The 'cold abscess' of skeletal tuberculosis lacks classical signs of inflammation. This is because:

• A M. tuberculosis secretes interleukin-10, which universally suppresses TNF-alpha
• B Mycobacterial cell wall lipids prevent vascular penetration to the abscess site
• C The granulomatous reaction and caseous necrosis evolve slowly with predominantly mononuclear (not neutrophilic) infiltrate and limited prostaglandin release, avoiding the heat and redness of acute pyogenic infection ✓
• D The hypoxic environment of caseous necrosis inhibits complement activation

Explanation

Cold abscesses in TB represent accumulations of liquefied caseous material within a granulomatous, predominantly mononuclear cell reaction. Unlike pyogenic infections driven by neutrophil-mediated acute inflammation (with prostaglandins causing redness, heat, and pain), the TB granulomatous process develops slowly with delayed-type hypersensitivity, minimal acute phase mediators, and fibrous encapsulation — hence no warmth or rubor despite fluctuant pus. Mycobacterial lipoglycans (cord factor, LAM) do modulate macrophage response but the key pathological distinction is mononuclear vs neutrophilic dominance.

Reference: Maheshwari Essential Orthopaedics, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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