Benign prostatic hyperplasia (BPH) represents the most commonly diagnosed urological disease in men after the fifth decade. Although BPH etiology remains uncertain in some aspects, several mechanisms have been proposed to be involved in the pathogenesis and progression of BPH.

First, aging represents the most significant risk factor for the development of BPH and the compliant of lower urinary tract symptoms (LUTS). In aging men, an interference in growth factor pathway occurs and a significant tissue-remodeling process takes place, leading to prostatic enlargement. Second, hormonal alterations have been proposed to be involved in BPH pathogenesis and progression. Indeed, the development of BPH requires the presence of testicular androgens, and BPH tissue has higher dihydrotestosterone activity than normal prostate gland tissue.

Additionally, insulin resistance with secondary hyperinsulinemia has been proposed to be involved in the development of BPH. Third, a role of increased sympathetic nerve activity has also been proposed. Finally, in the last few years, the role of prostatic inflammation as a crucial part of BPH pathogenesis and progression has emerged. The chronic inflammatory condition may contribute to tissue injury, activating cytokine release and increasing the concentration of growth factors, creating a local vicious cycle. In this context, the upregulation of proinflammatory cytokines has been widely reported in prostatic tissues of patients with BPH. Concluding, all these data support the hypothesis that tissue damage, hypoxia, and chronic process of wound healing lead to a persistent process of stimulation of stromal and epithelial prostatic tissues, potentially resulting in BPH [2, 3].

Risk factors for the development of BPH are poorly understood. Some studies have suggested a genetic predisposition, and some have noted racial differences. Approximately 50 % of men under the age of 60 who undergo surgery for BPH may have a heritable form of the disease. This form is most likely an autosomal dominant trait, and first-degree male relatives of such patients carry an increased relative risk of approximately fourfold.

Interestingly, it has been hypothesized that inflammatory infiltrate leads to tissue damage and to a chronic process of wound healing that might subsequently determinate prostatic enlargement [4].

BPH is the most common benign tumor in men, and its incidence is age related. The prevalence of histological BPH in autopsy studies rises from approximately 20 % in men aged 41–50 to 50 % in men aged 51–60 and to >90 % in men older than 80. Although clinical evidence of disease occurs less commonly, symptoms of prostatic obstruction are also age related. At age 55, approximately 25 % of men report obstructive voiding symptoms. At age 75, 50 % of men complain of a decrease in the force and caliber of their urinary stream [5, 6].

The symptoms of BPH can be divided into obstructive and irritative complaints. Obstructive symptoms include hesitancy, decreased force and caliber of stream, sensation of incomplete bladder emptying, double voiding (urinating a second time within 2 h of the previous void), straining to urinate, and post-void dribbling. Irritative symptoms include urgency, frequency, and nocturia. A detailed history focusing on the urinary tract excludes other possible causes of symptoms that may not result from the prostate, such as urinary tract infection, neurogenic bladder, urethral stricture, or prostate cancer.

A physical examination, digital rectal examination (DRE), and focused neurologic examination are performed on all patients. The size and consistency of the prostate is noted, even though prostate size, as determined by DRE, does not correlate with severity of symptoms or degree of obstruction. BPH usually results in a smooth, firm, elastic enlargement of the prostate. Induration, if detected, must alert the physician to the possibility of cancer and the need for further evaluation (i.e., prostate-specific antigen (PSA), transrectal ultrasound (TRUS), and biopsy) [7].

A urinalysis to exclude infection or hematuria and serum creatinine measurement to assess renal function are required. Renal insufficiency may be observed in 10 % of patients with prostatism and warrants upper-tract imaging. Patients with renal insufficiency are at an increased risk of developing postoperative complications following surgical intervention for BPH.

Serum PSA is considered optional, but most physicians will include it in the initial evaluation [8].

In some cases of benign prostatic hyperplasia are also observed high levels of PSA, but they are not considered index of malignant progression, but rather are due to the increase in prostate volume, consequently the most production of the antigen itself. PSA, compared with DRE alone, certainly increases the ability to detect CaP, but because there is much overlap between levels seen in BPH and CaP, its use remains controversial (see Screening for CaP) [9].

Benign prostatic hyperplasia is a disease characterized by an enlargement (hyperplasia or hypertrophy) of the prostate, more specifically in the prostatic epithelial cells and stromal cells, which leads to the formation of nodules in the periurethral region of the prostate. When these nodules become large enough to compress the urethral canal, causing a partial obstruction of the same, they interfere with normal urinary flow.

The hyperplastic prostate may consist of pure fibroleiomyomatous nodules or of pure glandular or of mixed glandular-atrophic-cystic areas. Frequently, these structures are intermixed. The smooth muscle fiber content of the prostate changes when concomitant chronic inflammatory processes are present. If, after transurethral resection in a recurrent hyperplastic gland, chronic transurethral resection (TUR)-prostatitis has developed, the fibromatous portion increases with little or no nodule formation. Vascularization and cellular content also change.

The prostate is an immunocompetent organ, and it is normally populated by a small number of inflammatory cells (i.e., T and B lymphocytes, macrophages, and mast cells).

Prostate tissue inflammatory patterns have been also widely assessed in patients with BPH. Robert et al. recently characterized the inflammatory infiltrate in a large cohort of patients surgically treated for BPH. Interestingly, 81 % of patients had T-lymphocytes infiltrates (CD-3), 52 % B cells (CD-20), and 82 % macrophage markers (CD-163) in BPH tissues. Thus, T cells represented the major component of the inflammatory infiltrate seen within the prostate gland. Moreover, an increased expression of B lymphocytes and macrophages was reported. These antigen-presenting cells play an important role in the activation of T lymphocytes and in the subsequent onset of an inflammatory state.

Prostatic calcifications are common in men with BPH and their incidence increases with age. Interestingly, calcifications were also seen in 47.2 % of younger men aged <50 years with urological complaints. In some studies [10], the incidence and significance of calcifications in patients with chronic pelvic pain syndrome were evaluated. In these patients, calcifications detected at TRUS were significantly associated with greater inflammation and longer symptoms duration. Other authors found that patients with larger stones were at higher risk of developing LUTS or prostatitis [11]. It could be speculated that in young patients, alterations in the prostatic fluid related to infections or inflammatory diseases might result in prostatic calcifications, which may obstruct intraprostatic ducts and subsequently enhance the inflammatory process. Particularly, calcifications could be the expression of previous infections leading to a chronic inflammatory process, with higher risk of subsequent BPH development over time.

In the last few years, magnetic resonance imaging (MRI) has been shown to be of great value in the imaging of the pelvis. Its advantages derive from the capability to obtain sections in direct axial, sagittal, and coronal planes and to show greater soft-tissue contrast than any other imaging modality [12]. In fact, CT does not easily provide direct coronal and sagittal images and does not visualize the internal architecture of prostate and seminal vesicles. Transrectal US is widely used as a first-choice exam in the study of prostatic pathology and gives a clear demonstration of the glandular texture. However, its limitation, when compared with MRI, is that it provides only a limited view of the pelvic structures surrounding the prostate and seminal vesicles.

T2-weighted MR imaging is the workhorse of prostate MR imaging. T2-weighted MR images have high spatial resolution and, thus, can clearly differentiate the normal intermediate- to high-signal-intensity peripheral zone (PZ) from the low-signal-intensity central and transition zones in young male subjects. In the aging man, owing to variable extension of the transition zone due to benign prostatic hyperplasia (BNH), the size and signal intensity of the prostate transition zone may vary. BPH itself is a round, well-defined, inhomogeneous area with (variable) intermediate signal intensity and a low-signal-intensity rim that surrounds the expanded transition zone. Because of transition zone expansion, the remainder of the compressed central zone is often indefinable on MR images (Fig. 7.1) [13, 14].

High-spatial-resolution T2-weighted rapid acquisition with refocused echo sequences with a small field of view, performed with endorectal and/or external body phased-array coils, is generally used to depict prostate anatomy. T1-weighted contrast in the prostate is very low. Therefore, it is not possible to appreciate the different anatomic zones on T1-weighted images. Therefore, a suggestion for minimal requirements for multiparametric MR imaging is a combination of T1- and T2-weighted imaging with DW or dynamic contrast-enhanced MR imaging. Owing to the presence of BPH, cancer in central and transition zones is more difficult to discern, BPH may have signal intensity similar to that of prostate cancer on T2-weighted images. However, it has been reported that features such as low-signal-intensity lesions with a wedge shape and a diffuse extension without mass may be reliable signs of benignity. Dynamic contrast-enhanced (DCE) MR imaging consists of a series of fast T1-weighted sequences covering the entire prostate before and after rapid injection (2–4 mL/s) of a bolus of a low-molecular-weight gadolinium chelate. A fast and direct method of characterizing prostatic vascular pharmacokinetic features is high temporal resolution DCE-MRI (<10 s). DCE-MRI consists of a series of axial T1WI gradient echo sequences covering the entire prostate during and after IV bolus injection of gadolinium contrast medium [15]. Diffusion-weighted imaging (DWI) is a powerful clinical tool, as it allows apparent diffusion coefficient (ADC) maps to be calculated, enabling qualitative and quantitative assessment of the prostate. Diffusion-weighted imaging should be acquired in the axial plane with an echo planar imaging sequence employing parallel imaging [16].

The MRI appearance of BPH is characteristic, though no tissue-specific diagnosis of benign disease can be made with certainty. The prostate is usually enlarged but can also be of normal size. On T1WI, the gland has a homogeneous intermediate-low signal intensity with no evidence of intraglandular zonal abnormalities. On T2WI, the appearance is that of a nonhomogeneous texture, mainly in the central gland, with alternating areas of intermediate and high signal (Fig. 7.1). The different signals of the various nodules are related to their relative stromal or epithelial components. The benign central gland is composed of two histologically distinct types of tissue: glandular tissue, which is hyperintense on T2-weighted images (Fig. 7.2), and stromal tissue, which is hypointense and can mimic CG cancer (Fig. 7.3). Like CG cancer, the majority of stromal hyperplastic foci could also demonstrate homogeneously low signal intensity and had ill-defined margins. The majority of glandular tissue foci are homogeneously hyperintense.

Sometimes each individual adenomatous nodule is surrounded by a hypointense rim of tissue (Figs. 7.1 and 7.4). MR images are usually obtained in more than one plane to allow accurate evaluation of prostatic volume. In addition, sagittal images are particularly suited to demonstrate impingement on the base of the bladder and the effect of the adenomatous nodules on the bladder neck and prostatic urethra. Stromal and sclerotic nodules of benign hyperplasia, if located in the peripheral zone where malignancy and inflammation usually occur, can appear the same as prostatitis or carcinoma.

Dynamic contrast-enhanced MRI in BPH can show accentuation of contrast already in the early phase after contrast administration but more frequently has a more delayed enhancement that increases progressively up to a plateau, reflecting the increased microvessel density in BPH (Figs. 7.2 and 7.5) [13].

Diffusion MR imaging parameters of central gland hyperplasia change according to the presence of stromal (ADC 1.27 × 10⁻³ mm²/s) or glandular hyperplasia (ADC: 1.73 × 10⁻³ mm²/s); therefore, it can be misleading to calculate a single diffusion parameter to represent the entire benign central gland. There is a considerable overlap between central gland carcinoma and stromal hyperplastic foci (Fig. 7.4).

After patients have been evaluated, they should be informed of the various therapeutic options for BPH. It is advisable for patients to consult with their physicians to make an educated decision on the basis of the relative efficacy and side effects of the treatment options.

Specific treatment recommendations can be offered for certain groups of patients. For those with mild symptoms (symptom score 0–7), watchful waiting only is advised.

On the other end of the therapeutic spectrum, absolute surgical indications include refractory urinary retention (failing at least one attempt at catheter removal), recurrent urinary tract infection from BPH, recurrent gross hematuria from BPH, bladder stones from BPH, renal insufficiency from BPH, or large bladder diverticula [18, 19].