevitably leads to hypoxia, parenchymal atrophy, and organ sclerosis.
Classification of Vascular Hyaline:
- Simple hyaline. Formed from minimally altered plasma components. Found in benign hypertension, atherosclerosis, and occasionally in healthy individuals.
- Lipohyaline. Contains lipids and $\beta$-lipoproteins. Specific for patients with diabetes mellitus.
- Complex hyaline. Consists of immune complexes, fibrin, and cellular detritus. Characteristic of diseases with an immunopathological component (e.g., rheumatic fever).
Clinically, hyalinosis and the preceding fibrinoid necrosis lead to severe consequences: cardiac valve deformities, loss of joint mobility, and acute kidney injury (when glomerular involvement occurs in malignant hypertension).