DISCUSSION

Osteoarthritis (OA) is a significant burden on both individuals and society. Although difficult to describe, it is defined by discomfort associated with the use and structural abnormalities of all synovial joint tissues, including ligaments, cartilage, subchondral bone, synovium, and capsule . ¹⁶

The relationship between OA and vascular damage has been recognized and researched previously. Surely, the vascular model cannot account for all clinical symptoms in OA, including osteophyte production, although this and some other traits are likely secondary responses to joint mechanical changes. According to Conaghan and colleagues, OA, or at least its structural evolution, maybe largely an atheromatous vascular disease of subchondral bone .¹⁶ In a recent systemic review published in 2020, proof from several studies suggested a positive association between the severity of vascular pathology and the likelihood of having hand or knee OA. The results of this systematic review support the hypothesis that vascular pathology may be involved in OA initiation and progression with consistent evidence for an association of vascular pathology with hand and knee OA .¹⁷ Pathological changes in blood vessels (vascular pathology), particularly atherosclerosis or thickening of the arterial wall, and OA are common chronic conditions associated with aging and obesity.⁵ Our study was carried out on a total of 56 patients (mean age of all studied patients was 56.2 ± 8.4 years), 12 males (21.4%) and 44 females (78.6%). In both male and female groups, the hand pain group was significantly higher in number than those who reported no hand pain at the time of assessment, and the figures were statistically similar between the male and female groups. The male "no pain" group had just two patients, and the low capillary density was found in the patient with severe X-ray severity classification. In the male group with pain, the highest morphological abnormalities and lower capillary density were found in the moderate X-ray severity classification. While in the females, the highest of both were found in the mild X-ray severity classification in the "No pain" group, and similar to the males in the "Pain" group. One of the earliest and most well-known works on Osteoarthritic capillaroscopic findings was that of Conners and McGrath .¹⁸

We contrasted the nailfold capillaries of 28 patients with distal interphalangeal joint OA to those of 23 age- and sex-matched controls without OA. Individuals with OA had a considerably decreased capillary density in their nail folds and substantially more capillary morphological anomalies, such as bleeding, 'drop out,' irregularity, and dilatation. Although we detected no hemorrhages or dropouts in our OA patients, the rest of their observations certainly agreed with our findings (Figure 3 A, B). We did not compare to normal controls in our study as we were more focused on describing the visible abnormalities found in the known pathologic group.

Fig. 3: A                                      B

Their assessment included the measurement of digital artery pressure using a doppler flowmeter. The pressure was determined in the finger in both the baseline and heated states, and the ratio of the finger pressure to the systolic brachial artery pressure was calculated. The results are given as a person's average digital to systemic blood pressure ratio per digit.

In their findings, It was discovered that individuals associated with OA had warmer fingertips and lowered finger to brachial blood pressure ratios. Additionally, they discovered strong relationships between the number of capillaries in the nailfold and the average joint discomfort, as well as between capillary morphological alterations and joint swelling. This agrees with our finding about clear higher morphological anomalies in the male pain group than the non-pain group.  These findings establish a link between interphalangeal joint OA and capillary anomalies and density in the Nailfold. The decreased capillary density in that location naturally results in decreased blood perfusion (shown in 73.2% of our OA patients).

 Vascular anomalies may play a role in the process and may explain why the condition is frequently found in the distal digit joints. Over a century ago, an ischemia process related to OA structural disease was proposed .¹⁹  Surprisingly, a minor investigation of this possibility was reported, although NFC has been an easily available and widespread tool to rheumatologists now for many years.  The observed defects may represent irregularities in the vascular supply of the synovium or juxta-articular bone in the underlying DIP joints, which may result in decreased oxygenation or nutritional intake, as well as vulnerability to reperfusion or immunological insult. On the other hand, vascular abnormalities may occur due to DIP joint disruption caused by OA and play no role in the pathophysiology of joint anomalies.

 Patients were checked once, at least three days after discontinuing anti-inflammatory treatment. This was also done in our study; we were careful not to examine patients who have had physiotherapy sessions on their hands 24 hours before the NFC assessment.

 Since both Conners and McGrath's and our studies are cross-sectional, the data cannot establish a causal association between these vascular anomalies and the onset or progression of OA.

Another interesting and more recent study was carried out by Fioverenti and colleagues ²⁰, who compared the capillaroscopic microvascular patterns in 56 patients with Erosive OA, 46 patients with Nodal OA, and 50 normal controls. The general classification was different from ours as well as the aim of assessment; they described that NFC in erosive OA was similar in findings described for psoriatic arthritis. One of their interesting findings that we did not encounter in our study group was detecting many capillary enlargements in the erosive OA group (about 40%). They also found a statistically significant difference between OA patients and controls regarding tortuous loops, which was one of our prominent morphological abnormalities in our OA patients. They did not assess capillary density. Morphological changes were found in almost all our OA subgroups, with varying degrees in different X-ray severity classes. The total morphological changes were found in 32 out of 56 patients (57%).

This is somewhat like Fioverenti's findings; they found regular-shaped capillaries in 53 percent of the erosive and 46 percent of the nodal group. So, about half of their total studied OA patients had morphological pathologies. They did find microhemorrhages in 11 out of their 23 OA patients; while we found no evident signs of microhemorrhages in our group, but we were keen to exclude any patient with recent hand trauma, autoimmune disease, peripheral vascular disease, or any other external possible cause of capillary hemorrhages from the beginning. Notable to say is that their OA age group was higher than ours, 60.5+-6.6 for erosive and 60.2+-7.0 for nodal, while (Ours was 56.2 ± 8.4). The male to female ratio in their study group was relatively like ours. Our study found low capillary density in most of the indeed studied OA group of patients (73.2%), but it was a mild affection (7-9 capillaries per mm), (Figure (4), A, B).

A                                                   B

Penin and colleagues worked on NFC in osteoarthritis and SSC patients, and they also found mildly reduced capillary density in OA. Additionally, there were statistically significant variations in the degree of density loss in individuals with systemic sclerosis compared to those with OA and other rheumatic diseases. ²¹

CONCLUSION

Our findings gave a general description of the NFC findings most likely to be encountered in OA patients; most of our patients were female, and, in both males and females, those with hand pain were significantly more than those without hand pain. No great NFC differences were found between male and female groups or between different severities of radiographic findings.

More research is needed on OA pathology and association with vascular abnormalities, and how utilization of NFC can be more helpful in diagnosis and follow-up of OA or help differentiate it from other rheumatic diseases affecting small joints of the hands, especially the DIP.

The limitations of our study were mainly the low number of patients and were performed as a single-center study. Indeed, a larger and more widespread cohort would have yielded more reliable results. The disease duration was not considered in our work, despite being a significant decisive factor on many variables in OA. Also, more clinical, and not just radiographic grouping and correlations were needed to help better understand the NFC changes observed in this group of patients.