Radiology/Pathology Correlation

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A 58-year-old man with a history of mining presents with progressive low-grade shortness of breath.


Imaging Findings:

Figure 1. Chest Radiograph

Describe the abnormality. Answer




Figure 2. HRCT

Describe the abnormality and indicate its location;

  • primarily centrilobular,
  • primarily along and in contact with interlobular septa and pleural surfaces,
  • random (equally in centrilobular, interlobular septal, and pleural locations).

Is emphysema present? Answers

What is the differential diagnosis? Answer


For more information about anatomy by HRCT, click here, here, and here.



Figure 3. Gross Pathology

This slice of lung from another patient shows circumscribed black nodules about a centimeter in diameter. The centrilobular location of the nodules is best seen in the lower lung where interlobular septa are prominent. Some nodules border the pleura. All are about the same size. Conglomerate masses are absent. Note the enlargement and fibrosis of the black-pigmented peribronchial lymph nodes. There is no emphysema in this lung.

Find 2 peribronchial lymph nodes. Click on the structure in the image to get verification.

In the region of the lung with well-defined fibrotic interlobular septa:

Find two centrilobular nodules.

Find a nodule at the periphery of the lobule in contact with the interlobar fissure.


Figure 4. Histopathology

The lesions all had a similar appearance. This one is made up of coalescent nodules, each with layers of collagen around an amorphous center that contains some black pigment. The surrounding histiocytes also contain black pigment.


What is this lesion?

What is the histologic differential diagnosis? Answers

Scroll down after answering the questions.













Silicosis is a disease resulting from the inhalation of crystalline silica (SiO2) particles, which are ubiquitous in the earth's crust. The disease occurs in metal or hard rock miners, and also in persons in a number of occupations where silica is used; e.g., ceramics and foundry work. A similar but distinct disease, coal worker's pneumoconiosis (CWP), results from the inhalation of coal dust [1,2].

Silicosis may be divided into acute silicoproteinosis or accelerated disease (not discussed here) and chronic silicosis. Chronic silicosis, occurring at lower doses than acute or accelerated disease and over many years, may be divided into simple or complicated forms; the latter is characterized by the development of conglomerate masses. Simple silicosis is often associated with few respiratory symptoms, whereas the development of complicated silicosis is usually accompanied by deterioration in pulmonary function [3,4]. Silicosis predisposes to tuberculosis and non-tuberculous mycobacterial infection, an association recently highlighted in South African gold miners with and without HIV infection [5].

Chest radiographs in patients with simple silicosis usually show well-defined nodules, 2-5 mm in diameter (range, 1-10 mm), that have an upper lobe and posterior lung zone predominance. Although silicosis and CWP are not easily distinguished by imaging methods, the nodules associated with silicosis tend to be more well-defined than those of CWP. In silicosis hilar lymphadenopathy may often be present, and may calcify in a peripheral pattern (so-called "eggshell" calcification) in 5% of cases.

The development of opacities greater than 1 cm in diameter (usually in the upper lobes) on a background of small nodules indicates the presence of complicated silicosis. These opacities tend to migrate toward the hila, leaving irregular airspace enlargement in their wake. Cavitation of these opacities suggests the diagnosis of tuberculosis [2].

HRCT scans in patients with silicosis typically reveal 2-5 mm, well-defined, centrilobular (sometimes subpleural) nodules that may calcify. The nodules favor the upper lobes, and tend to be more widely and evenly distributed than nodules that are seen with sarcoidosis. Hilar lymphadenopathy, occasionally calcified, may also be evident [6].

Although silica has been classified as a lung carcinogen in humans, the status of either silica exposure or silicosis as a lung carcinogen is still controversial [7].

A number of inflammatory cytokines including TNF-alpha and interleukin-1 (IL-1) have been shown to be elevated in the lungs of experimental animals breathing silica. These cytokines in turn stimulate the production of other inflammatory mediators. Recently, certain gene polymorphisms of TNF-alpha and IL-1 have been associated with susceptibility to [8] and severity of silicosis [8,9]. These polymorphisms help to explain the imperfect dose-response relationships between silica exposure and disease.

Comments on the Radiographic Features

Comments on the Pathologic Features

Final Diagnosis: Simple silicosis


1. Beckett W, et al. Adverse effects of crystalline silica exposure. Am J Respir Crit Care Med 1997; 155:761-765.

2. Silicosis and Silicate Disease Committee. Diseases associated with exposure to silica and nonfibrous silicate minerals. Arch Pathol Lab Med 1988; 112:673-720.

3. Bergin C, Müller N, Vedal S, Chan-Yeung M. CT in silicosis: correlation with plain films and pulmonary function tests. AJR Am J Roentgenol 1986; 146:477-483. abstract

4. Begin R, Ostiguy G, Cantin A, Bergeron D. Lung function in silica-exposed workers. A relationship to disease severity assessed by CT scan. Chest 1988; 94:539-545. abstract

5. Corbett E, Churchyard G, Clayton T, Williams B, Mulder D, Hayes R, De Cock K. HIV infection and silicosis: the impact of two potent risk factors on the incidence of mycobacterial disease in South African miners. AIDS 2000; 14:2759-2768. abstract

6. Akira M, Higashihara T, Yokoyama K, Yamamoto S, Kita N, Morimoto S, Ikezoe J, Kozuka T. Radiographic type p pneumoconiosis: high-resolution CT. Radiology 1989; 171:117-123. abstract

7. Wong O. The epidemiology of silica, silicosis and lung cancer: some recent findings and future challenges. Ann Epidemiol 2002; 12:285-287.

8. Yucesoy B, Vallyathan V, Landsittel D, Sharp D, Weston A, Burleson G, Simeonova P, McKinstry M, Luster MI. Association of tumor necrosis factor-alpha and interleukin-1 gene polymorphisms with silicosis. Toxicol Appl Pharmacol 2001; 172:75-82. abstract

9. Corbett EL, Mozzato-Chamay N, Butterworth AE, De Cock KM, Williams BG, Churchyard GJ, Conway DJ. Polymorphisms in the tumor necrosis factor-alpha gene promoter may predispose to severe silicosis in black South African miners. Am J Respir Crit Care Med 2002; 165:690-693. abstract


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Frontal chest radiograph shows numerous, small, scattered, well-defined nodules.




























HRCT shows numerous, well-defined nodules scattered throughout the lung parenchyma in a relatively even distribution. The nodules are primarily centrilobular in location, but some are located in the pleura. Note the variation in size of the nodules. Emphysema is absent.





























Differential diagnosis: Silicosis, coal worker's pneumoconiosis, mixed dust pneumoconiosis, sarcoidosis, and lymphangitic spread of carcinoma































Peribronchial lymph node





























Centrilobular nodule































Peripheral nodule in contact with the interlobar fissure




























































Answer: This is a silicotic nodule made up of a group of coalescent solitary nodules. Click here to see a solitary nodule. Histologically, the differential diagnosis includes the end, fibrotic stage of any fungal or mycobacterial granuloma or a granuloma of sarcoidosis. However, silicotic nodules do not begin as granulomas, but rather as collections of crystal-containing histiocytes that gradually become fibrotic.

Silicotic nodules should not be referred to as granulomas.

If it were of fungal origin, organisms could probably be found in it by a Gomori methenamine silver stain. Stains for acid fast organisms would be negative in a fibrotic granuloma such as this one even if it were of tuberculous origin.